naloxone has been researched along with Necrosis* in 10 studies
10 other study(ies) available for naloxone and Necrosis
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Imaging delta- and mu-opioid receptors by PET in lung carcinoma patients.
In the present study, we measured the kinetics and distribution in vivo of the selective delta-opioid antagonist 11C-methylnaltrindole (11C-MeNTI) and the mu-opioid agonist 11C-carfentanil (11C-CFN) in patients with lung carcinoma using PET.. Paired measurements of 11C-MeNTI and 11C-CFN binding were performed in biopsy-proven small-cell (n = 2), squamous (n = 2), and adenocarcinoma (n = 3) lung cancer patients. Dynamic PET scans of increasing duration (0.5-8 min) were acquired over 90 min after an intravenous bolus injection of 370 MBq of tracer. Time-activity curves for tumor and normal lung parenchyma binding were generated using the region-of-interest (ROI) method. The mean activity at equilibrium was measured, and the specific-to-nonspecific binding ratio (tumor - lung)/lung was calculated. Four of 7 patients underwent an additional static 18F-FDG PET scan for clinical indications. Three of 7 patients underwent surgery, and stained sections of tumor were inspected for inflammation, necrosis, and scar tissue.. Increased binding of 11C-MeNTI and 11C-CFN was detected in all tumor types studied. 11C-MeNTI binding in tumor and healthy lung tissue was significantly more intense than that of 11C-CFN. The average specific-to-nonspecific binding ratio across cell types for 11C-MeNTI (4.32 +/- 1.31; mean +/- SEM) was greater than that of 11C-CFN (2.42 +/- 1.17) but lower than that of 18F-FDG (7.74 +/- 0.53). Intravenous naloxone produced 50% and 44% decreases in the specific-to-nonspecific binding ratios of 11C-MeNTI and 11C-CFN, respectively.. These data provide in vivo evidence for the presence of delta- and mu-opioid receptor types in the 3 major human lung carcinomas and suggest the suitability of 11C-MeNTI and 11C-CFN as investigational probes of lung carcinoma biology. Topics: Adenocarcinoma; Aged; Carcinoma, Non-Small-Cell Lung; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Coloring Agents; Female; Humans; Inflammation; Lung Neoplasms; Male; Middle Aged; Naloxone; Narcotic Antagonists; Necrosis; Radionuclide Imaging; Radiopharmaceuticals; Receptors, Opioid, delta; Receptors, Opioid, mu; Tissue Distribution | 2007 |
The effect of post-burn local hyperthermia on the reducing burn injury: the possible role of opioids.
This paper studied the effect of post-burn local hyperthermia on burn induced injury.. A second-degree burn injury was induced on the right and left flanks of Balb/c mice. Thirty-two burn wounds were divided into four groups. Opioid receptor blocking was done for groups 3 and 4 by intra-peritoneal administration of Naloxone (NLX) 30 min before the thermal injury. Local hyperthermia (45 degrees C, 30 s) was applied only for the burn wounds of groups 2 and 4. Twenty-four hours after burn injury, the burned wounds were assessed for the level of iNOS (by immunohistochemistry) and the number of hair follicles (as an indicator of tissue injury).. The wounds that received hyperthermia (group 2) had significantly more hair follicles (p < 0.001) compared to the control wounds (group 1). There was no significant difference between the number of hair follicles and acute inflammation of group 1 and group 3 (NLX + burn). Group 4 (NLX + burn + hyperthermia) had significantly fewer hair follicles compared to group 1 (p < 0.001), group 2 (p < 0.001) and group 3 (p < 0.001). The level of iNOS in groups 1, 3 and 4 was not significantly different but significantly more than group 2 (p < 0.001, p < 0.001 and p < 0.001, respectively).. The results showed that local hyperthermia after second degree burn decreased the tissue injury and iNOS expression. It is also concluded that endogenous opioid response may have a key role in the above mentioned effects of post-burn local hyperthermia. Topics: Animals; Burns; Hair Follicle; Hyperthermia, Induced; Mice; Mice, Inbred BALB C; Naloxone; Narcotic Antagonists; Necrosis; Nitric Oxide Synthase Type II; Wound Healing | 2006 |
Preconditioning of the rat random-pattern skin flap: modulation by opioids.
Opioid receptors have been implicated in protecting several organ systems from ischaemic events. The authors have studied the effects of opioid receptors on random-pattern skin flap survival. Sixty-nine male Sprague-Dawley rats were used. Bipedicled dorsal skin flaps (2 x 8 cm) were elevated at the midline. Different doses of morphine (0.01, 0.1, 1 and 5 mg/flap) were administered locally in the cranial half of the flap and systemically through intraperitoneal injections (5 and 10 mg/kg). In another experiment, 0.4 mg/flap of naloxone was injected followed by 5 mg/flap injection of morphine to determine whether the effect of morphine is receptor mediated. The role of the opioid receptors in the ischaemic preconditioning (IPC) phenomenon was investigated by administration of naloxone (0.4 mg/flap) 1 h before clamping the cranial pedicle for 20 min followed by 40 min of reperfusion. Appropriate control groups were included. The cranial pedicle was cut 2 h after saline or drug administration in all groups and flap survival area was evaluated on the seventh postoperative day. Local administration of morphine in higher doses (1 and 5 mg/flap) significantly reduced the amount of flap necrosis when compared to that of the control cohort (P < 0.05). Naloxone abolished this protective effect of morphine. Furthermore naloxone significantly decreased the anti-ischaemic effect of the IPC. Systemic administrations of morphine had no significant effect on flap survival area in compare with the control group. Topics: Animals; Dose-Response Relationship, Drug; Injections, Intraperitoneal; Ischemia; Male; Morphine; Naloxone; Narcotic Antagonists; Narcotics; Necrosis; Rats; Rats, Sprague-Dawley; Receptors, Opioid; Skin; Surgical Flaps; Tissue Survival | 2005 |
Ischemic preconditioning attenuates calpain-mediated degradation of structural proteins through a protein kinase A-dependent mechanism.
It has been shown that sarcolemmal rupture can occur during reenergization in cardiomyocytes in which previous ischemia has induced sarcolemmal fragility by calpain-dependent hydrolysis of structural proteins. We tested the hypothesis that attenuated calpain activation contributes to the protection against reperfusion-induced cell death afforded by ischemic preconditioning (IPC), and investigated the involvement of protein kinase A (PKA) in this effect.. Calpain activity and degradation of different structural proteins were studied along with the extent of necrosis in isolated rat hearts submitted to 60 min of ischemia and 30 min of reperfusion with or without previous IPC (two cycles of 5 min ischemia-5 min reperfusion), and the ability of different treatments to mimic or blunt the effects of IPC were analyzed.. IPC accelerated ATP depletion and rigor onset during ischemia but reduced LDH release during reperfusion by 69% (P<0.001). At the end off reperfusion, calpain activity was reduced by 66% (P<0.001) in IPC, and calpain-dependent degradation of sarcolemmal proteins was attenuated. Addition of the calpain inhibitor MDL-28170 mimicked the effects of IPC on protein degradation and reduced LDH release by 48% (P<0.001). The effects of IPC on calpain, alpha-fodrin, and LDH release were blunted by the application of the PKA inhibitor H89 or alprenolol during IPC, while transient stimulation of PKA with CPT-cAMP or isoproterenol before ischemia attenuated calpain activation, alpha-fodrin degradation, and markedly reduced LDH release (P<0.001). In hearts exposed to Na(+)-free perfusion, IPC attenuated calpain activation by 67% (P<0.001) and reduced by 56% (P<0.001) LDH release associated to massive edema occurring during Na(+) readmission without modifying its magnitude.. These results are consistent with PKA-dependent attenuation of calpain-mediated degradation of structural proteins being an end-effector mechanism of the protection afforded by IPC. Topics: Adrenergic beta-Antagonists; Alprenolol; Animals; Calpain; Carrier Proteins; Cyclic AMP-Dependent Protein Kinases; Dipeptides; Enzyme Activation; Ischemic Preconditioning, Myocardial; Isoquinolines; L-Lactate Dehydrogenase; Male; Membrane Proteins; Microfilament Proteins; Myocardial Reperfusion Injury; Myocardium; Naloxone; Narcotic Antagonists; Necrosis; Perfusion; Rats; Rats, Sprague-Dawley; Sodium; Sulfonamides | 2004 |
Subcutaneous loperamide prevents gastric lesions induced by necrotizing agents in rats.
The effects of subcutaneous loperamide on gastric lesions induced by necrotizing agents were investigated in the rat. Loperamide produced a dose-dependent increase of gastric fluid volume and inhibition of gastric lesions caused by 0.6 N HCl or absolute ethanol. Pretreatment with naloxone almost completely blocked both fluid pooling effect and mucosal protective effect of loperamide. Omeprazole reduced the acidity of the gastric fluid in rats treated with loperamide without significantly decreasing the fluid volume. Various volumes of acid, given orally immediately before 0.6 N HCl, volume-dependently prevented gastric lesions. We conclude that subcutaneous loperamide protects the gastric mucosa against necrotizing agents through luminal dilution of irritants, which is mediated by naloxone-sensitive opiate receptors. Topics: Animals; Ethanol; Gastric Mucosa; Hydrochloric Acid; Injections, Subcutaneous; Irritants; Loperamide; Male; Naloxone; Necrosis; Omeprazole; Rats; Rats, Sprague-Dawley | 1997 |
Evidence for a central long-lasting antinociceptive effect of vapreotide, an analog of somatostatin, involving an opioidergic mechanism.
The antinociceptive effect of the octapeptide vapreotide, an analog of somatostatin, was studied after systemic injection in normal mice using the hot plate and abdominal stretching assays, and in normal rats using the paw pressure analgesiometric assay. Vapreotide was ineffective at 1 microgram/kg s.c. in the hot plate test in mice, but 30 min after injection it induced an antinociceptive effect at s.c. injected doses of 8, 64, 512 and 4096 micrograms/kg, with an ED50 of 213 +/- 5 micrograms/kg. For the three highest doses this effect persisted 24 hr after the injection (maximal increase: +80 +/- 23% for 512 micrograms/kg) and disappeared at 48 hr. In the phenylbenzoquinone stretching test, in mice, the ED50 was 186 +/- 6 micrograms/kg (maximal decrease: -63 +/- 5%); the effect persisted 24 hr only for the same two highest doses. Using the paw pressure test, in rats, a dose-dependent increase in paw withdrawal and vocalization thresholds was observed for 21 and 24 hr, respectively, after s.c. injections of 16, 64 and 512 micrograms/kg. Global scores obtained for vocalization thresholds were significantly increased (vs. paw withdrawal thresholds) for 64 and 512 micrograms/kg. Carrageenan-induced nociception in rats was reduced for 21 hr by 64 and 512 micrograms/kg s.c.; scores of the contralateral noninflamed paw were also increased. Vapreotide administered locally in the inflamed paw was inactive. No change in edema volume was obtained after systemic injection of vapreotide.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Amino Acid Sequence; Analgesics; Animals; Brain; Disease Models, Animal; Edema; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; In Vitro Techniques; Inflammation; Male; Membranes; Mice; Molecular Sequence Data; Morphine; Motor Activity; Naloxone; Necrosis; Nociceptors; Octreotide; Pain Measurement; Rats; Rats, Sprague-Dawley; Somatostatin; Spinal Cord; Time Factors; Tritium | 1994 |
Protective effect of nalmefene and naloxone on the ischemically damaged small bowel.
Topics: Animals; Intestine, Small; Ischemia; Mesenteric Arteries; Naloxone; Naltrexone; Narcotic Antagonists; Necrosis; Rats; Rats, Inbred Strains; Time Factors | 1991 |
Effect of naloxone on shock in a patient with fulminant hepatic failure.
Topics: Adult; Female; Humans; Liver Diseases; Naloxone; Necrosis; Shock | 1983 |
Hyper-endorphin syndrome in a child with necrotizing encephalomyelopathy.
Topics: Ataxia; Brain; Brain Chemistry; Brain Diseases; Cerebrospinal Fluid; Diagnosis, Differential; Endorphins; Enkephalins; Humans; Infant; Injections, Intravenous; Intellectual Disability; Male; Morphine; Naloxone; Necrosis; Spinal Cord Diseases; Syndrome | 1980 |
Endorphins in necrotizing encephalomyelopathy.
Topics: Brain Chemistry; Brain Diseases; Cerebrospinal Fluid; Endorphins; Enkephalins; Humans; Infant; Injections, Intravenous; Male; Naloxone; Necrosis; Spinal Cord Diseases | 1980 |