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)

The role of the celiac plexus in maintaining temperature homeostasis in rats during cold stress was studied histochemically, ultrastructurally, and electrophysiologically. Inhibition on efferent impulses in preganglionic (splanchnic) nerves and facilitation in postganglionic (superior mesenteric) nerves during a short-term cold exposure leading to slight hypothermia were found. In cold-exposed animals after the celiac plexus decentralization, the neurons showed an increase in the fluorescence intensity and activity of energy metabolism enzymes, hyperplasia of fine structures responsible for protein synthesis and energy supply of cells. It is suggested that during cold stress when efferent impulse flow in preganglionic nerves markedly decreases, the celiac plexus becomes a regulatory centre for autonomic functions involved in the maintenance of temperature homeostasis.
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PMID:[Cytophotometric and electrophysiologic analysis of the role of the celiac plexus in maintaining temperature homeostasis in cold stress in rats]. 149 77

Effects of temperature and emotive factors on the catecholamine content in intestinal and splenic adrenergic plexuses of celiac plexus-decentralized rats have been studied using histofluorescence and computer analysis. It is shown that the catecholamine content in the plexuses gets higher during hypothermia and remains unchanged during hyperthermia and emotional stress.
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PMID:[Effect of temperature and emotional factors on the catecholamine content in intestinal and splenic adrenergic plexuses of celiac plexus-decentralized rats]. 187 15

Many beta-adrenoceptor-blocking agents are well studied today. They differ from one another not only in their pharmacologic profiles (cardioselectivity, intrinsic sympathomimetic activity, membrane-stabilizing activity) but also in their metabolic and pharmacokinetic profiles. The profiles of the following 10 beta blockers have been compared: acebutolol, atenolol, labetalol, metoprolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, and timolol. Differences in the aromatic ring structure lead to differences in lipophilic characteristics. They in turn influence the pharmacokinetic parameters such as hepatic extraction ratio, protein binding, volume of distribution, and the ratio of renal versus hepatic clearance. Incomplete oral bioavailabilities are reported both for the lipophilic drugs (e.g., labetalol, oxprenolol, and propranolol) due to extensive first-pass metabolism and for the more hydrophilic drugs (e.g., atenolol, acebutalol, and nadolol) due to medium or low absorption. Low bioavailabilities (as in the case of propranolol) are the source of large biologic variations, nonlinearities, or increased plasma levels with food, with age, in nonsmokers, or in disease states (e.g., hypothermia and renal, hepatic, celiac, Crohn's, or inflammatory disease). The pharmacokinetic comparison in this series of beta blockers reveals that pindolol with its medium lipophilicity has some important advantages. A low daily dosage is possible because of the high bioavailability, the low first-pass effect, the moderate metabolism, and the potency of this drug. Due to the low first-pass effect and the low daily dosage there are no saturation effects, and a good dose linearity is observed. This, combined with moderate metabolism and low protein binding, results in small variability and a good predictability in plasma levels and drug effects. Due to the balanced renal and hepatic clearance, no relevant drug accumulation has to be expected in patients with liver or kidney impairment.
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PMID:Pharmacokinetic comparison of pindolol with other beta-adrenoceptor-blocking agents. 612 95

When using methods of perfusion to preserve the rat pancreas, we found that perfusion into the celiac axis was the most effective. The viability of the cadaver pancreas from decapitated rats preserved by perfusion into the celiac axis for 6 hours under various conditions of hypothermia, hyperbaria and oxygenation was investigated. The condition of perfusion affected the ratio of degenerative islets/normal islets in the pancreas. The ratio, under conditions of hypothermia and oxygenation was the lowest, while that under conditions of hyperbaria was the highest. Insulin-releasing activity of islets from 6-hour-perfusion-pancreas, under conditions of hypothermia and oxygenation was 86.5 per cent or more of that of the control. Stainings with fluorescent antibody and peroxidase antiperoxidase, revealed a large number of A and B cells in the islets of the pancreas, in cases of up to 6 hours of perfusion.
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PMID:Perfusion preservation of cadaver rat pancreas: I. Morphological observation and biological function of the islets. 637 97

The study was designed to test whether intact vagal innervation of the liver is required for the formation of tolerance to lipopolysaccharide (LPS). Wistar rats were subjected to either denervation of the liver (transection of the hepatic and both celiac branches of the abdominal vagus) or sham surgery. Two weeks later, each rat had an osmotic pump implanted subcutaneously. The pump was filled with either a suspension of Escherichia coli LPS (18 mg/ml) in saline or saline alone. Via a catheter, the pump delivered its content into the right jugular vein at a rate of approximately 0.72 microl/kg/h (approximately 13 microg/kg/h of LPS) over 28 d. On day 25 of the infusion, each animal had another catheter implanted into the left jugular vein. Three days later, each rat was injected with a lethal bolus dose of LPS (15 mg/kg) and had its colonic temperature recorded. The saline-infused sham-operated rats responded to the bolus injection of LPS with hypothermia followed by a fever (mean response magnitude 1.0+/-0.2 degrees C); 91% of the animals died within 24 h. The LPS-primed shams developed marked tolerance: When challenged with a lethal dose of LPS, they exhibited a significantly smaller thermal response (magnitude 0.5 +/- 0.2 degrees C) and none died. No group of the vagotomized animals, whether LPS- or saline-primed, became tolerant: Both groups exhibited similar hypothermic responses to the bolus LPS injection and a substantial mortality rate (40 and 100%, respectively). The study shows that prolonged infusion of low doses of LPS leads to the formation of tolerance and that vagal denervation of the liver by hepato-celiac vagotomy suppresses this process. The mechanisms of vagal control of the formation of LPS tolerance remain speculative.
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PMID:Does the formation of lipopolysaccharide tolerance require intact vagal innervation of the liver? 1118 17

The multiple effects of vagotomy on the thermoregulatory response to systemic inflammation are reviewed (primarily, for the model of intravenous lipopolysaccharide administration in the rat). The following conclusions are drawn. (1) Vagotomy-associated thermoeffector insufficiency is likely to account for the attenuation of the fever response observed in some--but not all--studies; such an insufficiency is, however, preventable by postoperative care, including the use of a liquid diet. (2) The febrile response to low doses of lipopolysaccharide (monophasic fever) is mediated by the hepatic (but not gastric or celiac) vagal fibers, presumably afferent; the same fibers are likely to be involved in the development of tolerance to low doses of circulating endotoxins. (3) Phase 1 of the polyphasic febrile response to moderate doses of lipopolysaccharide involves capsaicin-sensitive afferents (either nonvagal only or both nonvagal and vagal), does not involve cholecystokinin A-receptors, and may involve peripheral prostaglandins. (4) Febrile phase 2 does not require the integrity of abdominal nerve fibers, either vagal or nonvagal, at least in the rat. (5) Phase 3 of the febrile response to intravenous lipopolysaccharide (and perhaps the response to intraperitoneal lipopolysaccharide) involves capsaicin-insensitive vagal fibers, presumably efferent; the involvement of these fibers in febrigenic mechanisms is strongly modulated by an unknown factor. (6) A hepatoceliac vagal, presumably efferent, mechanism ('an anti-inflammatory pathway') counteracts the development of lipopolysaccharide-induced hypothermia and shock.
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PMID:Thermoregulatory manifestations of systemic inflammation: lessons from vagotomy. 1118 25

The primary risks associated with thoracoabdominal aortic aneurysm (TAAA) repair-namely operative death, paraplegia, and renal failure necessitating dialysis-are commonly related to the distal ischemia that occurs during aortic clamping and the disruption of vital branching arteries. Our technique for open TAAA repair has evolved over the course of 3 decades, from the unheparinized, simple "clamp-and-sew" approach learned directly from E. Stanley Crawford himself to a contemporary, multimodal strategy that uses an array of surgical adjuncts. Today, our approach to TAAA repair is largely standardized and based on the Crawford extents of TAAA repair, but we have maintained flexibility to explore new techniques and to adapt to the specific needs of patients. To protect the spinal cord, we routinely use mild passive hypothermia, cerebrospinal fluid drainage, left heart bypass, and reimplantation of crucial intercostal or lumbar arteries. The renal arteries are perfused with cold solution to protect the kidneys from ischemic damage, and the celiac axis and superior mesenteric artery are perfused with isothermic blood from the left heart bypass circuit, which minimizes the duration of abdominal-organ ischemia. The most extensive repair, Crawford extent II repair, typically replaces the aorta from just beyond the left subclavian artery to the aortic bifurcation; unsurprisingly, it commonly poses greater operative risk than do less extensive TAAA repairs (extent I, III, and IV). Subsequently, most surgical adjuncts used today were developed to ameliorate risk in extent II repair. Here, we provide a detailed description of our approach to open extent II TAAA repair.
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PMID:Extent II Thoracoabdominal Aortic Aneurysm Repair: How I Do It. 2804 22