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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fundamental physicochemical characteristics of the acid-base related constituents of extracellular and intracellular fluid spaces of vertebrates in relation to changes in temperature have been reviewed. Emphasis has been placed upon the dissociation constant of water, the solubility constant of CO2, the dissociation constant of histidine imidazole, the hydroxyl-hydrogen ion ratio, the protein charge state and the alpha-imidazole regulation concept. Because pN and pKIm change in parallel when temperature varies, the OH/H ratio and the alpha-imidazole value for any sample of blood or plasma held anaerobically in vitro are invariant with changing temperature, since a constant CO2 content is maintained. Thus, when blood or plasma cools, pH increases and PCO2 decreases, but relative alkalinity and the protein charge state remain constant. These responses are solely the consequence of physical constants, that is, equilibrium constants and gas solubility, changing with temperature. In vivo, the set of PCO2 is established in each poikilothermic species by its normal ventilatory pattern designed to maintain constant CO2 content. Regulation in vivo in poikilotherms consists of adjustments of ventilation per unit metabolism (VA/VCO2) appropriate to every temperature. When the ventilatory and renal mechanisms of human beings are suppressed by anesthesia and hypothermia, their extracellular and intracellular responses mimic those of poikilotherms. Clinical management of hypothermia in humans requires ventilatory control using oxygen-augmented room air without added CO2 monitored by pH measurements of arterial blood warmed anaerobically to 37 degrees C. Finally, the need for new techniques to measure intracellular pH as temperature is lowered and some areas for further investigation are suggested.
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PMID:The hydroxyl-hydrogen ion concentration ratio during hypothermia. 629 7

Intracisternal (IC) administration of neurotensin (NT) in a dose of 10 micrograms produced a significant hypothermia and antinociception in the hot-plate test in mice. Both of these effects of IC NT were completely antagonized by concomitant administration of equimolar doses of thyrotropin-releasing hormone (TRH) and several TRH congeners including 3-methyl-His-TRH (pGlu-3-methyl-His-Pro-NH2), MK-771 (pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide), beta-ala-TRH (pGlu-His-Pro-beta-ala-NH2), and RX-77368 (pGlu-His-dimethyl-Pro-NH2). The antagonism by TRH and TRH analogs on NT-induced hypothermia and antinociception was dose-dependent. Of particular interest was the finding that RX-77368 not only blocked the effects of NT but also produced hyperalgesia. It appears that TRH analogs that are more resistant to biologic degradation are, like TRH, capable of blocking NT-induced behaviors.
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PMID:Neurotensin-induced antinociception and hypothermia in mice: antagonism by TRH and structural analogs of TRH. 642 94

Two patients were rewarmed from hypothermia (esophageal temperature 27.2 degrees C, 27.5 degrees C respectively). The first case suffered from head-injury after alcohol ingestion and was deeply comatose. A metabolic or cardiovascular regulatory response to cold was not observed in this patient. The relationship between esophageal temperature and whole-body-oxygen consumption was quantified with a Q10 of 2.75 during rewarming (27.2-37.2 degrees C). His epinephrine levels were greatly elevated to 1,000 pg/ml whereas norepinephrine levels were only moderately increased to 250 pg/ml. Premature ventricular contractions (PVCs) during intubation or from the pulmonary artery catheter were not observed. The second patient was a 87 year old man with accidental hypothermia. He exhibited shivering at an esophageal temperature of 27.5 degrees C which indicated persistent thermoregulation. In contrast to the first case his norepinephrine levels were elevated to 1,500 pg/ml and his epinephrine levels only to 450 pg/ml. After onset of surface rewarming an additional increase in norepinephrine levels was observed and an increasing rate of PVC's (15/min) recorded, which ceased when temperature returned to normal. Our observations indicate that part of the cardiac complications during rewarming from deep hypothermia may result from thermoregulation and additional catecholamine liberation.
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PMID:[Rewarming from moderate to deep hypothermia: plasma catecholamine content, metabolism and circulatory function. 2 case reports]. 648 85

A 64-year-old male with an incomplete spinal cord injury had been taking baclofen 20 mg tid for 2 1/2 months without side effects. His blood urea nitrogen and serum creatinine rose from 13 and 0.9 mg%, respectively, to 59 and 2.8 mg% after ibuprofen 600 mg tid was begun. The patient displayed baclofen toxicity, developing confusion, disorientation, bradycardia, and hypothermia. His blood pressure dropped and he complained of blurred vision. Ibuprofen discontinuation and fluid repletion corrected the renal indices. Rapid tapering of baclofen was accompanied by reversal of baclofen toxicity. Patients taking baclofen must be monitored closely for toxicity when declining renal function is present. Clinicians should be alert to the possibility of renal insufficiency developing when ibuprofen is initiated. This case demonstrates the potential for ibuprofen-induced renal insufficiency to reduce baclofen clearance, thereby leading to baclofen toxicity. Published reports of ibuprofen-induced renal insufficiency are reviewed and pertinent pharmacokinetics of baclofen discussed.
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PMID:Baclofen toxicity associated with declining renal clearance after ibuprofen. 648 61

Atrioventricular conduction abnormalities have become more frequent since the reintroduction of cardioplegic techniques for myocardial preservation during cardiac surgery. An animal model was developed to clarify the role of atrial septal hypothermia in the preservation of the primary site of postoperative conduction delay, the AV node. In our study, 10 animals served as the control group. They were subjected to 40 min of cardioplegic arrest during which the heart was protected with multidose cold potassium cardioplegia. Atrial septal temperatures averaged 27.4 degrees +/- 1.2 degrees C during cardioplegic arrest. We treated 10 additional animals (study group) similarly, except that atrial hypothermia was augmented by intracavitary or specialized topical techniques, which resulted in an average atrial septal temperature of 20.8 degrees +/- 3.3 degrees C (p less than .05). Detailed electrophysiologic studies of both groups were performed at 37 degrees C before and after cardioplegic arrest. Significant prolongation of AV nodal, and to a lesser extent His-Purkinje, conduction times was noted in the control group, but no conduction abnormalities occurred in the study group receiving augmented atrial hypothermia. Thus, conduction block in the specialized conduction system after cardioplegic arrest appears to be related to the adequacy of hypothermic preservation of the atrial septum and can be prevented by augmented atrial hypothermia.
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PMID:Conduction block after cardioplegic arrest: prevention by augmented atrial hypothermia. 687 94

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether rat hearts could be predisposed to the calcium paradox by perfusion with Bretschneider's calcium-free histidine-buffered cardioplegic solution. Creatine kinase (CK) release during the reperfusion phase was used to quantitate cell damage. Perfusion with cardioplegic solution was performed at 37 degrees and 20 degrees C. Reperfusion after 10 minutes of perfusion with this solution at 37 degrees C resulted in a full calcium paradox. After 120 minutes of perfusion with cardioplegic solution at 20 degrees C, CK release during reperfusion amounted to 30% of the release during a full calcium paradox. This CK release could be further reduced by lowering the coronary flow rate or by adding 50 mumol X L-1 CaCl2 to the cardioplegic solution. It is concluded that a combination of hypothermia, a low coronary flow rate, and a limited duration of exposure to Bretschneider's histidine-buffered cardioplegic solution will minimize the risk of evoking the calcium paradox.
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PMID:Bretschneider's histidine-buffered cardioplegic solution and the calcium paradox. 688 57

A male alcoholic who presented with hypothermia and confusion was diagnosed as suffering from Wernicke's encephalopathy. He showed in addition signs of bulbar damage with cranial nerve signs, weakness of all limbs and absent oculo-vestibular responses. His course was complicated by recurrent episodes of aspiration pneumonia with death resulting from this cause. Neuropathological findings included typical features of Wernicke's encephalopathy as well as central pontine myelinolysis.
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PMID:Wernickes encephalopathy with central pontine myelinolysis presenting with hypothermia. 695 96

Acute administration of cyclo (His-Pro) to rats cause a dose-dependent decrease in ethanol-induced hypothermia. Bromination of the imidazole moiety of histidine in cyclo (His-Pro) resulted in a significant increase in its potency to attenuate ethanol hypothermia. In contrast, benzylation of the imidazole moiety of histidine or the substitution of one or both of the amino acids in cyclo(His-Pro) led to a total loss of its thermomodulatory activity. In conclusion, it appears from these preliminary data that it may be possible to design analogs of CHP that may be effective antagonists for ethanol hypothermia.
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PMID:Attenuation of alcohol-induced hypothermia by cyclo (His-Pro) and its analogs. 766 54

Central administration of exogenous cyclo(His-Pro) (CHP) is known to produce hypothermia in rodents. In the present study, we examined the role of endogenous CHP in cold-induced hypothermia in the desert rat, Mastomys natalensis. The results of these studies show that a rise in hypothalamic CHP content accompanied a decrease in rectal temperature during cold exposure. Immunoneutralization of endogenous CHP resulted in a significant decline in cold-induced hypothermia. In addition, central administration of cyclo(Ala-Gly), a structural analogue of CHP, also led to a decrease in cold-induced hypothermia. The results of these studies show that changes in endogenous CHP levels may affect body temperature regulation.
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PMID:Role of endogenous cyclo(His-Pro) in cold-induced hypothermia in the desert rat (Mastomys natalensis). 770 Aug 49

We presented a case of severe postoperative choreoathetosis which occurred in a 3-year-old boy with tetralogy of Fallot early postoperatively but almost completely recovered within two years after the operation. Because of the large coronary arterial branch on the right ventricular outflow, a small outflow incision and deep hypothermia (lowest rectal temperature was 13 degrees C) and short duration of circulatory arrest (8 minutes) were adopted. Postoperative course was uneventful till the onset of choreoathetosis on the fifth postoperative day. His symptoms and signs of choreoathetosis, oral-facial dyskinesias, hypotonia, affective changes and also pseudobulbar signs were becoming serious during the first week from the onset, but afterwards his condition started getting better gradually every week, and every month. Now, 20 months after the operation, he is almost completely recovered except for small and slow involuntary movements. Though investiations including CT, MRI and EEG were all almost normal, regional nonspecific low area of the frontal lobe and cerebellum was detected by SPECT (single photon emission computed tomography) on the 32nd and 94th postoperative days, respectively.
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PMID:[Postoperative choreoathetosis in a case of tetralogy of Fallot]. 788 49


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