Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93

The effects of alpha 2-adrenoceptor agonists on sulfobromophthalein (BSP) disposition in mice were studied. It was found that agents with both central and peripheral activities (clonidine, guanabenz, B-HT 920 and methyldopa) as well as peripherally acting alpha 2-adrenoceptor agonists (para amino-clonidine and St 91) inhibited sulfobromophthalein disposition in the mouse, and also caused substantial hypothermia. The effects of these agonists were inhibited by yohimbine, a specific alpha 2-antagonist, except for those of para amino-clonidine where only partial reversal was achieved. The effects of clonidine on BSP disposition were also reversed by piperoxan but not by the alpha 1-adrenoceptor antagonists, prazosin and phenoxybenzamine, nor by the beta-blocker, propranolol. These results suggest that, in mice, peripheral alpha 2-adrenoceptors are involved in the effects of the alpha-agonists on BSP disposition.
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PMID:Effects of adrenoceptor agonists and antagonists on sulfobromophthalein disposition in mice. 360 41

Morphine administration acutely reduced plasma clearance of sulfobromophthalein (BSP) in mice and increased hepatic retention of this dye. Increasing morphine doses from 5 to 40 mg/kg s.c. progressively raised plasma and liver BSP levels. Morphine-treated mice, warmed to reverse hypothermia, still had higher plasma and liver BSP levels. The narcotic also raised plasma levels of two dyes which are not conjugated, indocyanine green and dibromosulfophthalein. Naloxone reversed morphine-induced elevation of plasma BSP levels. In bile duct-ligated mice, plasma BSP levels were very high but hepatic BSP levels remained low, both after saline or morphine. Thus, the effects of morphine on BSP disposition differed from those of biliary occlusion. BSP content in bile was reduced by morphine, as dye levels were raised in plasma and hepatic parenchyma. In bile duct-cannulated mice morphine increased BSP levels in plasma and liver whereas reducing the amount of dye eliminated in bile.
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PMID:Opioid effects on hepatic disposition of dyes in mice. 397 20

Increasing doses of clonidine enhanced the retention of sulfobromophthalein (BSP) in plasma and liver, while reducing elimination of this dye into bile. The ED50 of clonidine for these effects was 0.05 to 0.2 mg/kg s.c. In clonidine-treated mice which were warmed to reverse drug-induced hypothermia, plasma and liver BSP levels were raised as compared to saline-treated mice. Clonidine also raised plasma and liver levels of the BSP analog, dibromosulfophthalein, which is not conjugated before biliary elimination. Hepatic glutathione levels, activity of glutathione-S-transferase and ratios of conjugated to unconjugated BSP were not affected by clonidine. In mice with cannulas in their common bile ducts to prevent duct spasm, clonidine reduced the amounts of BSP eliminated into bile. Thus, the alpha-2 adrenoceptor agonist, clonidine, raised plasma and liver levels of anionic dyes and reduced their levels in bile by mechanisms other than altered conjugation, hypothermia or bile duct spasm.
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PMID:Clonidine effects on sulfobromophthalein disposition in mice. 405 76

The hepatobiliary transport of glutathione (GSH) and methylmercury (MM) was investigated in male and female rats anesthetized with pentobarbital sodium. When bile flow was altered with either sodium dehydrocholate (DHC), hypertonic sucrose infusion, or by hypothermia, the absolute rates of GSH and MM secretion into bile were not affected, resulting in parallel concentration changes in the bile fluid for both GSH and MM. Indocyanine green and sulfobromophthalein (BSP), but not BSP-glutathione complex, inhibited the biliary secretion of free GSH. This inhibition was accompanied by a parallel inhibition of MM secretion into bile and occurred without any changes in liver GSH or MM levels. On the other hand, the intravenous administration of cysteine, GSH, and penicillamine was associated with an increase in the secretion rate of reduced sulfhydryl groups into bile and an increase in the biliary secretion rate of MM. The increased biliary secretion rate of MM after phenobarbital pretreatment was also associated with an increased rate of secretion of GSH into bile. In addition, sex differences and individual variability in the biliary secretion of MM were correlated with differing abilities to secrete GSH into bile. The results suggest the presence of a biliary transport system for GSH that determines the biliary secretion of MM.
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PMID:Biliary transport of glutathione and methylmercury. 683 49