naloxone and Atrophy

The objective of this study was to determine whether the opiate mu receptor antagonist naloxone would prevent atrophy of the gut in 24-h-fasted rats.. Male Sprague-Dawley rats (n = 76, body weight 200-225 g) were catheterized in the jugular vein on Day 0. The rats were fed standard rat chow for 4 days. On Day 4, the diet was changed to the standard liquid diet, and the rats were allowed free access to the liquid diet. On Day 7, the rats were randomized into five groups: (1) free fed, (2) free fed plus naloxone, (3) pair fed, (4) fasting, (5) free fed plus morphine, (6) fasting plus naloxone. Either naloxone (0.16 mg/kg/h) or morphine (0. 21 mg/kg/h) was continuously infused via venous catheter for 24 h. On Day 8, 24 h after fasting or free feeding, the animals were sacrificed.. Twenty-four hours of fasting caused atrophy of the jejunum and elevated morphine levels in the brain (free fed, 931. 3 +/- 122.3 fmol/g, vs fasting, 1419.0 +/- 150.0, P < 0.05). Morphine infusion reduced villus height, mucosal weight, and protein content in jejunum as compared with the free fed rats receiving saline. Administration of naloxone caused an increase in villus height (fasting, 587.0 +/- 25.8 microm, vs fasting plus naloxone, 670.0 +/- 17.4, P < 0.05), mucosal weight (fasting, 17.4 +/- 1.8 mg/cm, vs fasting plus naloxone, 22.6 +/- 1.9, P < 0.05), and protein content (fasting, 13.5 +/- 0.7 microg/cm, vs fasting plus naloxone, 16.7 +/- 0.6, P < 0.05) in jejunum.. Mucosal atrophy of the jejunum is caused by endogenous opioid in fasting rats.

Topics: Animals; Atrophy; Body Weight; Corticosterone; Fasting; Intestinal Mucosa; Jejunum; Leucine; Male; Morphine; Naloxone; Narcotic Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Opioid, mu

A role for endogenous opioids in central nervous system disorders has often been proposed. A case report is presented of a 47-year-old male, medicated only with carbamazepine and lithium, who developed a precipitous alteration of consciousness (Glascow coma scale = 4). An extensive medical workup did not reveal an underlying cause. He exhibited a graded awakening with two intravenous doses of naloxone, which gradually reversed as the last naloxone dose was eliminated. Immunoassay and thin-layer chromatography of two urine samples (to evaluate the possibility of a medication error, alcohol ingestion, or illicit drug use) revealed only the presence of carbamazepine. A dysregulation of the endogenous opioid system is believed to underlie this episode.

Topics: Atrophy; Coma; Dose-Response Relationship, Drug; Drug Administration Schedule; Frontal Lobe; Glasgow Coma Scale; Humans; Infusions, Intravenous; Male; Middle Aged; Naloxone; Narcotic Antagonists; Neurologic Examination; Opioid Peptides

Topics: Antipsychotic Agents; Atrophy; Brain; Cerebral Ventricles; Chronic Disease; Dopamine; Endorphins; GABA Antagonists; gamma-Aminobutyric Acid; Humans; Monoamine Oxidase; Naloxone; Neurotransmitter Agents; Receptors, Dopamine; Schizophrenia

Experimental and genetic hypertension in male rate is accompanied by a lower specific [3H]naloxone binding in the dorsal horn of the spinal cord, and in the hippocampus as compared to controls. Rats which are genetically resistant to hypertensive stimuli have a higher specific [3H]naloxone binding in the nucleus tractus solitarius and lower opiate receptor binding in the dorsal horn. Together with previous studies which demonstrated a correlation between blood pressure and pain sensitivity, these results support the notion that specific brain loci participate in co-regulation of pain perception and blood pressure.

Topics: Animals; Atrophy; Brain; Cell Membrane; Hippocampus; Hypertension, Renal; Kidney; Kinetics; Male; Naloxone; Organ Specificity; Rats; Rats, Inbred Strains; Receptors, Opioid; Spinal Cord