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)

Plasma cortisol and ACTH concentrations were measured in two groups of children (aged 1-16 yr). Ten children underwent routine (non-pulsatile) cardiopulmonary bypass and 10 underwent pulsatile bypass under moderate hypothermia (28-32 degrees C). Comparable increases in cortisol and ACTH concentrations were demonstrated at the onset of bypass and the concentrations of both hormones increased during bypass. In the post-bypass period plasma cortisol concentration increased sharply; there was no further increase in the plasma ACTH concentration. By 24 h the concentrations of both hormones had declined towards baseline values. There were no significant differences between the groups.
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PMID:Adrenocortical hormone concentrations in children during cardiopulmonary bypass with and without pulsatile flow. 283 62

To investigate the mechanism by which ACTH secretion is inhibited during hypothermia, hypophysial portal blood was collected from euthermic and hypothermic rats, and the concentrations of corticotropin-releasing factor (CRF), vasopressin (AVP), and oxytocin (OT) were measured by RIA. Whereas CRF levels in portal plasma were not different in the two groups, AVP and OT levels were significantly lower in hypothermic rats. The concentration of AVP and OT in peripheral plasma was also significantly lower in hypothermic rats compared with euthermic controls. The pituitary responsiveness to CRF during hypothermia was tested in vivo and in vitro. In pentobarbital-anesthetized male rats injected iv with 0.1 or 1.0 nmol CRF, the ACTH response was significantly smaller in hypothermic compared with euthermic animals. However, hemipituitaries superfused at 31 C released the same amount of ACTH in response to 1 nM CRF as hemipituitaries superfused at 37 C (31 C, 541 +/- 90 pg; 37 C, 563 +/- 29 pg) despite reduced baseline secretion (31 C, 77 +/- 10 pg/10 min; 37 C, 114 +/- 14 pg/10 min; P less than 0.05). The data suggest that the inhibition of ACTH secretion during hypothermia is mediated by decreased hypothalamic secretion of AVP and OT which in turn decreases the pituitary responsiveness to CRF.
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PMID:Inhibition of corticotropin release during hypothermia: the role of corticotropin-releasing factor, vasopressin, and oxytocin. 298 77

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
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PMID:Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease. 299 Nov 78

The hormonal changes were estimated after poisoning with an extremely toxic organophosphate, soman (pinacolyl methylphosphonofluoridate). Soman produced a significant (p less than or equal to 0.05) increase in serum corticosterone, thyroxine, and triidothyronine concentrations at 3, 6, and 9 hr after poisoning. However, by 22 hr the levels were not significantly different from control. Plasma ACTH levels were decreased at 3 hr after soman at 100 micrograms/kg but not after 287 micrograms/kg. Serum testosterone levels were decreased significantly (p less than or equal to 0.01) 6 and 9 hr after soman poisoning but had returned to control levels by 22 hr. Soman (100 micrograms/kg) produced an immunosuppressive response when administered at 24 hr after an antigen (sheep red blood cells). However, a similar response was obtained in adrenalectomized mice suggesting that some other mechanism other than elevated corticosterone was responsible for the immunosuppressive effect. Soman poisoning produced an intense hypothermia. It is possible that the hormonal changes noted after soman poisoning are due to a reduction in metabolism and excretion, a result of the hypothermia and not a direct action of soman.
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PMID:Hormonal consequences of organophosphate poisoning. 300 1

Mice were poisoned by an extremely toxic organophosphate anticholinesterase soman (pinacolyl methylphosphonofluoridate), 50 or 100 micrograms/kg at 1000, and the serum concentrations of corticosterone were determined fluorometrically at 3-h intervals for at least 24 h. The lower soman dose (50 micrograms/kg) produced a modest increase in serum corticosterone concentrations but by 24 h the levels were not significantly different from control. Following the higher soman dose (100 micrograms/kg) the serum corticosterone levels were elevated significantly (p less than 0.05), for at least 27 h. However, ACTH concentrations were not elevated. It is possible that the elevated levels of corticosterone were due to a reduced metabolism and excretion of corticosterone resulting from the intense hypothermia, following soman poisoning which may change cardiac output and organ (liver and kidney) perfusion and not due to an enhanced release from the adrenal gland.
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PMID:Effect of soman (pinacolyl methylphosphonofluoridate) on the blood levels of corticosterone and adrenocorticotropin in mice. 302 95

alpha-MSH within the septal region of the brain has been implicated in fever control; this peptide and ACTH (1-24), which contains the alpha-MSH amino acid sequence, reduce fever when given intracerebroventricularly (ICV) or peripherally. These peptides also cause hypothermia when given in doses larger than those required to reduce fever. Both peptides occur naturally within the preoptic PO region of the brain, the CNS locus of primary temperature control. alpha-MSH (350 ng) injected bilaterally into the PO region via chronic cannulas reduced fever caused in six rabbits by IV injection of IL-1 (interleukin 1, endogenous or leukocyte pyrogen) but had no effect in afebrile animals. A larger dose (1.5 micrograms) not only reduced fever but caused hypothermia in 12 rabbits. In separate experiments PO injections of ACTH (1-24) (1 microgram) reduced normal temperature. In the same six rabbits alpha-MSH (1 microgram) caused slightly smaller hypothermia. alpha-MSH (1.5 micrograms) also had no effect in 8 afebrile rabbits when injected into the septum. The primary conclusion is that alpha-MSH receptors within the PO region can contribute to both the antipyretic and hypothermic actions that are observed after ICV and peripheral administration of the peptide.
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PMID:Effects of preoptic microinjections of alpha-MSH on fever and normal temperature control in rabbits. 360 19

Morphine 50 mg/kg i.p. produced a hypothermic effect in unrestrained guinea-pigs and this effect was potentiated when animals were restrained. The morphine-induced hypothermia was antagonized by dexamethasone treatment (1 mg/kg 24 hr and 0.5 mg/kg i.p. 2 hr before morphine). Treatment with the inhibitor of peptide biosynthesis cycloheximide (10 mg/kg i.p. 24 and 2 hr before morphine) also inhibited the hypothermic effect of morphine. ACTH injected intracerebroventricular produced no changes in body temperature. These results are consistent with the hypothesis that anterior pituitary peptide beta-endorphin may play a role in the hypothermic effect produced by morphine in the guinea-pig.
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PMID:Possible mechanisms implicated on the hypothermic effect induced by morphine in guinea-pig. 609 6

The effects of some neuroleptic butyrophenones such as haloperidol, clofuperol, trifluperidol, lenperone, moperone, and floropipamide on pituitary-adrenal activity were studied in rats following a single i.p. administration. All the drugs examined caused a marked increase in the plasma and adrenal corticosterone concentrations. The actions of haloperidol, clofluperol, and trifluperidol were shown to be most potent, while floropipamide was the weakest among them. The stimulatory effect of the drugs on adrenocortical activity was completely inhibited by either dexamethasone pretreatment or hypophysectomy and was shown not to be merely due to a consequence of a drug-induced hypothermia. These results indicate that the release of ACTH from the adenohypophysis is necessary for the drug action.
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PMID:Effects of neuroleptic butyrophenones on pituitary-adrenal activity in rats. 611 Jul 13

In view of the close structural similarity between the pro-opiocortin fragment, gamma-MSH, and ACTH/MSH-type peptides, the behavioural profile of gamma-MSH was explored. Attention was first focused on behavioural procedures in which ACTH/MSH-related neuropeptides have been found effective. It was found that gamma-MSH and ACTH-like neuropeptides had opposite effects on avoidance behaviour. In this respect the activity of gamma-MSH resembles that of opiate antagonists rather than that of beta-endorphin. Accordingly, ACTH(1-24) induced excessive grooming which is blocked by opiate antagonists and is attenuated by gamma-MSH. In addition, gamma-MSH injected into the periaqueductal grey matter of the brainstem of opiate-naive rats elicited symptoms reminiscent of those seen after opiate withdrawal. Gamma-MSH attenuated several effects of intracerebroventricularly administered beta-endorphin (e.g. antinociception, hypothermia, alpha-MSH release) and decreased the acquisition of heroin self-administration. Although gamma-MSH at rather high doses displaced naloxone from its specific binding sites in brain homogenates, it did not interfere with beta-endorphin-induced effects on in vitro muscle preparations (guinea-pig ileum; rat rectum). Interestingly, gamma-MSH induced relaxation of the rat rectum in vitro. It is postulated that gamma-MSH may attenuate beta-endorphin-induced effects by acting via gamma-MSH receptor sites (functional antagonism), although a pharmacological antagonism cannot be excluded as yet.
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PMID:Gamma-melanotropin and brain function. 626 81

Adrenocorticotropin (ACTH) and alpha-melanotropin (alpha-MSH) occur in brain tissue known to be important to temperature control. These peptides cause hypothermia if they are injected centrally in sufficient doses, but they do not act on the central set point of temperature control. Instead they appear to inhibit central pathways for heat conservation and production. In addition to their hypothermic capability, these peptides are antipyretic when given centrally in doses that have no effect on normal body temperature. ACTH has previously been associated with fever reduction in both clinical and experimental studies, and it may be that endogenous central ACTH is important for limitation of maximal fever. The hypothermic and antipyretic effects of ACTH do not depend on stimulation of the adrenal cortex because they are also observed in adrenalectomized rabbits. Nor is the antipyretic effect limited to the rabbit inasmuch as a comparable effect has been demonstrated in the squirrel monkey. The two peptides may be involved in central mediation of normal thermoregulation and fever, perhaps limiting the febrile response and other rises in body temperature by acting as neurotransmitters or neuromodulators in central thermoregulatory pathways.
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PMID:ACTH and alpha-melanotropin in central temperature control. 627 99


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