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)

Bombesin (BN) and structurally related peptides, gastrin-releasing peptide (GRP) and neuromedin B (NMB), injected into the lateral ventricle produce multiple effects such as hypothermia, anorexia and hormone release. In this study, the pharmacological characteristics of BN receptors mediating hypothermia in the central nervous system (CNS) were investigated using free-moving male Wistar rats. Intracerebroventricular injections of BN, GRP and NMB produced hypothermia in a dose-dependent manner. The BN (0.3 microg)-induced effect showed a short latency and a 4-h duration with a potency increased by more than 100 times compared to the NMB-induced effect. Pretreatment with [D-Tyr(6)]BN(6-13)methylester, a GRP receptor antagonist, inhibited the BN (0.3 microg)- and NMB (7 microg)-induced hypothermia. On the other hand, BIM23127, an NMB receptor antagonist, did not influence the hypothermia. Of the protein kinase C (PKC) inhibitors, chelerythrine, Go6983, staurosporine and GF109203X, the first two partially blocked the BN-induced hypothermia. A PKC activator, phorbol-12,13-dibutyrate, decreased the rectal temperature. Genistein (a tyrosine kinase inhibitor), Y-27632 (a Rho kinase inhibitor) and PD98059 (a MAPK inhibitor) tended to suppress the BN-induced hypothermia, however, these were not significant. The inhibitory effect of a mixture of the three inhibitors, chelerythrine, genistein and Y-27632, on the BN-induced hypothermia was of a similar degree to that of chelerythrine alone. The BN receptor mediating the hypothermia seem to be the GRP subtype, and the effect involves activation of PKC.
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PMID:Pharmacological characteristics of bombesin receptor mediating hypothermia in the central nervous system of rats. 1267 68

Organ injury caused by ischaemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35 degrees C) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomised clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischaemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia,will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal "therapeutic window" for gene therapy.
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PMID:[Recent treatment of postischaemic anoxic brain damage after cardiac arrest by using therapeutic hypothermia]. 1906 51