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

The recovery of the myocardial contractility of blood-perfused papillary muscle from the rabbit hearts was used to determine if hypothermia would minimize the myocardial injury associated with intermittent aortic cross-clamping (IACC). Continuous normothermic coronary perfusion for 2 hours with either cross circulation or a membrane oxygenator had only minimal adverse effects on contractility. None of the hearts tolerated normothermic IACC (45 minutes of anoxia and 10 minutes of reperfusion, repeated twice), When the myocardial temperature was reduced to 32 degrees C., the recovery following IACC was 41.25 +/- 11.21 percent (n=8). With hypothermia of 28 degrees C., it was 70.43 +/- 13.03 percent (cross circulation group, n=7) or 68.36 +/- 13.11 percent (membrane oxygenator group, n=7). If the hearts were cooled to 24 degrees C., the recovery of the myocardial contractility following IACC was 90.95 +/- 5.42 percent (n=11). The improvement of the degree of recovery by hypothermia was statistically highly significant (p less than 0.005). Creatine phosphokinase (CPK) and isoenzymes (CPK-MB) were also measured in some groups, but the results warrrant further studies before they can be correlated with the myocardial function.
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PMID:Experimental evaluation of hypothermic intermittent coronary perfusion. 43 Oct 97

Signs of hypothermia injury were studied in rabbits cooled to a core temperature of 30 degrees C by immersion in ice water and thereafter rewarmed to 35 degrees C. Anaesthetized control rabbits were kept normothermic (37 degrees C) for a corresponding time (4 h). Creatine phosphokinase (CPK) activity increased 24 h after hypothermia to 20-fold in serum. In cerebrospinal fluid the activity was already significantly (5-fold) increased after hypothermia and was still as high at 24 h. Smaller increase was also found in the control normothermic rabbits both in serum (10-fold) and cerebrospinal fluid (2-fold). The values had returned to the initial level after 1 week. Small haemorrhages were observed in the brain at 24 h and slight scarring was seen in the myocardium of some rabbits which had lived 4 weeks following hypothermia. The results indicate that CPK can be a useful marker in the diagnostics of hypothermia death, especially in cerebrospinal fluid, which is less affected than blood by autolysis.
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PMID:Creatine phosphokinase in serum and cerebrospinal fluid, and microscopic findings in brain and heart in hypothermic rabbits. 322 8

Acute changes in cerebral perfusion and metabolism after subarachnoid hemorrhage (SAH) have been shown to contribute significantly to acute brain injury. The purpose of this study was to examine the effects of moderate hypothermia on the acute changes after massive experimental SAH as evaluated by diffusion-weighted imaging (DWI) and magnetic resonance spectroscopy (MRS). SAH in rats was induced by injection of 0.5 mL of arterial blood. Normothermic animals (NT, n = 10) were kept at 37.0 +/- 0.2 degrees C, while temperature was lowered to 32.0 +/- 0.2 degrees C in the primary hypothermia group (pHT, n = 10) prior to SAH and in the secondary hypothermia group (sHT, n = 10) immediately after SAH. DWI and MRS were performed from 30 min prior up to 3 h after injury. The apparent diffusion coefficient (ADC) was measured in cortical and hippocampal regions of interest (ROIs). MRS included lactate, N-acetyl aspartate (NAA), and creatine in a central voxel. DWI showed a generalized, significant decline in ADC after SAH in NT. Significant change in ADC in pHT was absent, and accelerated recovery for animals in sHT was noted. MRS analysis revealed significant lactate accumulation to 204 +/- 40% from baseline only in NT, while sHT was characterized by a transient, less pronounced increase of lactate (159 +/- 11%) and lactate in pHT did not change significantly (117 +/- 11%). NAA did not change significantly when compared to baseline or between groups for NT, pHT, or sHT. Creatine rose significantly to 166 +/- 27% in NT after the insult, indicating increased metabolic stress which was absent in pHT (106 +/- 8%) and sHT (124 +/- 18%). Hypothermia can ameliorate early development of cytotoxic edema, lactate accumulation, and a general metabolic stress response after SAH, even when started after the insult. Our study indicates that a potentially beneficial influence on metabolism and cerebral perfusion in this crucial phase is practicable and might hold the key to further improve outcome in SAH.
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PMID:Hypothermia reduces cytotoxic edema and metabolic alterations during the acute phase of massive SAH: a diffusion-weighted imaging and spectroscopy study in rats. 1862 60