buprenorphine and Hepatic-Encephalopathy

Portosystemic shunts were ligated over a gauged stainless steel rod in 160 dogs and 15 cats, using a midline celiotomy. The diameter of the rod varied with the size of the shunt and the diameter of the portal vein cranial to the shunt. Shunts were narrowed to the smallest diameter that did not cause signs of portal hypertension such as cyanosis of the stomach, pancreas, and small intestine. A slight discoloration was accepted only if the heart rate, end-expiratory CO2%, or arterial blood pressure (if available) did not deviate more than 15% from the values that were recorded at the beginning of the surgical procedure. The perioperative mortality (0-30 days) was 29%. The most common cause of death was euthanasia because of hypoplasia of the portal vein cranial to the shunt. Animals with intrahepatic shunts had a significantly lower probability of survival than animals with extrahepatic portocaval or portoazygos shunts. In dogs, large breed and a high body weight were also significant risk factors for non-survival. Age had a significant effect on risk of non-survival, with an increased risk for older dogs, irrespective of the breed of the dog (large breed vs. small breed). The probability of survival without recurrence of hepatoencephalopathy (HE) after 1 and 4 years was 61.3% and 55.7%, respectively. The only variable that was significantly associated with non-recurrence of HE was the breed of the dog, there being a lower probability for large breeds. Among the animals that survived surgery for more than 30 days, there was a significant higher probability of recurrence of HE in cats than in dogs.

Topics: Abdomen; Alanine Transaminase; Ammonia; Analgesics, Opioid; Animals; Bile Acids and Salts; Buprenorphine; Cat Diseases; Cats; Dog Diseases; Dogs; Female; Follow-Up Studies; Hepatic Encephalopathy; Hypotension; Ligation; Male; Narcotic Antagonists; Portal System; Portal Vein; Prognosis; Proportional Hazards Models; Sufentanil; Surveys and Questionnaires; Ultrasonography

Cocaine (COCA)-induced neurobehavioral symptoms, which can be observed simultaneously with exacerbation in biochemical markers, were evaluated in mice, and compared with the changes observed in a representative hepatic failure model induced by thioacetamide (TAA). The effects of pretreatment with buprenorphine (BUP) (0.25, 0.5 or 1 mg/kg i.p.), a mixed opioid agonist-antagonist and an antidote against fatal COCA toxicity, were also examined. At 5 min after the COCA administration (65 mg/kg i.p.), the liver ATP levels were attenuated, and an exacerbation of the CNS-stimulating effects of COCA could be characteristically observed for hepatotoxicity-related neurobehavioral symptoms (changes in alertness, interest, body tension, head movement and walking). At 24 h, the ALT (alanine aminotransferase) activity was elevated, and hepatotoxic attenuation was observed for all of the scores on the neurobehavioral symptoms; this was almost identical to the symptoms observed in the TAA-treated group of mice. Recovery was observed by 72 h for all of the morbid changes. The hepatotoxic biochemical changes and the sum score for all five neurobehavioral symptoms were significantly ameliorated by low doses (0.25 and 0.5 mg/kg) of BUP, both at 5 min and 24 h.

Topics: Adenosine Triphosphate; Alanine Transaminase; Animals; Antidotes; Behavior, Animal; Brain; Buprenorphine; Cocaine; Disease Models, Animal; Hepatic Encephalopathy; Liver; Mice; Mice, Inbred ICR; Motor Activity; Narcotic Antagonists; Narcotics