naloxone and Vomiting

naloxone has been researched along with Vomiting* in 58 studies

Reviews

4 review(s) available for naloxone and Vomiting

ArticleYear
Impact of prolonged-release oxycodone/naloxone on outcomes affecting patients' daily functioning in comparison with extended-release tapentadol: a systematic review.
    Clinical therapeutics, 2015, Jan-01, Volume: 37, Issue:1

    The objective of this systematic review was to assess the clinical efficacy, safety, tolerability, and health-related quality of life outcomes associated with management of moderate-to-severe chronic pain with oxycodone/naloxone and tapentadol, focusing on the effect of these treatments on patients' daily functioning.. Literature from a wide range of sources, including Embase, MEDLINE, MEDLINE In-Process, and the Cochrane Central Register of Controlled Trials, was searched to identify randomized controlled trials investigating tapentadol or oxycodone/naloxone for the treatment of patients with chronic pain. A network meta-analysis was conducted to determine the relative efficacy and safety profiles of these treatments.. Oxycodone/naloxone was significantly better than tapentadol with respect to the Patient Assessment of Constipation Symptoms total score (risk ratio = -3.60; 95% credible interval, -5.36 to -2.11) and revealed a significantly lower risk of dizziness (risk ratio = 0.72; 95% credible interval, 0.42-0.98). Oxycodone/naloxone was directionally favored, although not significantly superior to tapentadol for headache, fatigue, dry mouth, dyspepsia, and withdrawals due to lack of efficacy. For the AE outcomes of constipation, nausea, and vomiting, as well as pain efficacy and all-cause withdrawals from studies, tapentadol was directionally favored without any statistical difference from oxycodone/naloxone. However, the two treatments were not wholly comparable for the evaluation of pain efficacy because of differences in on-study rescue medication and a higher baseline pain severity in the tapentadol studies.. Oxycodone/naloxone offers significant improvements in Patient Assessment of Constipation Symptoms total score and dizziness and was directionally favored for fatigue and headache compared with extended-release tapentadol, which may translate to improved patient daily functioning and health-related quality of life.

    Topics: Chronic Pain; Constipation; Delayed-Action Preparations; Double-Blind Method; Drug Combinations; Headache; Humans; Naloxone; Nausea; Oxycodone; Phenols; Quality of Life; Tapentadol; Vomiting

2015
[Prevention by naloxone of adverse effects of epidural morphine analgesia for cancer pain].
    Annales francaises d'anesthesie et de reanimation, 1991, Volume: 10, Issue:2

    Forty cancer patients were randomly assigned to two groups (n = 20). All had incapacitating pain unresponsive to the usual non opioid analgesic drugs. An epidural catheter was set up at the level of the most painful metamere, and made to pass subcutaneously so as to exit either in the supraclacicular fossa, or on the patient's flank. At T0, the patients were given 4 mg morphine hydrochloride diluted in 10 ml normal saline. Thirty min later, patients in the naloxone group (group N) were given a 0.4 mg bolus, followed by a constant rate infusion of 5 micrograms.kg-1.h-1, of naloxone hydrochloride during 18 h. Patients in group P (placebo) were given normal saline instead. The degree of pain was studied with a visual analogue scale and analgesia was assessed by a clinician on a five point scale. These two parameters were obtained half an hour after the injection of morphine and 2, 4, 6 and 24 hours later. At the same time, the patients were questioned about adverse side-effects: nausea, vomiting, pruritus, dysuria, urinary retention. Respiratory depression was assessed clinically and biologically (blood gas measurements at the afore mentioned times). Heart rate, systolic and diastolic blood pressure were also measured. There was no statistically significant difference between the groups in quality and duration of analgesia. Pain reached its lowest level 4 h after the injection of morphine, returning to half its original value at the 24th h. This was also true for the incidence of nausea (11 in group N, 5 in group P), vomiting (3 in both groups), and urinary retention (6 in group P, 5 in group N).(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adult; Aged; Analgesia, Epidural; Chronic Disease; Double-Blind Method; Female; Humans; Male; Middle Aged; Morphine; Naloxone; Nausea; Neoplasms; Pain; Pain Measurement; Pruritus; Respiration Disorders; Urinary Retention; Vomiting

1991
Regulation of nausea and vomiting in cancer chemotherapy. A review with emphasis on opiate mediators.
    The American journal of pediatric hematology/oncology, 1988,Fall, Volume: 10, Issue:3

    Chemotherapy-induced nausea and vomiting are primarily regulated by chemoreceptor trigger zone (CTZ)-vomiting center (VC) pathways. Dopaminergic (D2), histaminic (H1), and muscarinic cholinergic (Ach) receptors are present in these sites, and specific receptor antagonists are potent but not "universal" antiemetics when used alone or in combination. Recently, neurons containing the endogenous opiate enkephalin were also identified near the CTZ and the VC. Furthermore, opiates stimulate vomiting at the CTZ and inhibit vomiting at the VC in dogs and in cats. A dose-related increase in nausea and vomiting in response to the opiate antagonist naloxone has also been demonstrated in patients receiving cancer chemotherapy. These observations support a role for endogenous opiates in regulating chemotherapy-induced nausea and vomiting; further, they suggest that narcotic agents may be effective antiemetics in this setting.

    Topics: Antineoplastic Agents; Chemoreceptor Cells; Child; Endorphins; Humans; Naloxone; Nausea; Neoplasms; Vomiting

1988
Advances in clinical toxicology.
    Pediatric clinics of North America, 1985, Volume: 32, Issue:1

    New data are reviewed in two areas in the management of the acute overdose: gastrointestinal decontamination and systemic antidotes. The mechanism and effectiveness of Ipecac syrup, gastric aspiration and lavage, activated charcoal, gastrointestinal dialysis, and saline cathartics are discussed. Special problems posed by disc batteries and packet ingestion of cocaine (in transporting contraband) are highlighted. The pharmacology and uses of pyridoxine and naloxone as antidotes are detailed.

    Topics: Antidotes; Cathartics; Charcoal; Child; Cocaine; Deglutition; Foreign Bodies; Gastric Lavage; Humans; Ipecac; Isoniazid; Naloxone; Narcotics; Poisoning; Pyridoxine; Substance-Related Disorders; Suction; Time Factors; Toxicology; Vomiting

1985

Trials

9 trial(s) available for naloxone and Vomiting

ArticleYear
The optimal dose of prophylactic intravenous naloxone in ameliorating opioid-induced side effects in children receiving intravenous patient-controlled analgesia morphine for moderate to severe pain: a dose finding study.
    Anesthesia and analgesia, 2011, Volume: 113, Issue:4

    Opioid-induced side effects, such as pruritus, nausea, and vomiting are common and may be more debilitating than pain itself. A continuous low-dose naloxone infusion (0.25 μg/kg/h) ameliorates some of these side effects in many but not all patients without adversely affecting analgesia. We sought to determine the optimal dose of naloxone required to minimize opioid-induced side effects and to measure plasma morphine and naloxone levels in a dose escalation study.. Fifty-nine pediatric patients (24 male/35 female; average age 14.2 ± 2.2 years) experiencing moderate to severe postoperative pain were started on IV patient-controlled analgesia morphine (basal infusion 20 μg/kg/h, demand dose 20 μg/kg, 5 doses/h) and a low-dose naloxone infusion (initial cohort: 0.05 μg/kg/h; subsequent cohorts: 0.10, 0.15, 0.25, 0.40, 0.65, 1, and 1.65 μg/kg/h). If 2 patients developed intolerable nausea, vomiting, or pruritus, the naloxone infusion was increased for subsequent patients. Dose/treatment success occurred when 10 patients had minimal side effects at a naloxone dose. Blood samples were obtained for measurement of plasma morphine and naloxone levels after initiation of the naloxone infusion, processed, stored, and measured by tandem mass spectrometry with electrospray positive ionization.. The minimum naloxone dose at which patients were successfully treated with a <10% side effect/failure rate was 1 μg/kg/h; cohort size varied between 4 and 11 patients. Naloxone was more effective in preventing pruritus than nausea and vomiting. Concomitant use of supplemental medicines to treat opioid-induced side effects was required at all naloxone infusion rates. Plasma naloxone levels were below the level of assay quantification (0.1 ng/mL) for infusion rates ≤0.15 μg/kg/h. At rates >0.25 μg/kg/h, plasma levels increased linearly with increasing infusion rate. In each dose cohort, patients who failed therapy had comparable or higher plasma naloxone levels than those levels measured in patients who did not fail treatment. Plasma morphine levels ranged between 3.52 and 172 ng/mL, and >90% of levels ranged between 10.2 and 61.6 ng/mL. Plasma morphine levels were comparable between patients who failed therapy and those patients who achieved symptom control.. Naloxone infusion rates ≥1 μg/kg/h significantly reduced, but did not eliminate, the incidence of opioid-induced side effects in postoperative pediatric patients receiving IV patient-controlled analgesia morphine. Patients who failed therapy generally had plasma naloxone and morphine levels that were comparable to those who had good symptom relief suggesting that success or failure to ameliorate opioid-induced side effects was unrelated to plasma levels.

    Topics: Adolescent; Analgesia, Patient-Controlled; Analgesics, Opioid; Antiemetics; Antipruritics; Baltimore; Child; Dose-Response Relationship, Drug; Female; Humans; Infusions, Intravenous; Male; Morphine; Naloxone; Narcotic Antagonists; Nausea; Odds Ratio; Pain Measurement; Pain, Postoperative; Prospective Studies; Pruritus; Regression Analysis; Severity of Illness Index; Spectrometry, Mass, Electrospray Ionization; Tandem Mass Spectrometry; Vomiting

2011
Pilot study of continuous co-infusion of morphine and naloxone in children with sickle cell pain crisis.
    American journal of hematology, 2008, Volume: 83, Issue:9

    Patients with sickle cell disease experience painful crises that often require hospitalization for a continuous infusion of morphine that may cause significant pruritus. We conducted a pilot study to determine the feasibility of simultaneous continuous co-infusion of naloxone with morphine, test novel assessment instruments for pruritus, and explore whether pruritus could be reduced while maintaining effective analgesia. Patients with sickle cell disease and painful crisis requiring continuous infusion morphine received continuous co-infusion of naloxone at 0.25 (low dose) or 1.0 mcg/kg x hr (high dose). Pain scores were obtained using the FACES scale and a 100-mm visual analog scale (VAS). Itching was quantified by a modified VAS score. Evaluable data were obtained on 16 patients. Simultaneous co-infusion of naloxone and morphine was feasible, did not seem to reduce the analgesic efficacy of morphine, and was associated with no adverse effects. The high dose group reported a lower median "VAS worst itch" score than the low dose group (4.8 vs. 7.3, P = 0.08). Simultaneous continuous infusion of naloxone with morphine in pediatric patients with sickle cell disease and pain crisis was feasible and well tolerated. A quantitative pruritus score allowed us to systematically measure pruritus. Further evaluation by randomized, placebo-controlled study of 1 mcg/kg x hr naloxone in this setting is required.

    Topics: Adolescent; Anemia, Sickle Cell; Child; Drug Therapy, Combination; Female; Humans; Hyperalgesia; Infusions, Intravenous; Male; Morphine; Naloxone; Narcotic Antagonists; Narcotics; Nausea; Pain; Pain Measurement; Pilot Projects; Pruritus; Vomiting

2008
Low-dose naloxone does not improve morphine-induced nausea, vomiting, or pruritus.
    The American journal of emergency medicine, 2005, Volume: 23, Issue:1

    We tested the hypothesis that low-dose naloxone delivered with intravenous (IV) bolus morphine to emergency department patients in pain would reduce nausea.. Randomized, double-blind, placebo-controlled trial. Patients receiving 0.10 mg/kg morphine IV bolus rated pain, nausea, and pruritus on 100-mm visual analog scales at enrollment and 20 minutes. Patients were randomized to 0.25 microg/kg naloxone or equal volume placebo administered with IV morphine.. One hundred thirty-one enrolled, 99 (76%) treated according to protocol with sufficient data for analysis. At 20 minutes the difference between groups (naloxone-placebo) was 1 mm (95% CI [confidence interval], -9 to 11) for nausea, 1 mm (95% CI, -3 to 3) for pruritus, 4% (95% CI, -1 to 9) for vomiting, and 0% (95% CI, -5 to 5) for rescue antiemetics. Pain was significantly reduced in both groups.. Addition of 0.25 microg/kg naloxone to bolus morphine does not improve nausea, pruritus, vomiting, or reduce use of rescue antiemetics when administered to emergency department patients in pain.

    Topics: Adult; Analgesia; Double-Blind Method; Female; Humans; Infusions, Intravenous; Male; Morphine; Naloxone; Narcotic Antagonists; Nausea; Pain Measurement; Prospective Studies; Pruritus; Treatment Outcome; Vomiting

2005
Naloxone partly counteracts apomorphine side effects.
    Clinical neuropharmacology, 1991, Volume: 14, Issue:5

    The effects of naloxone on side effects provoked by apomorphine (APO) administration in patients with parkinsonian syndrome have been studied. The group under study included eight patients with Parkinson's disease and four with parkinsonism who received 100 micrograms/kg s.c. APO acutely to test dopaminergic responsiveness. All patients were treated with 20 mg domperidone tablets t.i.d. and then for 2 consecutive days (in double blind fashion) were given a 2-hour i.v. saline infusion alone or with naloxone (8 mg) starting 30 min before APO administration. In both groups, naloxone delayed the appearance of sleepiness, and reduced the intensity of yawning, sleepiness, nausea, and vomiting as compared with saline. These findings indicate a potential usefulness of naloxone and other opioid antagonists in preventing acute APO side effects.

    Topics: Apomorphine; Double-Blind Method; Female; Humans; Male; Naloxone; Nausea; Parkinson Disease; Sleep Stages; Vomiting; Yawning

1991
[Prevention by naloxone of adverse effects of epidural morphine analgesia for cancer pain].
    Annales francaises d'anesthesie et de reanimation, 1991, Volume: 10, Issue:2

    Forty cancer patients were randomly assigned to two groups (n = 20). All had incapacitating pain unresponsive to the usual non opioid analgesic drugs. An epidural catheter was set up at the level of the most painful metamere, and made to pass subcutaneously so as to exit either in the supraclacicular fossa, or on the patient's flank. At T0, the patients were given 4 mg morphine hydrochloride diluted in 10 ml normal saline. Thirty min later, patients in the naloxone group (group N) were given a 0.4 mg bolus, followed by a constant rate infusion of 5 micrograms.kg-1.h-1, of naloxone hydrochloride during 18 h. Patients in group P (placebo) were given normal saline instead. The degree of pain was studied with a visual analogue scale and analgesia was assessed by a clinician on a five point scale. These two parameters were obtained half an hour after the injection of morphine and 2, 4, 6 and 24 hours later. At the same time, the patients were questioned about adverse side-effects: nausea, vomiting, pruritus, dysuria, urinary retention. Respiratory depression was assessed clinically and biologically (blood gas measurements at the afore mentioned times). Heart rate, systolic and diastolic blood pressure were also measured. There was no statistically significant difference between the groups in quality and duration of analgesia. Pain reached its lowest level 4 h after the injection of morphine, returning to half its original value at the 24th h. This was also true for the incidence of nausea (11 in group N, 5 in group P), vomiting (3 in both groups), and urinary retention (6 in group P, 5 in group N).(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adult; Aged; Analgesia, Epidural; Chronic Disease; Double-Blind Method; Female; Humans; Male; Middle Aged; Morphine; Naloxone; Nausea; Neoplasms; Pain; Pain Measurement; Pruritus; Respiration Disorders; Urinary Retention; Vomiting

1991
Increased nausea and vomiting induced by naloxone in patients receiving cancer chemotherapy.
    The American journal of pediatric hematology/oncology, 1988,Fall, Volume: 10, Issue:3

    To evaluate the role of endogenous opiates in chemo-therapy-induced nausea and vomiting, the narcotic-antagonist naloxone was administered to six pediatric patients receiving cancer chemotherapy. Naloxone was administered by continuous intravenous (i.v.) infusion after randomized, double-blind controlled assignment at a dose of 0, 10 or 40 micrograms/kg/h for 12 h. Each patient was studied for four consecutive and identical courses of chemotherapy (eight courses for each naloxone dose or 24 courses in all). A dose-related increase in nausea (nausea score 2.5 +/- 2.24, 3.83 +/- 2.73, and 5.75 +/- 2.86/12 h, p = 0.003), vomiting (emetic events 6.0 +/- 7.50, 8.08 +/- 6.71, and 10.3 +/- 8.91/12 h, p = 0.035), and patient aversion (course preference rank 1.5 +/- 0.45, 2.83 +/- 1.17, and 3.25 +/- 0.42/4 courses, p = 0.014) was observed. The infusion of naloxone in the absence of chemotherapy was without effect. These results support a role for endogenous opiates in regulating chemotherapy-induced nausea and vomiting, and further suggest that narcotic agents may be effective antiemetics in this setting.

    Topics: Adolescent; Antineoplastic Agents; Chemoreceptor Cells; Child; Child, Preschool; Clinical Trials as Topic; Drug Synergism; Endorphins; Female; Humans; Male; Naloxone; Nausea; Neoplasms; Random Allocation; Vomiting

1988
Enhancement of the antiemetic action of metoclopramide against cisplatin-induced emesis by transdermal electrical nerve stimulation.
    Journal of clinical pharmacology, 1986, Volume: 26, Issue:2

    In a double-blind sequential trial, the influence of transdermal electrical nerve stimulation (TENS) was studied in patients who were treated with total infusions of metoclopramide 3.5 mg/kg to counter the emetic action of cisplatin 60-90 mg/m2. Transdermal electrical nerve stimulation further reduced the emetic episodes in ten of 11 treatment pairs (2 alpha = .10). This effect was blocked by naloxone. More surprisingly, TENS reduced the incidence of extrapyramidal effects of metoclopramide (i.e., akathisia and dystonia). These effects may be explained by the involvement of central nervous and peripheral TENS-induced production of opioid neuromodulators. An alternate hypothesis is the stimulation of serotonergic mechanisms via neuromodulation by opioid peptides, or by involvement of both systems.

    Topics: Adult; Aged; Cisplatin; Clinical Trials as Topic; Double-Blind Method; Electric Stimulation; Female; Humans; Male; Metoclopramide; Middle Aged; Naloxone; Nausea; Neoplasms; Random Allocation; Skin; Vomiting

1986
The effects of naloxone and nalorphine during the development of morphine dependence in rhesus monkeys.
    Pharmacology, 1977, Volume: 15, Issue:1

    A randomized and blind experimental design was used to study the effects of naloxone and nalorphine on the development of morphine dependence in monkeys. The results suggest: (a) that significant dose-related differences existed for combined numbers of withdrawal symptoms times frequency of occurrences; (b) that naloxone and nalorphine were qualitatively similar; (c) antagonists are more effective as dependence develops; (d) naloxone is approximately 10 times more potent than nalorphine, and (e) vomiting was the only withdrawal sign with which ED50s could be calculated. Dependence on morphine still increases up to 9 months after the commonly accepted 90-day stabilization period as measured by the ED50 for vomiting for naloxone.

    Topics: Animals; Dose-Response Relationship, Drug; Female; Haplorhini; Humans; Macaca mulatta; Male; Morphine; Morphine Dependence; Nalorphine; Naloxone; Substance Withdrawal Syndrome; Vomiting

1977
The antagonist effect of naloxone hydrochloride after neuroleptanaesthesia during neurosurgery.
    Acta anaesthesiologica Scandinavica, 1976, Volume: 20, Issue:3

    The effects of naloxone were studied in 82 patients undergoing intracranial surgery under general anaesthesia with fentanyl or phenoperidine. After the operation was finished the patients' alertness, sensitivity to pain, blood pressure, pulse rate, respiratory rate, tidal and minute volume were recorded parallel with arterial blood gas analyses prior to and immediately after the administration of varying amounts of naloxone i.v. in a single dose. These parameters were also repeatedly controlled for several hours in the postoperative period. The results show that a single i.v. naloxone dose of 1 mug/kg b.w. is effective in the rapid and definite reversal of the respiratory depression caused by the analgesics. This dose was neither correlated to the total amount of analgesics given, nor to the time period which elapsed between the last dose of the analgesic drug and the administration of naloxone. No side effects or complications were encountered when the indicated doses of naloxone were given. It is concluded that, even in a small single dose, naloxone effectively antagonises the respiratory depression caused by fentanyl and phenoperidine without totally eliminating the immediate postoperative analgesic effects of these agents.

    Topics: Adolescent; Adult; Aged; Anesthesia, General; Blood Pressure; Clinical Trials as Topic; Dose-Response Relationship, Drug; Drug Evaluation; Female; Fentanyl; Humans; Male; Middle Aged; Naloxone; Nausea; Neuroleptanalgesia; Neurosurgery; Partial Pressure; Phenoperidine; Pulse; Respiration; Shivering; Tidal Volume; Vomiting

1976

Other Studies

46 other study(ies) available for naloxone and Vomiting

ArticleYear
Case 6-2019: A 29-Year-Old Woman with Nausea, Vomiting, and Diarrhea.
    The New England journal of medicine, 2019, 02-21, Volume: 380, Issue:8

    Topics: Acetaminophen; Adult; Buprenorphine; Cocaine-Related Disorders; Diagnosis, Differential; Diarrhea; Drug Combinations; Female; Humans; Illicit Drugs; Naloxone; Narcotic Antagonists; Nausea; Opioid-Related Disorders; Oxycodone; Substance Abuse Detection; Vomiting

2019
Effects of naloxone on motion sickness in cats alone and with broad spectrum antiemetics.
    Autonomic neuroscience : basic & clinical, 2017, Volume: 202

    Doses of naloxone far below those which elicit emesis increase the sensitivity to motion sickness. In order to evaluate the possible interaction with broad spectrum antiemetics, low doses of naloxone were tested alone and in combination with 8-hydroxy-2-(di-n-propylamine)tetralin (DPAT), fentanyl and the NK1 antagonist CP-99994. A modified autonomic symptom rating scale was unaffected by any drug and thus considered of little value. Fentanyl and NK1 antagonists decreased the duration of the retch/vomit sequence. Naloxone alone and in combination with each of the drugs increased the duration of retching/vomiting. Naloxone also increased the number of vomiting sequences. The results are interpreted in terms of possible site(s) of action of the antiemetic drugs.

    Topics: 8-Hydroxy-2-(di-n-propylamino)tetralin; Animals; Antiemetics; Cats; Dose-Response Relationship, Drug; Drug Interactions; Emetics; Female; Fentanyl; Models, Animal; Motion Sickness; Naloxone; Neurokinin-1 Receptor Antagonists; Physical Stimulation; Piperidines; Vomiting

2017
Central effects of morphine on GI motility in conscious dogs.
    Brain research, 2007, Aug-29, Volume: 1166

    It has been suggested that morphine has dual effects; emetic effects and anti-emetic effects. The chemoreceptor trigger zone, which is outside the BBB, mediates the emetic effect. In contrast, the vomiting center mediates the anti-emetic effect of opioids. Thus, naloxone methiodide, which does not cross the BBB, antagonizes emetic effects of opioids. We studied whether naloxone methiodide alters abnormal motility pattern induced by morphine in gastrointestinal (GI) tract. Strain gauge force transducers were sutured on the serosal surface of upper GI tract to record the circular muscle contractions in eight dogs. The ventricular access system was implanted to inject morphine intracerebroventricularly (icv). Effects of icv-injection of morphine (0.3-3.0 mug/kg, bolus) on GI motility were studied during intravenous infusion of naloxone hydrochloride or naloxone methiodide. Icv-injection of morphine (3.0 mug/kg) induced retching and vomiting in all dogs tested. Phasic contractions of the jejunum were observed after icv-injection of morphine. These contractions in the jejunum migrated orally to the antrum (retrograde peristaltic contractions; RPCs). Both naloxone hydrochloride and naloxone methiodide treatment virtually abolished the emetic effects of morphine. Naloxone hydrochloride completely abolished morphine-induced RPCs in all dogs, whereas naloxone methiodide converted morphine-induced RPCs to anterograde peristaltic contractions (APCs) in 6 of 8 dogs. Our current study suggests that central opioids may induce APCs and prevent emesis in conscious dogs. Naloxone methiodide may be useful to prevent the undesired side effects of morphine.

    Topics: Analgesics, Opioid; Animals; Dogs; Drug Antagonism; Emetics; Female; Gastrointestinal Motility; Injections, Intraventricular; Jejunum; Male; Morphine; Naloxone; Narcotic Antagonists; Peristalsis; Pyloric Antrum; Vomiting

2007
Suboxone (buprenorphine/naloxone) toxicity in pediatric patients: a case report.
    Pediatric emergency care, 2007, Volume: 23, Issue:9

    Suboxone, a combination of buprenorphine and naloxone in sublingual tablet form, was recently approved in the United States for management of opioid dependence. Little information exists regarding the potential for opioid toxicity after Suboxone exposure in the pediatric population. We report a case of opioid toxicity after exposure to Suboxone in a pediatric patient and a review of other cases of pediatric Suboxone ingestion in the literature.. A previously healthy 2-year-old boy was found with 1 tablet of Suboxone (8 mg buprenorphine/2 mg naloxone) in his mouth. Remnants of the partly dissolved tablet were immediately removed from the child's oropharynx. The child experienced 1 episode of spontaneous emesis and became drowsy en route to the emergency department 30 minutes after the exposure. The patient was observed in the emergency department; no interventions were necessary, and the child was discharged asymptomatic and stable 6 hours post ingestion.. Suboxone, a combination of buprenorphine and naloxone, may produce opioid toxicity via sublingual absorption or ingestion by children. We present the case of a child with mild central nervous system depression after exposure to Suboxone. Pediatric case reports that demonstrate more significant central nervous system and respiratory depressant effects from Suboxone ingestion are emerging.

    Topics: Buprenorphine; Buprenorphine, Naloxone Drug Combination; Child, Preschool; Humans; Male; Naloxone; Narcotic Antagonists; Vomiting

2007
Effects of acupuncture on vasopressin-induced emesis in conscious dogs.
    American journal of physiology. Regulatory, integrative and comparative physiology, 2005, Volume: 288, Issue:2

    Although acupuncture has a significant clinical benefit, the mechanism of acupuncture remains unclear. Vasopressin, a posterior pituitary hormone, is involved in nausea and vomiting in humans and dogs. To investigate the antiemetic effects of acupuncture on vasopressin-induced emesis, gastroduodenal motor activity and the frequency of retching and vomiting were simultaneously recorded in conscious dogs. In seven dogs, four force transducers were implanted on the serosal surfaces of the gastric body, antrum, pylorus, and duodenum. Gastroduodenal motility was continuously monitored throughout the experiment. Vasopressin was intravenously infused at a dose of 0.1 U x kg(-1) x min(-1) for 20 min. Electroacupuncture (EA, 1-30 Hz) at pericardium-6 (PC6), bladder-21 (BL21), or stomach-36 (ST36) was performed before, during, and after the vasopressin infusion. To investigate whether the opioid pathway is involved in EA-induced antiemetic effects, naloxone (a central and peripheral opioid receptor antagonist) or naloxone methiodide (a peripheral opioid receptor antagonist) was administered before, during, and after EA and vasopressin infusion. Intravenous infusion of vasopressin induced retching and vomiting in all dogs tested. Retrograde peristaltic contractions occurred before the onset of retching and vomiting. EA (10 Hz) at PC6 significantly reduced the number of episodes of retching and vomiting. EA at PC6 also suppressed retrograde peristaltic contractions. In contrast, EA at BL21 or ST36 had no antiemetic effects. The antiemetic effect of EA was abolished by pretreatment with naloxone but not naloxone methiodide. It is suggested that the antiemetic effect of acupuncture is mediated via the central opioid pathway.

    Topics: Acupuncture Points; Animals; Central Nervous System; Dogs; Electroacupuncture; Female; Gastrointestinal Motility; Male; Naloxone; Narcotic Antagonists; Quaternary Ammonium Compounds; Receptors, Opioid; Vagus Nerve; Vasopressins; Vomiting

2005
Adverse events after naloxone treatment of episodes of suspected acute opioid overdose.
    European journal of emergency medicine : official journal of the European Society for Emergency Medicine, 2004, Volume: 11, Issue:1

    An increasing and serious heroin overdose problem in Oslo has mandated the increasing out-of-hospital use of naloxone administered by paramedics. The aim of this study was to determine the frequencies and characteristics of adverse events related to this out-of-hospital administration by paramedics.. A one-year prospective observational study from February 1998 to January 1999 was performed in patients suspected to be acutely overdosed by an opioid. A total of 1192 episodes treated with naloxone administered by the Emergency Medical Service system in Oslo, were included. The main outcome variable was adverse events observed immediately after the administration of naloxone.. The mean age of patients included was 32.6 years, and 77% were men. Adverse events suspected to be related to naloxone treatment were reported in 45% of episodes. The most common adverse events were related to opioid withdrawal (33%) such as gastrointestinal disorders, aggressiveness, tachycardia, shivering, sweating and tremor. Cases of confusion/restlessness (32%) might be related either to opioid withdrawal or to the effect of the heroin in combination with other drugs. Headache and seizures (25%) were probably related to hypoxia. Most events were non-serious. In three episodes (0.3%) the patients were hospitalized because of adverse events.. Although adverse events were common among patients treated for opioid overdose in an out-of-hospital setting, serious complications were rare. Out-of-hospital naloxone treatment by paramedics seems to save several lives a year without a high risk of serious complications.

    Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Confusion; Drug Overdose; Emergency Medical Services; Female; Headache; Humans; Male; Middle Aged; Naloxone; Narcotic Antagonists; Narcotics; Nausea; Norway; Prospective Studies; Seizures; Substance-Related Disorders; Tachycardia; Tremor; Vomiting

2004
An arterially perfused decerebrate preparation of Suncus murinus (house musk shrew) for the study of emesis and swallowing.
    Experimental physiology, 2002, Volume: 87, Issue:5

    Arterially perfused, decerebrate preparations of the insectivore, Suncus murinus were made to determine whether the emetic reflex could be activated in such a preparation using a range of stimuli shown to be emetic in conscious or anaesthetised Suncus. Efferent phrenic and vagus nerve activities and electromyograms (EMGs) from the temporalis, abdominal oesophagus and trapezius muscles were recorded, as well as longitudinal shortening of the oesophagus and dorso-ventral movements of the thorax. The preparations swallowed spontaneously every 0.6 to 6.5 min. The duration of a swallow was 3.1 +/- 0.3 s (recorded as the time taken for the oesophagus to shorten and recover to its resting position) and the oesophagus shortened by 3.5 +/- 0.4 mm during a swallow. The emetic reflex was activated by electrical stimulation (30 Hz, 10-20 V, 0.2 ms pulse width, for 30 s) of abdominal vagal afferents (latency < 30 s) or by arterial perfusion with either 40 nM of the capsaicin analogue resiniferatoxin (latency 1.7 +/- 0.6 min), 6 microM nicotine (latency 1.6 +/- 0.1 min) or 1 microM of the phosphodiesterase IV inhibitor CP-80,633 (latency 8.9 +/- 3.9 min). These emetic stimuli produced somatic and visceral movements in Suncus preparations indicative of activation of the emetic reflex. There were pronounced contractions of the thorax that occurred simultaneously with oesophageal shortening and mouth opening, separated by thorax expansion and a burst of phrenic nerve activity. During emetic-like episodes, oesophageal shortenings were only 0.84 +/- 0.1 s in duration, faster than the duration of shortening observed during swallowing (cf. swallowing, 3.1 +/- 0.3 s; P < 0.0001). The shortening of the oesophagus during emetic-like episodes was 6.2 +/- 0.4 mm, which was greater than the shortening seen during swallowing (cf. swallowing, 3.5 +/- 0.4 mm; P < 0.0001). We conclude that the emetic reflex can be activated in our Suncus preparations and that this non-sentient small adult animal model can now be used to study the neurophysiology and pharmacology of swallowing and emesis.

    Topics: Animals; Aorta, Thoracic; Decerebrate State; Deglutition; Disease Models, Animal; Diterpenes; Electric Stimulation; Esophagus; Female; Heart Rate; Male; Naloxone; Narcotic Antagonists; Nicotine; Nicotinic Agonists; Perfusion; Phrenic Nerve; Physical Stimulation; Pyrimidinones; Reflex; Respiratory Mechanics; Shrews; Vagus Nerve; Video Recording; Vomiting

2002
Opioid receptor involvement in the adaptation to motion sickness in Suncus murinus.
    Pharmacology, biochemistry, and behavior, 2001, Volume: 68, Issue:4

    The aim of the present study was to investigate an opioid receptor involvement in the adaptation response to motion sickness in Suncus murinus. Different groups of animals were treated intraperitoneally with either saline, morphine (0.1 and 1.0 mg/kg), naloxone (1.0, 10.0 and 5.0 mg/kg) or a combination of naloxone plus morphine in the absence or 30 min prior to a horizontal motion stimulus of 1 Hz and 40 mm amplitude. For the study of adaptation, different groups received saline on the first trial, and in subsequent trials (every 2 days) they received either saline, naloxone (1.0 and 10.0 mg/kg, i.p.) or morphine (0.1 mg/kg, i.p.) 30 min prior to the motion stimulus. Pretreatment with morphine caused a dose-related reduction in emesis induced by a single challenge to a motion stimulus. Pretreatment with naloxone alone did not induce emesis in its own right nor did it modify emesis induced by a single challenge to a motion stimulus. However, pretreatment with naloxone (5.0 mg/kg, i.p.) revealed an emetic response to morphine (P<.001) (1.0 mg/kg, i.p.) and antagonised the reduction of motion sickness induced by morphine. In animals that received saline or naloxone (1.0 mg/kg), a motion stimulus inducing emesis decreased the responsiveness of animals to a second and subsequent motion stimulus challenge when applied every 2 days for 11 trials. However, the animals receiving naloxone 10.0 mg/kg prior to the second and subsequent challenges showed no significant reduction in the intensity of emesis compared to the first trial. The data are revealing of an emetic potential of morphine when administered in the presence of a naloxone pretreatment. The administration of naloxone is also revealing of an additional inhibitory opioid system whose activation by endogenous opioid(s) may play a role in the adaptation to motion sickness on repeated challenge in S. murinus.

    Topics: Adaptation, Psychological; Analgesics, Opioid; Animals; Female; Ganglionic Stimulants; Male; Morphine; Motion Sickness; Naloxone; Narcotic Antagonists; Nicotine; Receptors, Opioid; Shrews; Vomiting

2001
Modulation of emesis by fentanyl and opioid receptor antagonists in Suncus murinus (house musk shrew).
    European journal of pharmacology, 1999, Jun-11, Volume: 374, Issue:1

    The anti-emetic mechanism of action of fentanyl to inhibit nicotine (5 mg/kg, s.c.)-induced emesis was investigated in Suncus murinus. The anti-emetic action of fentanyl (40 microg/kg, s.c.) was antagonised by the opioid receptor antagonists naltrexone (1 mg/kg, s.c.), naloxone (1 mg/kg, s.c.), M8008 (16S-methylcyprenorphine; 1 mg/kg, s.c.) and MR 2266 (5,9-diethyl-2-(3-furylmethyl)2'-hydroxy-7,7-benzomorphan; 1 mg/kg) but not by naloxone methylbromide (1 mg/kg, s.c.), naloxone methyliodide (1 mg/kg, s.c.), naltrindole (1 mg/kg, s.c.), DIPPA (2-(3,4-dichlorophenyl)-N-methyl-N-[1S)-1-(3-isothiocyanatophenyl)-2-(1- pyrrolidinyl)-ethyl]acetamide; 3 mg/kg, i.p.) or naloxonazine (35 mg/kg, i.p.). This indicates an involvement of mu2-opioid receptors within the brain to mediate the anti-emetic effect of fentanyl. In other studies, naloxone 10-60 mg/kg, s.c. induced dose-related emesis but naltrexone was only emetic at 60 mg/kg, s.c. and naloxone methylbromide failed to induce emesis at doses up to 60 mg/kg, s.c. The emesis induced by a high dose of naloxone 60 mg/kg, s.c. was antagonized by CP-99,994 ((+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine; 3-30 mg/kg, i.p.), 8-OH-DPAT, ((+/-)-8-hydroxy-dipropylaminotetralin; 0.003-0.3 mg/kg, s.c.), buspirone (3 mg/kg, s.c.) and fluphenazine (1-3 mg/kg, i.p.) but not by naltrexone (1-30 mg/kg, s.c.), metoclopramide (0.3-3 mg/kg, i.p.), sulpiride (0.3-3 mg/kg, i.p.), domperidone (0.1-3 mg/kg, i.p.), ondansetron (0.3-3 mg/kg, i.p.), granisetron (0.3-3 mg/kg, i.p.), scopolamine (0.3-3 mg/kg, i.p.) or promethazine (0.3-3 mg/kg, i.p.). The data is discussed in relation to opioid receptor mechanisms moderating emesis and the identification of potential sites of drug action available to inhibit the emetic reflex.

    Topics: Animals; Antiemetics; Female; Fentanyl; Male; Naloxone; Naltrexone; Narcotic Antagonists; Nicotine; Receptors, Opioid; Shrews; Vomiting

1999
The role of alpha-adrenergic mechanisms within the area postrema in dopamine-induced emesis.
    European journal of pharmacology, 1995, Jan-05, Volume: 272, Issue:1

    Intracerebroventricular injection of dopamine (0.5-4.0 mg) produced dose-dependent and short-lasting emesis (1-8 min) in cats, which was abolished after ablation of the area postrema. Relatively selective alpha 2-adrenoceptor antagonists (yohimbine and idazoxan) and a mixed alpha 1- and alpha 2-adrenoceptor antagonist (tolazoline), but not a non-selective alpha 1-adrenoceptor antagonist (prazosin), injected intracerebroventricularly inhibited the emesis induced by intracerebroventricular dopamine. However, dopamine receptor antagonists (chlorpromazine, droperidol, spiperone, domperidone, triflupromazine, sulpiride and metoclopramide), an antimuscarinic drug (atropine), a ganglionic blocking agent (mecamylamine), an opioid receptor antagonist (naloxone) and a 5-HT receptor antagonist (methysergide), all injected intracerebroventricularly, had no significant effect on emesis evoked by intracerebroventricular dopamine. The emetic response to intracerebroventricular dopamine was attenuated in cats pretreated with intracerebroventricular reserpine, 6-hydroxydopamine, alpha-methyl-p-tyrosine and hemicholinium-3. It is postulated that dopamine-induced emesis is mediated through the release of noradrenaline acting at alpha 2-adrenoceptors and that it depends on the integrity of monoaminergic and possibly cholinergic structures within the area postrema. It appears, therefore, that the emetic effect of intracerebroventricular dopamine is mediated by adrenergic rather than dopaminergic mechanisms in the area postrema, at least in the cat.

    Topics: Adrenergic alpha-Antagonists; alpha-Methyltyrosine; Animals; Atropine; Cats; Cerebral Ventricles; Dioxanes; Disease Models, Animal; Dopamine; Dopamine Antagonists; Dose-Response Relationship, Drug; Female; Hemicholinium 3; Idazoxan; Injections, Intraventricular; Male; Mecamylamine; Methyltyrosines; Methysergide; Naloxone; Oxidopamine; Prazosin; Reserpine; Tolazoline; Tyrosine 3-Monooxygenase; Vomiting; Yohimbine

1995
Naloxone does not prevent apomorphine-induced emesis or hypotension in dogs.
    Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 1994, Volume: 4, Issue:6

    Previous data have shown that apomorphine-induced respiratory depression can be reversed by the opiate antagonist, naloxone. The present study investigates the influence of naloxone on cardiovascular changes and vomiting elicited by apomorphine in dogs. In chloralose-anaesthetized animals, naloxone (0.02 mg/kg i.v.) failed to modify either the decrease in blood pressure and the biphasic changes (bradycardia followed by a long-lasting tachycardia in heart rate or the characteristics (occurrence, latency, duration) of the emesis elicited by apomorphine (200 micrograms/kg i.v.). In contrast, in conscious animals, naloxone (0.02 mg/kg i.v.) increased both the number and the duration (but not latency) of vomiting induced by a lower dose of apomorphine (30 micrograms/kg i.v.). These data show that apomorphine-induced vomiting and arterial hypotension do not involve opiate receptors.

    Topics: Anesthetics; Animals; Apomorphine; Blood Pressure; Chloralose; Dogs; Female; Heart Rate; Hypotension; Male; Naloxone; Vomiting

1994
Absence of emetic effects of morphine and loperamide in Suncus murinus.
    European journal of pharmacology, 1994, May-02, Volume: 256, Issue:3

    The house musk shrew Suncus murinus recently has been introduced for the study of emesis. We investigated the emetic effects of the opioids morphine (0.1-21.5 mg/kg i.p.) and loperamide (0.01-10 mg/kg i.p.) and found a complete lack of emetogenic potential. Nicotine, however, dose dependently induced vomiting in the Suncus with an ED50 of 8.8 mg/kg s.c. and a 100% incidence at 20 mg/kg. This drug-induced vomiting was reduced by morphine or loperamide: ED50 values obtained were 1.2 mg/kg i.p. for morphine and 0.7 mg/kg i.p. for loperamide. Naloxone (2 mg/kg s.c.) antagonised the inhibitory effect of morphine (2 mg/kg i.p.) or loperamide (10 mg/kg i.p.). Serotonin (20 mg/kg s.c.) had less reliable emetogenic potency than nicotine in the Suncus with incidences between 50 and 100%. However, the serotonin-induced vomiting was abolished by morphine and loperamide and this inhibition was antagonised by naloxone. These results suggest that systemically administered opioids are pure antiemetics in Suncus murinus in contrast to other animal models and man. Naloxone antagonism indicates that this antiemetic effect is mediated by opioid receptors.

    Topics: Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Injections, Intraperitoneal; Injections, Subcutaneous; Loperamide; Male; Morphine; Naloxone; Nicotine; Serotonin; Serotonin Antagonists; Shrews; Vomiting

1994
Emetic reflex arc revealed by expression of the immediate-early gene c-fos in the cat.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 1994, Volume: 14, Issue:2

    The organization of the central neuronal circuitry that produces vomiting was explored by mapping the distribution of c-fos protein (Fos)-like immunoreactivity (FLI) as a monitor of functional activity. The brainstem and spinal cord were examined in cats administered multiple emetic drugs (cisplatin, lobeline, protoveratrine, naloxone, apomorphine) or control saline injections. Some animals were decerebrated, paralyzed, and artificially ventilated to avoid possible Fos expression induced by sensory feedback or fluid depletion during vomiting. Fictive vomiting was identified in these animals by a characteristic pattern of respiratory muscle nerve (phrenic and abdominal) coactivation. Tissues were immunoprocessed using an antibody raised against amino acids 1-131 of Fos and the avidin-biotin peroxidase complex method. Enhanced nuclear FLI was observed in experimental animals along portions of the sensorimotor emetic reflex arc, including the nodose ganglia, area postrema, nuclei of the solitary tract (especially medial and subpostrema subnuclei), intermediate reticular zone of the lateral tegmental field, nucleus retroambiguus, C2 inspiratory propriospinal cell region, and dorsal vagal and phrenic motor nuclei. Enhanced FLI was also detected in the raphe magnus, subretrofacial nucleus, and spinal dorsal horn. Regions showing no recognizable differences in FLI between experimental and control animals included the vestibular, cochlear, spinal trigeminal, subtrigeminal, and lateral reticular nuclei. Only minor differences were observed in the distributions of FLI between intact and decerebrate animals. No unique, well-defined group of labeled neurons that might function as a "vomiting center" could be identified. Instead, the pattern of c-fos expression suggests that neurons involved in coordinating the emetic response may radiate from the area postrema and nucleus of the solitary tract to an arc in the lateral tegmental field implicated in somato-autonomic integration.

    Topics: Animals; Apomorphine; Brain Stem; Cats; Cervical Plexus; Cisplatin; Decerebrate State; Emetics; Gene Expression; Genes, fos; Genes, Immediate-Early; Lobeline; Medulla Oblongata; Naloxone; Neurons; Organ Specificity; Phrenic Nerve; Proto-Oncogene Proteins c-fos; Protoveratrines; Reflex; Spinal Cord; Vomiting

1994
The effects of different antiemetic agents on morphine-induced emesis in ferrets.
    European journal of pharmacology, 1993, Sep-07, Volume: 241, Issue:1

    There is interest in the development of antiemetics other than dopamine receptor antagonists for the treatment of postoperative nausea and vomiting. A ferret model of morphine-induced emesis may have wider application in evaluating newer agents than the apomorphine dog model. This study describes the conditions for morphine-induced emesis in ferrets and evaluates five antiemetics that are prototypical of three different mechanisms. The average numbers of vomiting and retching episodes induced by morphine (0.1-2.5 mg/kg s.c.) were distributed as a bell-shaped curve. Maximum number of vomits occurred at 0.3 mg/kg (11.8 +/- 2.1 vomits; 45 +/- 12.5 retches). Antiemetics or vehicle were given i.v. 5 min prior to morphine while each ferret was maintained under isoflurane-O2 anesthesia. Ondansetron, a 5-HT3 receptor antagonist, reduced vomiting episodes by 47% and 70% (3 and 10 mg/kg). Granisetron, a 5-HT3 receptor antagonist was inactive at doses of 0.1, 1.0, 3.0 and 10 mg/kg. Metoclopramide reduced vomiting episodes by 48% and 82% (3 and 10 mg/kg). Droperidol reduced vomiting episodes by 84% at 3 mg/kg. Naloxone reduced vomiting episodes by 91% and 43% at doses of 0.1 and 1.0 mg/kg. In most cases, prolonged latency times to the first episodes accompanied the reduction in total numbers of episodes. The significant reduction of morphine-induced emesis in the ferret by ondansetron, metoclopramide and droperidol is consistent with the reduction of postoperative emesis in man by these compounds when morphine was a component of the anesthetic regimen. These results suggested that the morphine ferret model may be useful for evaluating compounds having the potential for preventing and treating postoperative vomiting.

    Topics: Anesthesia; Animals; Antiemetics; Droperidol; Ferrets; Granisetron; Injections, Intravenous; Isoflurane; Male; Metoclopramide; Morphine; Naloxone; Ondansetron; Vomiting

1993
Stimulation of gastrointestinal motility by cisplatin in the ferret: activation of an intrinsic cholinergic mechanism dissociated from emesis.
    Naunyn-Schmiedeberg's archives of pharmacology, 1993, Volume: 347, Issue:5

    Motility was recorded from the corpus, antrum and small intestine of the urethane anaesthetised ferret. The gastrointestinal effects of the highly emetic cytotoxic anticancer agent, cisplatin were investigated following intravenous administration (10 mg/kg i.v.). Following injection, cisplatin induced a prompt onset (< 2 min) increase in motility (tone and contraction amplitude) in all regions with a duration of < 15 min. Acute vagotomy did not abolish the effect but reduced the peak amplitude in the antrum only. Chronic subdiaphragmatic vagotomy significantly enhanced the cisplatin-induced rise in tone in the corpus, the contraction amplitude in the antrum and the duration of the response in the duodenum. The stimulatory effect of cisplatin was blocked in all regions by atropine but not naloxone or the 5-HT3 receptor antagonist ondansetron. This study reports a previously undescribed gastrointestinal motility effect of cisplatin in vivo that is temporally dissociated from emesis. It is proposed that the results provide evidence for a neuroactive effect of cisplatin on enteric cholinergic neurones.

    Topics: Animals; Atropine; Cisplatin; Female; Ferrets; Gastrointestinal Motility; Male; Muscle Contraction; Muscle, Smooth; Naloxone; Ondansetron; Receptors, Serotonin; Vomiting

1993
Morphine 6-glucuronide: a metabolite of morphine with greater emetic potency than morphine in the ferret.
    British journal of pharmacology, 1992, Volume: 106, Issue:1

    1. The emetic potencies of morphine and its metabolite morphine 6-glucuronide have been determined in the ferret by constructing dose-response curves for mean total retches and vomits for subcutaneous doses of 0.05 mg kg-1 to 5 mg kg-1. Morphine 6-glucuronide induced retching and vomiting at lower doses than morphine and at a maximal dose induced more retching and vomiting than morphine. 2. The emesis induced by both morphine and morphine 6-glucuronide was abolished by the preadministration of naloxone (0.5 mg kg-1 s.c.). 3. The 5-HT3 receptor antagonists granisetron and ondansetron (1 mg kg-1, s.c.) failed to abolish or reduce emesis induced by either compound. 4. At a high-dose (5 mg kg-1), morphine but not morphine 6-glucuronide failed to induce emesis and abolished the emesis induced by the cytotoxic drug, cyclophosphamide (200 mg kg-1, i.p.). 5. Preliminary pharmacokinetic studies of intravenous and subcutaneous morphine and morphine 6-glucuronide revealed that morphine 6-glucuronide accounts for less than 1% of the metabolic product of morphine in the ferret. Peak plasma levels of the two compounds after their subcutaneous administration were obtained within 10 min. The metabolic profile of morphine was not dose-dependent. There was no relationship between plasma level and emetic response for either compound.

    Topics: Animals; Cyclophosphamide; Dose-Response Relationship, Drug; Emetics; Ferrets; Granisetron; Imidazoles; Indazoles; Injections, Subcutaneous; Morphine; Morphine Derivatives; Naloxone; Ondansetron; Vomiting

1992
Naloxone or haloperidol but not yohimbine reverse apomorphine-induced respiratory depression.
    Clinical neuropharmacology, 1992, Volume: 15, Issue:5

    Intravenous injection of low doses of naloxone was found to reverse the respiratory depression induced by apomorphine in chloralose-anesthesized dogs. Similar results were obtained with haloperidol, whereas yohimbine remained ineffective. These data suggest that apomorphine depresses respiratory rate through a mechanism involving both dopamine and opiate mechanisms but not alpha 2-adrenoceptors. Respiratory arrest induced by overdosages of apomorphine can be treated with naloxone.

    Topics: Animals; Apomorphine; Dogs; Drug Interactions; Female; Haloperidol; Injections, Intravenous; Male; Naloxone; Respiratory Insufficiency; Vomiting; Yohimbine

1992
The actions of fentanyl to inhibit drug-induced emesis.
    Neuropharmacology, 1991, Volume: 30, Issue:10

    The ability of fentanyl to inhibit drug-induced emesis was investigated in the ferret. Initial studies established that morphine, in small doses (0.025-0.5 mg/kg s.c.), induced emesis in the ferret that decreased at the larger doses of 1 and 2 mg/kg (s.c.). Fentanyl (10-80 micrograms/kg s.c.) failed to induce emesis but in this dose range prevented the emesis induced by morphine (0.5 mg/kg s.c.), apomorphine (0.25 mg/kg s.c.), copper sulphate (100 mg/kg intragastric) and cisplatin (10 mg/kg i.v.). The antiemetic effects could be obtained in the absence of sedation or motor impairment. The antagonism by fentanyl of apomorphine-, copper sulphate- and cisplatin-induced emesis was inhibited by naloxone (0.1 or 0.5 mg/kg s.c.). It is concluded that fentanyl exerts a broad spectrum of actions to inhibit drug-induced emesis. An autoradiographic study of the binding of [3H]DAGO to the brainstem of the ferret indicated high densities of mu recognition sites in the area postrema, nucleus tractus solitarius, dorsal motor nucleus of the vagus, reticular medulla and other sites. The results are discussed in terms of balanced facilitatory and inhibitory opioid systems, regulating emesis and that the antiemetic actions of fentanyl reflect an important, although not necessarily an exclusive, action at mu opioid receptors.

    Topics: Animals; Antiemetics; Apomorphine; Autoradiography; Brain Stem; Cisplatin; Copper; Copper Sulfate; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Female; Fentanyl; Ferrets; Male; Morphine; Naloxone; Receptors, Opioid; Receptors, Opioid, mu; Vomiting

1991
The safety of prehospital naloxone administration by paramedics.
    Annals of emergency medicine, 1990, Volume: 19, Issue:8

    We performed a retrospective review to investigate the safety of prehospital naloxone administration by paramedics as part of a protocol for all patients presenting with an acutely depressed level of consciousness (LOC). The prevalence of naloxone-induced vomiting, seizures, hypotension, hypertension, and cardiac arrest was sought from the prehospital records of 813 patients treated during a 12-month period. The mean age of the treated patients was 42.4 +/- 9.7 years. The initial dose of naloxone was 0.4 to 0.8 mg, and the mean total dose was 0.9 +/- 0.6 mg. No patients lost a pulse within ten minutes of receiving naloxone. Two patients (0.2%) experienced a significant drop in systolic blood pressure, and one patient (0.1%) demonstrated a significant rise in systolic blood pressure within five minutes of naloxone administration. Vomiting occurred in two patients (0.2%), and one patient (0.1%) suffered a tonic-clonic seizure within five minutes of naloxone administration. Of the 813 patients treated, 60 patients (7.4%: mean age, 32.3 +/- 6.7 years) were judged to have an improved LOC after naloxone, with 27 (3.3%) regaining a normal LOC. We conclude that in the above doses, naloxone is safe as part of prehospital protocols for paramedics treating patients with an acutely depressed LOC. However, the vast majority of patients treated empirically with naloxone in the field demonstrated no benefit.

    Topics: Adult; Emergencies; Emergency Medical Services; Female; Heart Arrest; Humans; Hypotension; Male; Middle Aged; Naloxone; Pennsylvania; Retrospective Studies; Safety; Seizures; Unconsciousness; Vomiting

1990
Apomorphine-induced emesis in the dog--routes of administration, efficacy and synergism by naloxone.
    Journal of veterinary pharmacology and therapeutics, 1990, Volume: 13, Issue:2

    Apomorphine proved to be more effective as an emetic in dogs after s.c. administration than after i.m. injection with doses of 0.04 and 0.1 mg/kg. This effect is explained by an anti-emetic effect mediated by mu-receptors in the vomiting centre in the brain, which, in contrast to the chemoreceptor trigger zone, is within the blood-brain barrier. A certain delay between the stimulation of D2-receptors in the chemoreceptor trigger zone (causing emesis) and mu-receptors in the vomiting centre (producing anti-emesis) therefore results, leading to a self-limiting emesis. Blockade of the mu-receptors by naloxone increased and prolonged the effect of apomorphine. A relatively narrow range of apomorphine concentrations on s.c. administration is then effective to stimulate the chemoreceptor trigger zone, but can hardly inhibit the vomiting centre, and must therefore be considered the most suitable route for administration of apomorphine.

    Topics: Animals; Apomorphine; Dog Diseases; Dogs; Drug Synergism; Female; Injections, Intramuscular; Injections, Intravenous; Injections, Subcutaneous; Male; Naloxone; Vomiting

1990
Functional localization of specific receptors mediating gastrointestinal motor correlates of vomiting.
    The American journal of physiology, 1989, Volume: 256, Issue:1 Pt 1

    The gastrointestinal motor correlates of vomiting consist of two contractile events, 1) a giant retrogradely propagated contraction of the upper small intestine, the retrograde giant contraction (RGC) and 2) a series of post-RGC phasic contractions that occur primarily in the lower small intestine. The effects of cholinergic, dopaminergic, serotonergic, and opioid receptor antagonists and an opioid receptor agonist on vomiting and its gastrointestinal motor correlates initiated by apomorphine (APO), CuSO4, or cholecystokinin octapeptide (CCK-8) were determined in awake dogs. Atropine blocked the retrograde giant contraction only, and hexamethonium blocked all jejunoileal motor responses activated by APO, CuSO4, or CCK-8. Domperidone blocked all effects of APO only, whereas haloperidol, methysergide, 1-(1-naphthyl) piperazine, and fentanyl blocked or inhibited responses to both APO and CuSO4. None of the dopaminergic, serotonergic, or opioid receptor antagonists or the opioid receptor agonist affected the gastrointestinal motor responses to CCK-8. Cinanserin or Sch 23390 had no effect on any of the responses activated by APO, CuSO4, or CCK-8. These results suggested that D2 dopaminergic and 5-HT2 serotonergic receptors of the emetic central pattern generator mediate vomiting and its gastrointestinal motor correlates, whereas opioid receptors may mediate tonic inhibition of these responses. In addition, peripheral muscarinic or nicotinic cholinergic receptors but not peripheral 5-HT2, dopaminergic, or opioid receptors mediate the gastrointestinal motor correlates of vomiting.

    Topics: Animals; Apomorphine; Atropine; Copper; Copper Sulfate; Digestive System; Dogs; Domperidone; Female; Gastrointestinal Motility; Haloperidol; Hexamethonium; Hexamethonium Compounds; Male; Muscle Contraction; Naloxone; Receptors, Cholinergic; Receptors, Dopamine; Receptors, Neurotransmitter; Receptors, Opioid; Receptors, Serotonin; Serotonin Antagonists; Sincalide; Vomiting

1989
Evidence for the involvement of alpha 2-adrenoceptors in the emetic action of xylazine in cats.
    American journal of veterinary research, 1989, Volume: 50, Issue:8

    Intramuscular injection of xylazine induced dose-dependent vomiting in cats (ED50 = 0.277 mg/kg); administration of standard dose of xylazine (2 mg/kg, 2 times the 100% emetic dose) induced vomiting in 100% of the cats studied. The xylazine-induced vomiting was antagonized by adrenoceptor antagonists possessing alpha 2-blocking activity, which were yohimbine, tolazoline, and phentolamine. Of these antagonists, yohimbine was the most effective; the maximal antagonistic effect was seen at 1 mg of yohimbine/kg, a dose at which the other drugs had little or no effect. At the doses studied, prazosin and phenoxybenzamine, adrenoceptor antagonists with alpha 1-blocking activity, did not prevent vomiting induced by xylazine. Beta-Adrenoceptor (propranolol), dopamine receptor (domperidone and chlorpromazine), a cholinoceptor (atropine), an opiate receptor (naloxone), and a histamine-receptor (diphenhydramine) antagonists, at the doses studied, did not prevent xylazine-induced vomiting. Pretreatment with 6-hydroxydopamine failed to prevent xylazine-induced vomiting. These results indicated that xylazine-induced vomiting in cats is mediated by alpha 2-adrenoceptors and suggested that the alpha 2-adrenoceptors mediating the vomiting attributable to xylazine may not be presynaptic alpha 2-receptors located on noradrenergic nerve terminals.

    Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Animals; Atropine; Cat Diseases; Cats; Chlorpromazine; Diphenhydramine; Domperidone; Female; Hydroxydopamines; Male; Naloxone; Oxidopamine; Propranolol; Random Allocation; Receptors, Adrenergic, alpha; Thiazines; Vomiting; Xylazine

1989
Role of endogenous opioids and histamine in morphine induced emesis.
    Indian journal of experimental biology, 1989, Volume: 27, Issue:1

    The role of opioid and histaminergic system in morphine induced emesis was investigated in dogs. Morphine (25 micrograms, icv) consistently evoked emesis with an average latency of 195 +/- 29 sec which was fully accounted for by an action on the chemoreceptor trigger zone (CTZ) as its ablation rendered animals refractory to vomiting. Intraventricular pretreatment with opioid antagonist naloxone, histamine H1 antagonist mepyramine and H2 antagonists metiamide and cimetidine afforded protection to icv morphine emesis. The CSF histamine concentration was significantly raised 5 min after icv morphine administration. The results suggest that both endogenous opioid and histamine are involved in morphine emesis. Naloxone in high doses (1600 micrograms, icv) elicited emesis which was not blocked by CTZ ablation confirming our earlier report.

    Topics: Animals; Cimetidine; Dogs; Endorphins; Histamine; Metiamide; Morphine; Naloxone; Pyrilamine; Vomiting

1989
Epidural morphine for postoperative pain: experience with 1085 patients.
    Acta anaesthesiologica Scandinavica, 1985, Volume: 29, Issue:1

    A prospective study of the effect and side-effects of epidural morphine for pain relief in 1085 patients after thoracic, abdominal, urologic, or orthopaedic surgery was performed. Morphine chloride was diluted in saline or bupivacaine and administered through an epidural catheter placed at a segmental level appropriate for the type of surgery. The initial dose was 4 or 6 mg morphine and supplementary doses were given when needed to obtain complete freedom from pain during deep breathing or nursing care. The total dose of epidural morphine from end of surgery until the next morning varied from 4 to 18 mg. 97% of hip arthroplasty patients, 91% of prostatectomy patients and thoracotomy patients, 90% of patients after major lower extremity surgery and 88% of patients after laparotomy were completely satisfied with the postoperative course. For hip arthroplasty and major extremity surgery, an initial dose of 4 mg of epidural morphine was as effective as 6 mg. After prostatectomy, laparotomy, and thoracotomy, an initial dose of 6 mg gave significantly better effect than 4 mg. Pruritus occurred in 11%, nausea or vomiting in 34%, and respiratory depression in 0.9% of the total patient population. Urinary retention occurred in 42% of patients not having urinary catheters in place. Postoperative nausea or vomiting was more frequent in women than in men (P less than 0.001). There was a higher incidence of nausea or vomiting in men experiencing pain than in men who were completely pain-free after abdominal surgery (P less than 0.001). Respiratory depression was rare and occurred as a gradually decreasing respiratory rate.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Anesthesia, Epidural; Catheterization; Depression, Chemical; Epidural Space; Humans; Morphine; Naloxone; Nausea; Pain, Postoperative; Prospective Studies; Pruritus; Respiration; Time Factors; Vomiting

1985
Influence of peripheral and central administration of apomorphine and morphine on intragastric pressure in the dog.
    European journal of pharmacology, 1985, Jan-02, Volume: 107, Issue:2

    Apomorphine was about 30 times more potent in inducing gastric relaxation when applied intracerebroventricularly (i.c.v.) than when injected intravenously (i.v.) in the conscious dog. In the anesthetized dog, the dose of apomorphine producing gastric relaxation via the vertebral artery was at least 10 times lower than that needed to produce gastric relaxation via the i.v. route. For morphine, similar doses had to be given i.c.v. and i.v. to obtain the same degree of gastric relaxation in the conscious dog; in the anesthetized dog, morphine was 3 times more potent via the vertebral artery than i.v. The results suggest that apomorphine-induced gastric relaxation in the dog is mediated via a central site located in the region supplied by the vertebral artery, but that the gastric relaxatory effect of morphine is mediated by both a peripheral and a central site of action.

    Topics: Animals; Apomorphine; Brain; Chemoreceptor Cells; Dogs; Domperidone; Female; Injections, Intravenous; Injections, Intraventricular; Morphine; Naloxone; Pressure; Stomach; Vomiting

1985
Naloxone induced suppression of feeding in tigers.
    Physiology & behavior, 1985, Volume: 34, Issue:4

    Naloxone suppresses, but does not eliminate feeding in Siberian tigers. Naloxone administration paired with novel foods appeared to induce emesis.

    Topics: Animals; Behavior, Animal; Carnivora; Depression, Chemical; Feeding Behavior; Female; Naloxone; Vomiting

1985
Review of the current status of prokinetic agents in gastroenterology.
    The American journal of gastroenterology, 1985, Volume: 80, Issue:12

    Topics: Benzamides; Chemical Phenomena; Chemistry; Cisapride; Dexamethasone; Digestive System; Domperidone; Gastric Emptying; Gastroesophageal Reflux; Gastrointestinal Diseases; Gastrointestinal Motility; Humans; Kinetics; Metoclopramide; Naloxone; Phenytoin; Piperidines; Proglumide; Vomiting

1985
Antiemetic activity of butorphanol against cisplatin-induced emesis in ferrets and dogs.
    Cancer treatment reports, 1982, Volume: 66, Issue:10

    The analgesic agent butorphanol was evaluated for its ability to block cisplatin-induced emesis in ferrets and dogs. In ferrets, butorphanol (0.15, 0.3, or 0.45 mg/kg; expressed in terms of the tartrate salt) administered sc 30 minutes prior to cisplatin (8 mg/kg iv) reduced the number of emetic episodes but did not eliminate them. When these doses of butorphanol were administered 30 minutes before and 30 and 90 minutes after cisplatin, they caused a dose-related reduction in the number of emetic episodes; there was complete protection at a dose of 0.45 mg/kg/injection. In dogs, butorphanol (0.185 or 0.37 mg/kg/injection, expressed in terms of the tartrate salt) was administered sc on the same multiple-dose schedule used in the ferrets; this caused a nearly complete elimination of the emetic response to cisplatin (3 mg/kg iv). Butorphanol caused some sedation in both species at effective antiemetic doses but had no effect on the antitumor activity of cisplatin against murine L1210 leukemia. Naloxone blocked the antiemetic effect of butorphanol in ferrets, indicating the involvement of opiate receptors. The results of these studies suggest that butorphanol may be useful clinically in mitigating the emetic effects of cisplatin.

    Topics: Animals; Butorphanol; Cisplatin; Dogs; Dose-Response Relationship, Drug; Female; Ferrets; Male; Mice; Morphinans; Naloxone; Time Factors; Vomiting

1982
Gastric relaxation and vomiting by apomorphine, morphine and fentanyl in the conscious dog.
    European journal of pharmacology, 1981, Jan-16, Volume: 69, Issue:2

    Apomorphine (0.03 mg . kg-1 s.c.) and morphine (0.5 mg . kg-1 s.c.) produced gastric relaxation and vomiting in the conscious dog. Domperidone (0.1-1 mg . kg-1 i.v.), haloperidol (0.1 mg . kg-1 i.v.) and pimozide (0.025 mg . kg-1 i.v.) selectively blocked the gastric relaxation as well as the vomiting caused by apomorphine. Naloxone (0.07 mg . kg-1 i.v.) selectively blocked the gastric relaxation and the vomiting caused by morphine; after naloxone, morphine produced a delayed gastric relaxation in 2 experiments out of 7. These results suggest that for gastric relaxation as well as for vomiting, apomorphine and morphine act on different receptors. Fentanyl elicited marked gastric relaxation, blocked by naloxone, but did not elicit vomiting. After fentanyl, morphine and apomorphine no longer produced gastric relaxation and vomiting. This observation shows that the known blocking effect of fentanyl at the vomiting center does not affect its gastric relaxing effect.

    Topics: Animals; Apomorphine; Dogs; Dopamine Antagonists; Drug Interactions; Female; Fentanyl; Morphine; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Naloxone; Pressure; Stomach; Vomiting

1981
Failure of naloxone to prevent the emetic activity of apomorphine in dogs.
    Journal of veterinary pharmacology and therapeutics, 1981, Volume: 4, Issue:4

    Topics: Animals; Apomorphine; Dogs; Droperidol; Female; Fentanyl; Haloperidol; Injections, Intravenous; Male; Naloxone; Time Factors; Vomiting

1981
Control of radiation-induced emesis with promethazine, cimetidine, thiethylperazine, or naloxone.
    American journal of veterinary research, 1979, Volume: 40, Issue:8

    Promethazine (2 mg/kg), cimetidine (4 mg/kg), thiethylperazine (0.86 mg/kg), and naloxone (0.08 mg/kg) were each evaluated for their ability to increase the threshold of radiation-induced emesis in the dog. Each dog was fed a can of dog food (ca 0.4 kg) and then injected IM with the appropriate drug 1 hour before being irradiated by a 60Co teletherapy unit. The total radiation dose given an individual dog was determined by an up-and-down exposure schedule. Dogs were then observed continuously for 10 hours while the number, time of onset, and duration of each emetic episode were monitored. The dose of radiation causing emesis in 50% (ED50 +/- SEM) of control dogs was 170 +/- 38.5 rad. The ED50 +/- SEM was increased to 402 +/- 18.6 rad by promethazine, to 331 +/- 27.3 rad by cimetidine, and to 320 +/- 38.5 rad by thiethylperazine. This increased tolerance was significant at P less than 0.05 for each drug. The ED50 for naloxone was 262.5 +/- 92.9 rad, which was not a statistically significant increase in threshold.

    Topics: Animals; Chemoreceptor Cells; Cimetidine; Dog Diseases; Dogs; Guanidines; Male; Naloxone; Promethazine; Radiation Injuries; Radiation Injuries, Experimental; Thiethylperazine; Vomiting

1979
Gastric relaxation by morphine, apomorphine and fentanyl in the conscious dog.
    Archives internationales de pharmacodynamie et de therapie, 1979, Volume: 242, Issue:2

    Topics: Animals; Apomorphine; Benzimidazoles; Dogs; Domperidone; Fentanyl; Haloperidol; Morphine; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Naloxone; Piperidines; Stomach; Vomiting

1979
Overdose of Lomotil.
    British medical journal, 1978, Jan-21, Volume: 1, Issue:6106

    Topics: Atropine; Child, Preschool; Diphenoxylate; Drug Combinations; Female; Humans; Isonipecotic Acids; Male; Naloxone; Vomiting

1978
Overdose of Lomotil.
    British medical journal, 1978, Apr-15, Volume: 1, Issue:6118

    Topics: Atropine; Diphenoxylate; Drug Combinations; Humans; Isonipecotic Acids; Naloxone; Vomiting

1978
Beta-endorphin: pharmacologic and behavioral activity in cats after low intravenous doses.
    Life sciences, 1978, Nov-20, Volume: 23, Issue:21

    Topics: Animals; Behavior, Animal; Cats; Dose-Response Relationship, Drug; Endorphins; Injections, Intravenous; Male; Motor Activity; Muscle Relaxation; Muscle, Smooth; Naloxone; Nictitating Membrane; Vomiting

1978
Reversible, titrated deep sedation for major office surgery.
    Plastic and reconstructive surgery, 1977, Volume: 59, Issue:1

    We have operated upon 446 consecutive patients in the office, using the controlled titrated method of sedation which we have described. We believe the results are superior to the methods in more common use. A major factor in choosing a narcotic as our one basic drug was the availability of a safe, swift, and effective antidote to it.

    Topics: Adolescent; Adult; Aged; Anesthesia, Local; Arrhythmias, Cardiac; Bradycardia; Humans; Hypotension; Injections, Intravenous; Male; Meperidine; Middle Aged; Morphine; Naloxone; Respiratory Insufficiency; Surgery, Plastic; Vomiting

1977
Emetic and hyperthermic effects of centrally injected methionine-enkephalin in cats.
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 1977, Volume: 154, Issue:4

    Topics: Animals; Body Temperature; Cats; Enkephalins; Injections, Intraventricular; Morphine; Naloxone; Oligopeptides; Vomiting

1977
Naloxone antagonizes narcotic self blockade of emesis in the cat.
    The Journal of pharmacology and experimental therapeutics, 1977, Volume: 203, Issue:1

    Morphine, levorphanol, fentanyl and methadone given by intracerebroventricular (i.c.v.) injection blocked the vomiting response to a standard emetic test dose of apomorphine subsequently injected i.c.v. Of these narcotics, only morphine initially evoked vomiting. Systemic pretreatment with naloxone (5 mg/kg i.p. or i.v.) uniformly abolished the antiemetic activity of all the represented narcotic agents, moreover, naloxone thus administered was followed consistently by emetic responses to those narcotics which separately failed to evoke vomiting. When naloxone was injected i.c.v. in addition to being given systemically, both antiemetic and emetic activities of the narcotic agents were essentially abolished, whereas apomorphine continued to evoke vomiting. In the presence of systemic naloxone, given to counteract self-blockade of vomiting, the narcotics were shown to induce vomiting through excitation of the medullary emetic chemoreceptor trigger zone and emetic receptor tolerance as well as cross-tolerance developed acutely. The present differentiation by naloxone of the emetic and antiemetic properties of narcotic agents placed in the cerebrospinal fluid indicates that the opposing narcotic actions are exercised at different sites in the brain and that the narcotic receptor specificity of the chemoreceptor trigger zone does not encompass the emetic action of apomorphine.

    Topics: Animals; Cats; Drug Tolerance; Female; Injections, Intraventricular; Male; Medulla Oblongata; Naloxone; Narcotic Antagonists; Narcotics; Vomiting

1977
Intestinal myoelectric activity after activation of central emetic mechanism.
    The American journal of physiology, 1977, Volume: 233, Issue:3

    Topics: Action Potentials; Animals; Apomorphine; Cats; Epinephrine; Female; Injections, Intraperitoneal; Injections, Intraventricular; Intestine, Small; Ketamine; Male; Morphine; Naloxone; Phentolamine; Vomiting

1977
Pethidine compared with pethidine-naloxone administered during labour. A study of analgesic treatment by a sequential method.
    British journal of anaesthesia, 1976, Volume: 48, Issue:6

    In a restricted sequential trial in healthy parturient women, the pain relief from pethidine 100 mg and pethidine 100 mg combined with naloxone 0.4 mg was compared. Pethidine alone gave better relief. The incidence of minor side-effects was high with both treatments but dizziness was reduced slightly by naloxone. It was concluded that naloxone antagonized the analgesia without abolishing the side-effects of pethidine.

    Topics: Anesthesia, Obstetrical; Female; Humans; Labor Stage, First; Labor, Obstetric; Meperidine; Naloxone; Nausea; Pregnancy; Time Factors; Vomiting

1976
[High doses of fentanyl as the sole anaesthetic agent and naloxone as its antagonist (author's transl)].
    Der Anaesthesist, 1975, Volume: 24, Issue:4

    In 70 patients (maxillo-facial-, neurosurgical-, abdominal- and gynaecological operations) the technique of "analgetic anaesthesia" using high doses of fentanyl (0.025 mg/kg body weight) and naloxone as its antagonist (0.02 mg/kg body weight) has been employed. All patients were artificially ventilated with N2O/O2 in a 3:1 ratio. Muscle relaxation was achieved with pancuronium-bromide (0.08 mg/kg). The patients had no apparent heart or lung disease. The youngest patient was 4 years of age, the oldest 82 years of age (average age 48.9). The necessity for a reinjection of fentanyl (half the initial dose) was determined by continously monitoring heart rate. This variable appeared to be the most subtle index indicating a reduction in analgesia. Sufficient analgesia was maintained once the heart rate stayed 20% below preanaesthetic levels. At the end of the operation naloxone reversed the respiratory depression. There was no evidence indicating postoperative pain, which may have required administration of additional analgesics. If deep analgesia was maintained up to the last surgical procedures no emesis appeared in the post operative period. The incidence of emesis was higher 10% compared to the classical neuroleptanalgesia with droperidol this was often noted in cases where blood accumulated in the stomach (maxillo-facial operations) (70%). In 3% of all cases psychomotor agitation with delirium appeared right after the injection of naloxone. This lasted for about 15 minutes. We suspect that due to the sudden and powerful effect of naxolone, in replacing fentanyl from its receptor site, acute withdrawal symptoms may be precipitated.

    Topics: Adolescent; Adult; Aged; Analgesia; Autonomic Nervous System; Child; Child, Preschool; Female; Fentanyl; Genital Diseases, Female; Humans; Hypertension; Hypotension; Male; Maxilla; Middle Aged; Naloxone; Nausea; Neurosurgery; Tachycardia; Vomiting

1975
The management of propoxyphene poisoning.
    The Journal of pediatrics, 1974, Volume: 85, Issue:1

    Topics: Adult; Dextropropoxyphene; Female; Humans; Ipecac; Naloxone; Poisoning; Respiratory Insufficiency; Seizures; Vomiting

1974
Reversal of morphine anesthesia with naloxone.
    Anesthesiology, 1974, Volume: 41, Issue:4

    Topics: Adult; Anesthesia, Intravenous; Carbon Dioxide; Humans; Infusions, Parenteral; Male; Mental Processes; Morphine; Naloxone; Partial Pressure; Respiration; Spirometry; Time Factors; Vomiting

1974
Toxicity from Lomotil. Accidental ingestion by a 22-month-old child.
    Clinical pediatrics, 1973, Volume: 12, Issue:1

    Topics: Atropine; Drug Combinations; Gastrointestinal Agents; Humans; Infant; Ipecac; Isonipecotic Acids; Male; Naloxone; Poisoning; Respiration, Artificial; Seizures; Tachycardia; Vomiting

1973
Treatment of overdose and withdrawal of abused drugs.
    Postgraduate medicine, 1973, Volume: 54, Issue:6

    Topics: Amphetamine; Cathartics; Charcoal; Diuretics; Gastric Lavage; Hallucinogens; Humans; Hypnotics and Sedatives; Methadone; Naloxone; Opium; Parasympatholytics; Pulmonary Edema; Renal Dialysis; Respiration, Artificial; Substance Withdrawal Syndrome; Substance-Related Disorders; Tranquilizing Agents; Vomiting

1973
Narcotic-antagonist assay procedures in dogs.
    Advances in biochemical psychopharmacology, 1973, Volume: 8, Issue:0

    Topics: Analgesics; Animals; Behavior, Animal; Cyclazocine; Dental Pulp; Dogs; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Drug Tolerance; Electroshock; Hemodynamics; Intestines; Meperidine; Morphine; Muscle Tonus; Muscle, Smooth; Nalorphine; Naloxone; Narcotic Antagonists; Pentazocine; Reflex, Stretch; Respiration; Spinal Cord; Vomiting

1973