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

The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.
 ...
PMID:Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. 29 52

Blood glucose, lactate, plasma free fatty acid and plasma and tissue individual free amino acid levels were followed in newborn rabbits exposed for 10 h to an environmental temperature of 25 degrees C. Severe hypothermia developed with an increase of blood lactate and accumulation of total free amino acids in plasma and liver. Alanine, isoleucine, leucine, valine, phenylalanine, tyrosine, ornithine and taurine were elevated in the plasma; alanine and ornithine in the liver; leucine and isoleucine in the muscle.
 ...
PMID:The metabolic effects of cold exposure in the newborn rabbit. 48 11

The intensity of [14C]leucine incorporation into heart, liver, brain, muscle, and blood plasma protein in gophers under deep artificial hypothermia has been studied. It was shown that the intensity of protein synthesis decreased sharply under these conditions. Insignificant incorporation of [14C]leucine into proteins was observed during the first two hours after the onset of hypothermia and then ceased completely.
 ...
PMID:[Protein synthesis during hyperthermia in ground squirrels]. 139 Dec 21

We recently reported that H-Lys psi (CH2NH)Lys-Pro-Tyr-Ile-Leu-OH (JMV 449), a pseudopeptide analogue of neurotensin-(8-13) with a reduced CH2NH bond in position 8-9, was about 3 times more potent than neurotensin in binding to mouse brain membranes and in contracting the guinea-pig ileum, and was markedly more resistant to degradation than neurotensin when exposed to rat brain membranes. In the present study, we compared the time courses and dose-response relationships for the ability of i.c.v. injected neurotensin and JMV 449 to elicit hypothermia and analgesia (tail-flick test) in the mouse. The results show that the pseudopeptide analogue behaved as a highly potent and long-lasting neurotensin agonist in these two in vivo bioassays. The analogue should prove very useful for studying the effects of chronic neurotensin receptor stimulation in vitro and in vivo.
 ...
PMID:JMV 449: a pseudopeptide analogue of neurotensin-(8-13) with highly potent and long-lasting hypothermic and analgesic effects in the mouse. 142 58

The aim of the present study was to investigate if a physical dependence could be induced by chronic activation of the endogenous enkephalinergic system. We have therefore evaluated naloxone-induced withdrawal syndrome in rats after central infusion during 7 days of comparable antinociceptive doses of RB 38 A ((R,S)HONH-CO-CH2-CH(CH2C6H5)-CONH-CH(CH2C6H5)-COOH), a mixed enkephalin catabolism blocker and of the selective mu, DAGO (Tyr-D-Ala-Gly-(Me)Phe-Gly-ol) and delta, DSTBULET (Tyr-D-Ser(OtBu)-Gly-Phe-Leu-Thr), opioid agonists. The responses were compared to those induced by RB 38 B ((S,S)HONH-CO-CH2-CH(CH2C6H5)-CONH-CH(CH2C6H5)-COOH), a selective inhibitor of the 24.11 neutral endopeptidase (NEP) 'enkephalinase'. DAGO induced a severe withdrawal syndrome evidenced by a large weight loss, hypothermia, jumping, mastication, teeth chattering, diarrhoea, lacrimation and salivation. In contrast, DSTBULET and RB 38 A produced only a moderate physical dependence. Only two signs were statistically different in these two groups: wet dog shakes and temperature. Chronic i.c.v. administration of DAGO, DSTBULET and RB 38 A produced a time-dependent reduction in analgesia, but 120 h after continuous infusion only RB 38 A was able to still induce a significative antinociceptive effect. The present data suggest that even in the drastic conditions used here long-term complete inhibition of enkephalin catabolism induces a weak tolerance and a moderate physical dependence, similar to that produced by delta opioid agonists. This effect was not observed after chronic selective inhibition of NEP by RB 38 B.
 ...
PMID:Differences in physical dependence induced by selective mu or delta opioid agonists and by endogenous enkephalins protected by peptidase inhibitors. 216 53

Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and MIF-1 (Pro-Leu-Gly-NH2) can increase GABA-stimulated benzodiazepine binding in brain tissue can block the hypothermia induced by several other compounds. Since benzodiazepines can also cause hypothermia, colonic temperatures were measured in mice after administration of chlordiazepoxide (CDP) and these two brain peptides. In several experiments involving different doses and times of administration of CDP, MIF-1, and Tyr-MIF-1, there were no significant effects of the peptides in altering the reliable decrease in colonic temperature induced by the benzodiazepine. The results indicate that the interaction of Tyr-MIF-1 and MIF-1 with benzodiazepines does not involve thermoregulation.
 ...
PMID:MIF-1 and Tyr-MIF-1 fail to alter benzodiazepine-induced hypothermia. 257 Nov 69

The effect of hypoxia, cold and hypoxic-cold stress was studied on plasma and brain amino acid levels of rats. Hypoxia caused a considerable increase in plasma taurine and phosphoserine levels, while the remaining amino acids (except valine, cystine, iso-leucine, leucine and anserine) decreased significantly. On the other hand cold stress significantly increased the plasma taurine, asparagine and decreased glutamine, glycine, alanine, methionine and histidine levels. The hypoxic-cold stress combination produced marked decrease in most of the plasma levels of amino acids (except phosphoserine, taurine and anserine). During brain amino acid studies, hypoxia significantly elevated taurine, aspartic acid, valine and leucine levels while the concentrations of other amino acids were not significantly altered. Cold stress was found to elevate taurine and valine levels, while leucine and phenyl-alanine levels were significantly decreased. Exposure of animals to hypoxic-hypothermia affected significantly the brain levels of valine, methionine, leucine and arginine. Since, the change in amino acid levels in brain is less prominent, as compared with plasma, in response to stress, it appeared that brain possesses higher adaptive mechanisms to counteract the stress induced amino acid level imbalance.
 ...
PMID:Effect of hypoxia and/or cold stress on plasma and brain amino acids in rat. 274 Jun 20

Earlier it was found that oxytocin (OXT) treatment inhibited the development of tolerance to ethanol. In the present study the possibility was investigated whether the effect of OXT on ethanol tolerance was related to peptide fragments derived from the C-terminal part of the molecule. The actions of different doses of the C-terminal tripeptide (prolyl-leucyl-glycinamide, PLG) and of a synthetic dipeptide derivative (Z-prolyl-D-leucine, Z-Pro-D-Leu) on the development of tolerance to the hypothermic effect of ethanol in CFLP mice were therefore investigated. Peptide treatment did not affect body temperature in ethanol-naive animals. The acute effects (hypothermia, sleeping time) of a single ethanol injection were also unaffected by these peptides. In contrast, both PLG and Z-Pro-D-Leu inhibited the development of tolerance to the hypothermic effect of ethanol. Accordingly, it might be speculated that a sequence active in affecting ethanol tolerance is located in the C-terminal part of the OXT molecule.
 ...
PMID:C-terminal fragments of oxytocin (prolyl-leucyl-glycinamide and Z-prolyl-D-leucine) attenuate the development of tolerance to ethanol. 288 3

Acute intraventricular administration of human beta-endorphin (15 microgram) produced analgesia, hypothermia and catalepsy in male Sprague-Dawley rats. Injections of beta-endorphin given every 8 hr for 3 days resulted in the development of tolerance to all of the above mentioned pharmacological effects. Tolerance developed rapidly to the hypothermic effect and less rapidly to the analgesic and cataleptic effects. After the third or the fourth injection of beta-endorphin, pronounced hyperthermia, rather than hypothermia, was observed. After seven or eight injections of beta-endorphin, tolerance to the analgesic effect was complete and the cataleptic effect was reduced to 50% of the original. Daily s.c. administration of Pro-Leu-Gly-NH2 (MIF) or cyclo(Leu-Gly) (2 mg/kg each) blocked the development of tolerance to the analgesic and cataleptic effects of beta-endorphin. The hyperthermic effect of beta-endorphin in beta-endorphin-tolerant rats was partially blocked by both MIF and cyclo(Leu-Gly). Multiple injections of MIF or cyclo(Leu-Gly) did not alter beta-endorphin-induced analgesia, catalepsy and hypothermia in rats which were given repeated intraventricular injections of saline. Since MIF is a naturally occurring peptide of hypothalamic origin, these studies suggest that the hypothalamus may be an important site in regulating the pharmacological effects of chronically administered endogenous opiates.
 ...
PMID:Inhibition of tolerance to the pharmacological effects of human beta-endorphin by prolyl-leucyl-glycinamide and cyclo(leucylglycine) in the rat. 611 70

The effects of melanotropin release inhibiting factor (Pro-Leu-Gly-NH2; MIF) and its three analogs Pro-ILeu-Gly-NHi2, Leu-Gly-NH2 (a metabolite of MIF) and cyclo (Leu-Gly) (an analog derived theoretically from MIF) on tolerance to morphine-induced hyperthermia, hypothermia and catalepsy were studied in male Sprague-Dawley rats. Subcutaneous implantation of four morphine pellets (each containing 75 mg of morphine-free base) during a 3-day period resulted in the development of tolerance to these pharmacological effects of morphine as evidenced by decreased intensity of responses to designated i.p. doses of morphine. Concurrent daily s.c. administration of each peptide, injected 24 hr apart for 3 days, resulted in blockade of tolerance to the pharmacological effects of morphine as evidenced by a greater pharmacological response in peptide plus morphine-treated rats as compared with the vehicle plus morphine-treated rats. Multiple injections of peptides did not modify morphine-induced responses in rats implanted with placebo pellets. The blockade of tolerance to morphine by these peptides was not associated with changes in the distribution of morphine in brain and plasma. These studies indicate that the following changes do not modify the inhibitory action of MIF tolerance: 1) substitution of ILeu in place of Leu in MIF; 2) cleavage of the Pro-Leu bond which gives rise to Leu-Gly-NH2; and 3) possible cyclization (diketopiperazine formation) of Leu-Gly-NH2 which yields cyclo (Leu-Gly), and that linear and cyclic peptides either derived from the hypothalamus or synthesized may provide agents to block opiate-induced tolerance.
 ...
PMID:Structure activity relationship studies with hypothalamic peptide hormones. I. Effect of melanotropin release inhibiting factor and analogs on tolerance to morphine in the rat. 612 Feb 29


1 2 3 4 5 Next >>