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

To evaluate the effect of selective brain cooling on cortical cerebral blood flow, we reduced brain temperature in nitrous oxide anesthetized adult rats using a high speed fan while keeping rectal temperature at 37-38 degrees C. During selective brain cooling, cortical cerebral blood flow, as measured by laser-Doppler flowmetry, increased to 215 +/- 26% (mean +/- SE) of baseline at a cortical brain temperature of 30.9 +/- 0.5 degrees C and a rectal temperature of 37.5 +/- 0.1 degrees C. During rewarming, as brain temperature increased, cortical cerebral blood flow decreased. The cerebral vasodilatory response to hypothermia may explain its protective effects during and after cerebral ischemia.
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PMID:Selective brain cooling increases cortical cerebral blood flow in rats. 821 16

A research program in cerebral ischemia was initiated by our laboratory to determine optimal strategies for cerebroprotection. Four studies relating to cerebroprotection using nuclear magnetic resonance spectroscopy in a sheep model of hypothermic cardiopulmonary bypass are summarized. These showed, first, that low-flow bypass, with a flow as low as 10 mL.kg-1 x min-1, maintained normal cerebral metabolism; second, that hypothermia increases the high-energy phosphate content and the intracellular pH of the brain; third, that hyperglycemia causes a profound intracellular acidosis; and, finally, that barbiturates prevent the normal increase in high-energy phosphates associated with hypothermia.
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PMID:Low-flow cardiopulmonary bypass and cerebral protection: a summary of investigations. 826 75

Deep to moderate hypothermia (24 degrees to 30 degrees C) during focal cerebral ischemia reduces infarct volume but must be initiated before the onset of ischemia to be effective and has deleterious pulmonary, myocardial and neurological effects. It is not known whether mild hypothermia (32 degrees to 33 degrees C) protects against ischemic neuronal damage, whether hypothermia induced after the onset of ischemia has protective effects, or whether these effects are associated with alterations in cortical blood flow. In this study, mild whole-body hypothermia was induced in rats just before or 10, 30, or 60 minutes after the onset of 2 hours of temporary middle cerebral artery occlusion; rewarming began immediately after reversal of occlusion and normothermia was maintained throughout 22 hours of reperfusion. Infarct volume, measured 24 hours after the end of reperfusion, was significantly smaller in rats made hypothermic within 30 minutes after the onset of ischemia than in normothermic controls; hypothermia induced at 60 minutes of ischemia did not reduce infarct volume. Cortical blood flow, measured by laser Doppler ultrasound flowmetry, was not significantly different between groups during ischemia; however, postischemic cortical blood flow correlated positively with total infarct volume. These results indicate that mild hypothermia initiated during temporary focal ischemia in rats can reduce infarct volume without attenuating the reduction in cortical blood flow.
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PMID:Delayed induction of mild hypothermia to reduce infarct volume after temporary middle cerebral artery occlusion in rats. 827 Sep 97

Considerable evidence indicates that brain temperature during ischemia affects the extent and distribution of ischemic injury. However, only limited data have been presented concerning the influence of temperature on ischemic damage after reversible focal cerebral ischemia. Because focal ischemic events of this type resemble conditions observed in the clinic, studies were undertaken to examine the effects of mild and moderate hypothermia on the extent of cerebral infarction after focal neocortical ischemia. Under halothane anesthesia, the left middle cerebral artery and both carotid arteries were occluded reversibly for a period of 3 hours in adult Sprague-Dawley rats. The animals were killed 3 days later. Brain sections were stained with triphenyltetrazolium chloride and analyzed for infarction using a computerized image analysis system. Temporal muscle temperature and rectal temperature were monitored continuously. The following groups with different intraischemic temporal muscle temperatures were analyzed: 1) control, 35.8 to 36.2 degrees C; 2) mild hypothermia, 33.0 to 33.5 degrees C; and 3) moderate hypothermia, 27.5 to 29.2 degrees C. The volumes of infarction were 214.5 +/- 17.9, 166.5 +/- 6.8, and 108.2 +/- 5.9 mm3 (mean +/- SEM) for the control, mild hypothermia, and moderate hypothermia groups, respectively. These findings demonstrate that both mild and moderate hypothermia reduce the impact of temporary focal ischemia in Sprague-Dawley rats.
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PMID:Effects of intraischemic hypothermia on cerebral damage in a model of reversible focal ischemia. 832 2

A technique for remotely controlling the degree of carotid artery occlusion in the gerbil model of cerebral ischaemia has been developed. The technique relies on manually adjustable nylon snares around the carotid arteries, in conjunction with a computer-based monitoring system, to control the degree of occlusion. This has allowed us to determine the dependence of energy metabolism (as assessed by 31P NMR spectroscopy) on blood flow in greater detail than was possible in our previous studies. Data obtained show that energy changes first appear at flows of 25-30 mL/100 g/min, while at flows below 20 mL/100 g/min there is a major derangement of energy metabolism. The model was used to determine the sensitivity of cerebral energy metabolism to reduced cerebral blood flow under normothermic conditions and in mild hypothermia (30 degrees C). Hypothermia had a protective effect in that energy metabolites were maintained at flows significantly below the normothermic threshold.
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PMID:Controllable graded cerebral ischaemia in the gerbil: studies of cerebral blood flow and energy metabolism by hydrogen clearance and 31P NMR spectroscopy. 834 51

Protein synthesis, measured as [14C]-leucine incorporation into proteins, was studied in the normothermic rat brain following 15 min of transient cerebral ischaemia and 1 h, 24 h and 48 h of recirculation, and in the hypothermic (33 degrees C) brain following 1 h and 48 h of recirculation. Ischaemia was induced by bilateral common carotid occlusion combined with hypotension. Following normothermic ischaemia, incorporation of [14C]-leucine was depressed by 40-80% at 1 h of recirculation in all brain regions studied. At 48 h postischaemia, incorporation returned to normal or above normal levels in the inner layers of neocortex, the CA3 region, the striatum and the dentate gyrus, while in the outer layers of neocortex and in the hippocampal CA1 region the incorporation was persistently decreased by 26% and 40% respectively. At 24 and 48 h postischaemia, protein synthesis in the CA1 region and the striatum could be attributed to proliferating microglia. Intra-ischaemic hypothermia ameliorated the persistent depression of protein synthesis in the CA1 region at 48 h postischaemia, and a two-fold increase compared to the normothermic group was observed both in the CA1 region and the striatum. In the cortex, eucaryotic initiation factor 2 activity transiently decreased at 30 min postischaemia. In animals subjected to intra-ischaemic hypothermia, the eucaryotic initiation factor 2 activity was reduced by 50% of control at 30 min of recirculation compared with 77% in normothermic animals. We conclude that the postischaemic depression of protein synthesis is in part caused by a decrease in eucaryotic initiation factor 2 activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postischaemic changes in protein synthesis in the rat brain: effects of hypothermia. 840 56

The change in the subcellular distribution of Ca2+/calmodulin-dependent protein kinase II was studied in the rat hippocampus following normothermic and hypothermic transient cerebral ischemia of 15 min duration. A decrease in immunostaining of Ca2+/calmodulin-dependent protein kinase II was observed at 1 h of reperfusion which persisted until cell death in the CA1 region. In the CA3 and dentate gyrus areas immunostaining recovered at one to three days of reperfusion. The CA2+/calmodulin-dependent protein kinase II was translocated to synaptic junctions during ischemia and reperfusion which could be due to a persistent change in the intracellular calcium ion homeostasis. The expression of the messenger RNA of the alpha-subunit of Ca2+/calmodulin-dependent protein kinase II decreased in the entire hippocampus during reperfusion, and was most marked in the dentate gyrus at 12 h of reperfusion. This decrease could be a feedback downregulation of the mRNA due to increased Ca2+/calmodulin-dependent protein kinase II activation. Intraischemic hypothermia protected against ischemic neuronal damage and attenuated the ischemia-induced decrease of Ca2+/calmodulin-dependent protein kinase II immunostaining in all hippocampal regions. Hypothermia also reduced the translocation of Ca2+/calmodulin-dependent protein kinase II and restored Ca2+/calmodulin-dependent protein kinase II alpha messenger RNA after ischemia. The data suggest that ischemia leads to an aberrant Ca2+/calmodulin-dependent protein kinase II mediated signal transduction in the CA1 region, which is important for the development of delayed neuronal damage. Hypothermia enhances the restoration of the Ca2+/calmodulin-dependent protein kinase II mediated cell signalling.
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PMID:Alterations of Ca2+/calmodulin-dependent protein kinase II and its messenger RNA in the rat hippocampus following normo- and hypothermic ischemia. 854 77

Neurologic injury that occurs after ischemia results from a cascade of events involving the release of various endogenous neurotoxins. A portion of the release of excitatory neurotransmitters is calcium dependent and may be attenuated by administration of calcium channel blockers. Using an in vivo model of ischemia, we studied the effects of omega-conopeptide MVIIC, a voltage-sensitive calcium channel blocker, and hypothermia (32 degrees C) on hippocampal glutamate and aspartate release in the peri-ischemic period. Thirty-four New Zealand white rabbits of either sex were anesthetized with halothane, intubated, and mechanically ventilated. Monitored variables included blood gases, mean arterial blood pressure, and the electroencephalogram. Microdialysis catheters were transversely inserted through the anterior portion of the dorsal hippocampus and perfused with artificial cerebrospinal fluid at a rate of 2 microliters/min. After stabilization period, animals were randomly assigned to one of the following groups: Control group (n = 8), 10 microM omega-conopeptide MVIIC group (n = 7), 100 microM omega-conopeptide MVIIC group (n = 7), Hypothermia group (n = 6; cranial temperature = 32 degrees C), and omega-conopeptide MVIIC + hypothermia group (n = 6; 100 microM omega-conopeptide MVIIC and cranial temperature 32 degrees C). All the rabbits were subjected to 10 minutes of global cerebral ischemia produced by neck tourniquet inflation combined with hypotension during halothane anesthesia. Conopeptide MVIIC was administered in the artificial cerebrospinal fluid used to perfuse the microdialysis catheter. In control animals, ischemia caused a significant increase in glutamate (9.7 fold) and aspartate (11.3 fold) concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transient brain ischemia in rabbits: the effect of omega-conopeptide MVIIC on hippocampal excitatory amino acids. 854 94

For surgical removal of a malignant choroid melanoma, it is necessary to reduce systolic blood pressure to around 50-60 mmHg in order to prevent choroidal haemorrhages. However, blood pressure reduction is associated with the risk of cerebral ischaemia. We report a patient with a malignant choroid melanoma in whom waves I and II of the brainstem auditory evoked potentials (BAEP) disappeared during surgery under controlled arterial hypotension and hypothermia (31.1 degrees C). The waves could be recorded again immediately after the mean arterial pressure was increased from 48 to 77 mmHg. The oesophageal temperature had dropped by 0.3 degrees C at this time. The 2-channel electroencephalogram (EEG) showed no irregularities during this time period. A bilateral, reversible, apparently blood-pressure-dependent loss of waves I and II during arterial hypotension despite a normal EEG has to our knowledge not been previously described in the literature. The isolated loss of waves I and II with maintenance of waves III, IV, and V is unusual. The literature contains reports of acoustic neurinoma patients in whom only wave V could be recorded. This is regarded as an indication of continued impulse conduction despite the loss of waves I to IV. Others have observed a patient with temporary and reversible loss of BAEP wave I due to vasospasm of the internal auditory artery that apparently occurred during or shortly after manipulation of the internal auditory meatus. Assuming anatomic peculiarities in the blood supply to the generators of the BAEP waves, a stenosis of the basilar artery could be considered as the cause of the bilateral reversible loss of waves I and II. Another potential source could be induced hypothermia, but this does not seem very likely because the patient's temperature was 0.3 degrees C lower at the return of the waves than at their loss.
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PMID:[Loss of brain stem auditory evoked potential waves I and II during controlled hypotension]. 867 70

The energy state and intracellular pH of the rat brain during and after transient cerebral ischemia was measured by the method of 31P magnetic resonance spectroscopy in vivo for the purpose of the evaluation of the protective effect of hypothermia. The rat's chest was opened and the bilateral subclavian arteries were ligated. The transient cerebral ischemia was induced by occlusion of the bilateral cerebral arteries using the balloon occluders. The rat's brain was cooled to 20 degrees C by the surface cooling using the ice bags and was heated to 37 degrees C in the control group, respectively. The animal's temperature was adjusted and regulated by a water blanket placed under the animal's body. After 30 min cerebral ischemia, the level of phosphocreatine (PC) was decreased to 58 +/- 4% versus to 36 +/- 4%, 20 degrees C versus 37 degrees C, respectively (p < 0.01). ATP was decreased to 73 +/- 5% versus 52 +/- 4% (< 0.01). Intracellular pH was decreased from 7.23 to 6.48 at 20 degrees C, from 7.22 to 6.08 at 37 degrees C (p < 0.01). After 60 min ischemia, PC was decreased to 52 +/- 5% versus to 33 +/- 6%, 20 degrees C versus 37 degrees C (p < 0.01). ATP was decreased to 62 +/- 6% versus 36 +/- 6% (p < 0.01). At 37 degrees C either PC or ATP was not recovered to the pre-ischemic level. Intracellular pH was decreased to 6.38 at 20 degrees C, to 5.80 at 37 degrees C (p < 0.01). It is concluded the hypothermia saved the high energy phosphates and keeps intracellular pH high and this beneficial effects contribute the brain protection during cerebral ischemia.
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PMID:[The protective effect of hypothermia in a new transient cerebral ischemic model of the rat--A 31P magnetic resonance spectroscopy in vivo study]. 868 62


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