naloxone and Respiratory-Distress-Syndrome

The effect of pentazocine, a strong analgesic with a weak opiate antagonistic activity, on fentanyl-induced respiratory depression was studied after anaesthesia in patients undergoing gynaecological laparotomy. Pentazocine (1 mg/kg) was given intravenously at the end of operation. The postoperative respiratory depression in these patients was compared with that in patients who received strong opiate antagonists, nalorphine and naloxone, or no opiate antagonists. Respiratory depression was evaluated by measuring respiratory rate, respiratory minute volume and blood gases. The results show that pentazocine has a clear antagonistic effect on fentanyl-induced respiratory depression but the effect of 1 mg/kg is weaker and shorter than that produced by 5 mg of nalorphine or 0.4 mg of naloxone. Postoperative analgesia in patients who received pentazocine was not longer than that in patients who received no opiate antagonists at the end of the operation.

Topics: Adult; Anesthesia, General; Female; Fentanyl; Humans; Middle Aged; Nalorphine; Naloxone; Pentazocine; Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS), a severe medical condition, is among the major causes of death in critically ill patients. Morphine is used as a therapeutic agent against severe pain. The mechanisms of its reactions over ARDS are not fully understood. The aim of this study was to assess the mechanism of morphine in rats with ARDS.. Rats were injected with lipopolysaccharide to induce ARDS, and some rats were pre-treated with graded doses of morphine in the lateral ventricles to assess survival and non-infected mortality. Immunohistochemical and HE staining were performed to measure MPO and CD68 activity in the lungs and lung injury. ELISA was conducted to detect the inflammatory factor levels in the plasma and BALF. Co-labeling of μ-opioid receptor (MOR) and c-Fos was observed in the brain tissues. MOR-positive cells in brain tissues were evaluated using immunohistochemistry. The effect of MOR antagonists on ARDS was examined in rats by pre-injection of naloxone or methylnaltrexone. The expression of MyD88, TLR4, and NF-κB was lastly assessed.. Dose-independent improvement was observed in respiratory capacity and lung injury in ARDS rats after morphine pre-injection, along with reduced inflammatory factors in the plasma and BALF. MOR-positive cells were elevated after morphine, which occurred within the ventral part of the gigantocellular reticular nucleus (GiV). Naloxone and methylnaltrexone blocked the effects of morphine via central and peripheral MOR. Morphine activated TLR pathway in a MyD88-dependent manner.. Morphine activates MOR within the GiV and the TLR pathway to attenuate ARDS in rats.

Topics: Animals; Lipopolysaccharides; Lung Injury; Morphine; Myeloid Differentiation Factor 88; Naloxone; Rats; Receptors, Opioid; Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) due to methadone (MTD) toxicity is a known but rather uncommon phenomenon. In most of the previously reported cases of MTD-related ARDS, MTD was ingested orally in the form of tablets in high or unknown amounts. Despite the findings from the available literature, this case report is aimed at demonstrating that even small amounts of MTD syrup can cause ARDS earlier than it is usually expected. We present a non-addicted MTD-overdosed patient who developed ARDS after ingesting a very small amount of MTD syrup. We suggest close monitoring of MTD-overdosed patients from at least 48 h to 72 h for possible respiratory complications such as pulmonary oedema.

Topics: Administration, Oral; Adult; Coma; Drug Compounding; Drug Overdose; Female; Humans; Male; Methadone; Naloxone; Narcotic Antagonists; Respiratory Distress Syndrome

The inability to appropriately ventilate neonates shortly after their birth could be related in rare cases to chest-wall rigidity caused by the placental transfer of fentanyl. Although this adverse effect is recognized when fentanyl is administered to neonates after their birth, the prenatal phenomenon is less known. Treatment with either naloxone or muscle relaxants reverses the fentanyl effect and may prevent unnecessary excessive ventilatory settings.

Topics: Cesarean Section; Female; Fentanyl; Humans; Infant, Newborn; Infant, Premature, Diseases; Muscle Rigidity; Naloxone; Narcotic Antagonists; Narcotics; Pregnancy; Pregnancy Complications, Infectious; Pyelonephritis; Respiratory Distress Syndrome; Thoracic Wall

We describe a case-report of an 85-year-male patient with a patient-controlled analgesia (PCA) after a total hip arthroplasty. Four hours after surgery, acute respiratory distress secondary to a morphine overdose occurred, requiring an antagonisation with naloxone. Morphine overdose during a PCA was always caused by a wrong use of the pump. In this case-report, no mistake of programming or administration's use was found. Too important morphine's doses managed in comparison with the patient's age and his renal failure could explain this morphine's accumulation and the respiratory distress. This observation reminds us the obligation to determine the optimal posology in accordance with the rate of glomerular filtration estimated by Cockcroft and Gault formula for patients using a PCA.

Topics: Acute Kidney Injury; Adjuvants, Anesthesia; Aged, 80 and over; Analgesia, Patient-Controlled; Analgesics, Opioid; Arthroplasty, Replacement, Hip; Droperidol; Glomerular Filtration Rate; Humans; Male; Morphine; Naloxone; Narcotic Antagonists; Oxygen Inhalation Therapy; Pain, Postoperative; Respiratory Distress Syndrome

Non-cardiogenic pulmonary oedema is an uncommon complication of both methadone and heroin overdose, often requiring a period of invasive ventilation due to its severity. We report the successful, early use of non-invasive ventilation in the management of non-cardiogenic pulmonary oedema secondary to a non-fatal overdose of oral methadone.

Topics: Administration, Oral; Continuous Positive Airway Pressure; Drug Overdose; Humans; Male; Methadone; Middle Aged; Naloxone; Narcotic Antagonists; Narcotics; Respiratory Distress Syndrome

Intragastric enteral feeding intolerance, common in the intensive care setting, is attributed to many causes. Opioid antagonists such as naloxone may have a role in reversing the intolerance when it is associated with intravenous opioid infusions. A 38-year-old woman hospitalized for acute respiratory distress syndrome was supported with low tidal volume mechanical ventilation. She required lorazepam and morphine administered by continuous intravenous infusion to achieve ventilator synchrony and pain control. While receiving these therapies, the patient developed persistent intolerance to intragastric feeding. Intravenous metoclopramide and laxatives did not decrease gastric volume residuals, and insertion of a jejunal tube was deemed unsafe due to worsening of her respiratory status. Total parenteral nutrition was begun to meet her caloric needs, but she experienced repeated catheter-related bloodstream infections. Naloxone 2 mg by gastric tube every 8 hours for 8 days was started; the dosage then was increased to 4 mg every 8 hours. Tube feeding was restarted, which provided the patient with more than 90% of her daily caloric needs and allowed for discontinuation of parenteral nutrition. With this dosage of naloxone, tolerance to intragastric feeding was maintained until the patient's death due to refractory respiratory failure. Enterally administered naloxone is an effective, noninvasive means of reversing intolerance to intragastric feeding associated with opioids.

Topics: Adult; Catheters, Indwelling; Cross Infection; Drug Administration Schedule; Enteral Nutrition; Fatal Outcome; Female; Food Hypersensitivity; Gastric Emptying; Gastrointestinal Motility; Humans; Infusions, Intravenous; Intubation, Gastrointestinal; Lorazepam; Morphine; Naloxone; Narcotics; Pregnancy; Respiratory Distress Syndrome; Respiratory Insufficiency; Time Factors

Adult respiratory distress syndrome (ARDS) is a common and serious complication of septic shock. Pulmonary trapping of platelets (PPT) and leukocytes, and release of vasoactive and toxic substances such as prostaglandins, lysozymes and oxygen-radicals have been implicated as mediators of the lung injury. beta-Endorphin is regarded as one of the substances released during shock, and has been shown to cause cell damage similar to that seen with endotoxin, and also PPT. We recently reported that combined treatment with methylprednisolone, ibuprofen and naloxone significantly increased lasting survival in an LD100 canine endotoxin shock model. In the present study the effects of these drugs in various combinations were evaluated as regards blood pressure, hematocrit, peripheral platelet and leukocyte counts, intestinal damage and PPT in the same model. The effects of combined treatment were significantly decreased PPT, rise in blood pressure and abolition of bloody diarrhea. We concluded that ibuprofen and naloxone have additive action and that methylprednisolone has no effect on PPT.

Topics: Animals; Blood Platelets; Blood Pressure; Diarrhea; Dogs; Endotoxins; Escherichia coli; Female; Hematocrit; Ibuprofen; Leukocyte Count; Male; Methylprednisolone; Naloxone; Platelet Count; Respiratory Distress Syndrome; Shock, Septic

The opiate antagonist, naloxone, has been shown to obviate hypotension and to improve survival of animals with shock induced by endotoxin, hypovolemia, and spinal transection. This study was done to evaluate the effects of naloxone on pulmonary platelet trapping (PPT) and on platelet aggregability in dogs with endotoxin shock. Dogs with 51Cr labelled platelets were treated with naloxone before and after induction of endotoxin shock. PPT was assessed by measuring 51Cr activity in lung and blood using a gamma scintillation counter. ADP induced platelet aggregability was measured in an aggregometer. PPT seen in endotoxin shocked controls was obviated by naloxone treatment; this effect was more pronounced in pretreated dogs. Naloxone treated animals did not show the increased platelet aggregability normally seen in endotoxin shocked dogs. These results suggest the applicability of naloxone therapy for adult respiratory distress associated with shock.

Topics: Animals; Blood Platelets; Blood Pressure; Dogs; Endotoxins; Escherichia coli; Female; Lung; Male; Naloxone; Platelet Aggregation; Respiratory Distress Syndrome; Shock, Septic

Adult respiratory distress syndrome (ARDS) is a serious complication of trauma and sepsis. We have earlier shown naloxone, an opiate antagonist, and cyproheptadine, an antiserotonin drug, to be effective in reducing pulmonary platelet trapping (PPT), which is thought to play an important role in the evolution of ARDS in endotoxin-shocked dogs. Endorphins are implicated as pathophysiologic factors in shock, and serotonin is a possible mediator of their action. The present study shows naloxone and cyproheptadine to be equally effective in protecting against PPT in dogs subjected to trauma, and when naloxone is given before the trauma it also obviates the hypotension associated with trauma. In addition, the naloxone- and cyproheptadine-treated animals did not show the increased platelet aggregability usually seen in traumatized dogs.

Topics: Animals; Blood Platelets; Blood Pressure; Chromium Radioisotopes; Cyproheptadine; Dogs; Female; Hindlimb; Hypotension; In Vitro Techniques; Isotope Labeling; Lung; Male; Naloxone; Organ Size; Platelet Aggregation; Respiratory Distress Syndrome; Wounds and Injuries

Narcotic analgesics and related drugs act as agonists on several receptors that are responsible for their effects on pain perception, mood and feeling state, and respiration, as well as other pharmacologic actions. Naloxone is the first discovered antagonist that is devoid of agonistic activity and appears to be a competitive antagonist at several receptors. The ability of naloxone to displace or prevent the binding of agonistic narcotics is partly responsible for its antagonistic effects. The ability of naloxone to rectify narcotic-depressed homeostats and precipitate abstinence is also related to its antagonistic activity. Certain cautions and principles apply in the use of naloxone in treating narcotic overdose, reversing surgical analgesia, and the treatment of neonates and children. Unapproved uses of naloxine include reversing the psychotomimetic effects of certain agonists-antagonists, terminating narcotic-induced convulsions and coma, reversing non-narcotic depression, diagnosing physical dependence, and treating narcotic addicts.

Topics: Adult; Analgesics; Animals; Child; Coma; Female; Guinea Pigs; Humans; Infant, Newborn; Infant, Newborn, Diseases; Mice; Naloxone; Narcotic Antagonists; Narcotics; Pregnancy; Receptors, Opioid; Respiratory Distress Syndrome; Seizures; Substance Withdrawal Syndrome; Substance-Related Disorders