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)

We analyzed cerebral protection of twenty-five patients, 11 of whom underwent ascending-arch aortic replacement and 14 underwent aortic arch replacement, supported with cardiopulmonary bypass. Twenty of patients underwent selective cerebral perfusion (SCP) with moderate hypothermic circulatory support; 12 of single SCP, 8 of double SCPs. Major arch branch reconstruction were performed with 11 patients; 3 of triple branches, 2 of double branches and 6 of single branch reconstruction. Cerebral impairment was found in 7 patients (25%) with SCP; 3 of them died of low output syndrome and major bleeding during perioperative period. Four of 17 patients, who survived more than one month, showed cerebral infarction in 2 patients and temporary neurological deficit in 2 patients. Our strategies for cerebral protection are (1) careful cerebral four vessels study, (2) SCP with perfusion pressure more than 40 mmHg and flow rate of 7-10 ml/kg/min under moderate hypothermia, (3) bilaterally double branches perfusion minimally for arch replacement, (4) intensive cerebral monitoring from multiple aspect, (5) pharmacological support with barbiturate or aprotinin, (6) gentle maneuver and reliable major branch cannulation to prevent debris embolism.
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PMID:[Strategy for cerebral protection during aortic arch replacement]. 837 23

The effectiveness of monitoring somatosensory evoked potentials (SEPs) intraoperatively to detect brain damage early remains controversial. To assess the diagnostic accuracy of this modality, a study was conducted between 1991 and 1994, recording SEPs in 287 consecutive patients undergoing cardiac and aortic surgery using cardiopulmonary bypass (CPB) with moderate hypothermia or deep hypothermic circulatory arrest. From P1 to N2 of the SEPs occurring within 50 ms latency in response to electrical stimulation of the median nerve were recorded over the contralateral postcentral cortex at 5-min intervals using a Neuropack-2 (Nihon Koden, Tokyo, Japan). Normal SEPs were recovered in 247 patients postoperatively; however, 2 of these patients had suffered a cerebral infarction and 1, a transient stroke intraoperatively, demonstrating a false-negative incidence of 1.2%. On the other hand, three different types of abnormal SEPs were recorded postoperatively. P1 and N1 absence, probably caused by a subcortical lesion, was observed in 4 patients; P2 and N2 absence, probably caused by a cortical lesion, was observed in 8 patients; and a flat SEP, representing diffuse damage, was observed in 2 patients. Among these 14 patients with abnormal SEPs, 7 showed no neurologic disturbance at all, demonstrating a false-positive incidence of 50%. Thus, we concluded that when normal SEPs are recovered during weaning from CPB, the incidence of brain damage could be predicted at below 5%. Conversely, when abnormal SEPs are demonstrated, the incidence of brain dysfunction impeding a return to active life is estimated to be about 70%.
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PMID:Continuous monitoring of short-latency somatosensory evoked potentials during cardiac and aortic surgery. 872 17

Intraischemic mild hypothermia has been shown to attenuate cerebral infarction occurring after transient focal ischemia. In contrast, the capacity of mild hypothermia to provide a protective effect when administered postischemically has not been clearly defined for transient focal events such as occur in many types of stroke. The present study addressed this issue by investigating the influence of timing and duration of mild hypothermia on cerebral infarction in a rat model of reversible focal ischemia. Sprague-Dawley rats (n = 45) were subjected to 3 h of focal neocortical ischemia by occluding reversibly one middle cerebral artery and both carotid arteries. Mild hypothermia was established after reperfusion and maintained for brief (1 h) or prolonged (21 h) periods. Animals were sacrificed 24 or 48 h after ischemia. A significant reduction (32%) in the volume of infarction was obtained when hypothermia was established immediately after reperfusion and maintained for a prolonged (21 h) period. In contrast, immediate but brief (1 h) hypothermia did not reduce infarction volume. Delaying hypothermia until 30 min post reperfusion and maintaining it for 21 h reduced infarction volume by 22%; however, this effect did not achieve statistical significance. These findings demonstrate that mild postischemic hypothermia is capable of protecting against cerebral injury following transient focal ischemia but that prolonged hypothermia is required to achieve this effect. These findings are consistent with increasing evidence that the window of therapeutic opportunity after transient focal ischemia is rather brief and that critical mechanisms involved in this form of ischemic injury remain activated over a rather lengthy postischemic interval.
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PMID:Mild postischemic hypothermia limits cerebral injury following transient focal ischemia in rat neocortex. 877 89

Skin surface temperature was examined using thermography in 26 patients with unilateral ischemic cerebrovascular disease (5 with pontine lesions, 5 with lateral medullary lesions and 16 with hemispheric lesions). Three of the 5 patients with pontine lesions and 4 of the 5 with medullary lesions showed hemihyperthermia on the ipsilateral body surface. However, the face showed no impairment with pontine lesions, whereas it appeared as a hyperthermic area with medullary lesions. Ten of 11 patients with lesions of the internal capsule or putamen had hypothermia on the contralateral body surface except for the face. All the patients with thalamic lesions showed no skin temperature asymmetry. These observations suggest the following: (1) sympathetic skin vasomotor fibers descend through the ipsilateral side of the brainstem; (2) at the level of the medulla, skin vasomotor fibers innervating the body trunk and limbs and those innervating the face descend contiguously, while at the level of the pons the two fiber groups descend separately; (3) hypothermia in patients with cerebral infarction could be explained by interruption of the inhibitory neural pathway that controls vasomotor function on the contralateral side of the body; (4) these inhibitory pathways descend in the vicinity of the pyramidal tract.
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PMID:[A study of skin surface temperature in patients with unilateral cerebral infarction--with special reference to central autonomic regulation of skin vasomotor response]. 877 99

In animal stroke models, treatment with mild hypothermia (30-34 degrees C) for 3-4 hours may reduce the size of cerebral infarction if started within three hours of the initiation of cerebral ischaemia. The mechanism by which hypothermia exerts its neuroprotective effect is unknown, but experimental studies have shown the release of neurotoxic excitatory amino acids and free oxygen radicals to be reduced during hypothermic ischaemia. In patients with acute stroke, body temperature above 37.5 degrees C are associated with poor outcome, and temperatures below 36.5 degrees C with improved outcome, compared to normothermic patients. Due to the unpleasantness of cooling and side effects as shivering, hypothermia may not be tolerated by stroke patients without sedation of light anaesthesia which may increase the risk of hypotension and respiratory complications. However, lowering body temperature by 1-2 degrees C may suffice to improve functional outcome in acute stroke patients, and such mild hypothermia should be tested in randomized controlled clinical trials.
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PMID:[Can acute stroke be treated with hypothermia?]. 946 99

The present study investigates the neuroprotective effects of temporary mild systemic hypothermia and selective brain cooling against focal cerebral infarction in the rat and the changes of cortical blood flow, and compares these two treatment modalities. In permanent middle cerebral artery (MCA) model, the treatments were induced 15 min following the artery occlusion. The animals were kept at the desired rectal or brain temperature (about 32 degrees C) for 30 min; (each, n = 6) and for 1 hr (each, n = 6), and then allowed to rewarm spontaneously, whereas control animals were kept at normothermia throughout the experiment. The volumes of brain infarction and edema were assessed 24 hr post-occlusion. The blood flow of the dorsolateral cortex was monitored by Laser-Doppler flowmetry (LDF) in the other experiments. Hemispheric infarct volume was attenuated only in the animals treated for 1 hr with systemic hypothermia (49.2%, P < 0.001) and selective brain cooling (26.7%, P < 0.01). The volume of brain swelling was diminished only in the animals treated with systemic hypothermia for 1 hr (23.6%, P < 0.05). LDF examination revealed a sharp drop in blood flow upon MCA occlusion and maintaining in low blood flow throughout the experiment in the control and systemic hypothermia. However, in the selective brain cooling, the reduced blood flow increased from 40% to 70% of baseline value while the brain was rewarmed. The present study indicates that mild systemic hypothermia has much stronger protective effects against focal cerebral infarction and edema than selective brain cooling. The lack of protective effects of selective brain cooling may be caused by post-cooling cerebral hyperemia in the ischemia area.
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PMID:Effects of systemic hypothermia and selective brain cooling on ischemic brain damage and swelling. 977 91

Anoxic depolarization (AD) is one of the major physiological characteristics in the ischemic core. The effect of mild hypothermia on the appearance of AD and subsequent brain injury following profound ischemia is studied to evaluate the protective mechanism of hypothermia against severe ischemia. Sprague-Dawley rats were subjected to transient ischemia by hypotension (50-20 mmHg) and bilateral carotid artery occlusion (BCA-O) for 20 min in normothermia and 30 min in hypothermia. The temperature of body and temporal muscles was maintained at 37.5 degrees C and 36.5 degrees C in normothermia and 33.0 degrees C and 31.0 degrees C in hypothermia, respectively. Recording of the DC potential shift and electrocorticogram and monitoring of the cortical blood flow (CoBF) with a laser Doppler flowmeter were done epidurally on the right parietal cortex. The right parietal cortex pathology was examined 24 h after ischemia in normothermia and after 30 days in hypothermia. AD appeared in all seven normothermic rats with a fall in the CoBF to 9%-10% of the control flow. However, in spite of CoBF reduction to 8%-9% of the control flow, it did not appear in five hypothermic rats. Intra-ischemic CoBF was not statistically different between these two groups. AD appeared with the CoBF decreasing to 4%-5% of the control flow in seven hypothermic rats. Intra-ischemic CoBF in hypothermic rats exhibiting AD was significantly lower than the other two groups. The interval between BCA-O and the appearance of AD in hypothermic rats was 5.1 +/- 0.3 min (mean +/- SE), which was significantly longer than the 2.2 +/- 0.5 min observed in normothermia (p < 0.0005). Of seven normothermic rats exhibiting AD, two died within 24 h and four revealed massive neuronal injury. Of seven hypothermic rats with AD, four died between day 2 and day 13, and one revealed diffuse cerebral infarction. However, no severe ischemic injury or ischemic death was observed in all five hypothermic rats without AD. The incidence of severe neuronal injury or ischemic death was significantly lower in hypothermic rats without AD compared with normothermic rats with AD (p < 0.02) or hypothermic rats with AD (p < 0.05). Although mild hypothermia delays AD, it is suggested that raising the cerebral blood flow threshold for AD appearance has a key role in the hypothermic protection of a severely ischemic area such as the ischemic core.
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PMID:Mild hypothermia on anoxic depolarization and subsequent cortical injury following transient ischemia. 1055 90

Delayed resistance to ischemic injury can be induced by a variety of conditioning stimuli. This phenomenon, known as delayed ischemic tolerance, is initiated over several hours or a day, and can persist for up to a week or more. The present paper describes recent experiments in which transient hypothermia was used as a conditioning stimulus to induce ischemic tolerance. A brief period of hypothermia administered 6 to 48 hours prior to focal ischemia reduces subsequent cerebral infarction. Hypothermia-induced ischemic tolerance is reversed by 7 days postconditioning, and is blocked by the protein synthesis inhibitor anisomycin. Electrophysiological studies utilizing in vitro brain slices demonstrate that hypoxic damage to synaptic responses is reduced in slices prepared from hypothermia-preconditioned animals. Taken together, these findings indicate that transient hypothermia induces tolerance in the brain parenchyma, and that increased expression of one or more gene products contributes to this phenomenon. Inasmuch as hypothermia is already an approved clinical procedure for intraischemic and postischemic therapy, it is possible that hypothermia could provide a clinically useful conditioning stimulus for limiting injury elicited by anticipated periods of ischemia.
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PMID:Hypothermia-induced ischemic tolerance. 1066 11

Cerebral ischemia is a frequent and dangerous consequence of some cerebrovascular diseases. Ischaemia may be used also electively in the course of neurosurgery. Therefore new possible ways are sought how to reduce the danger of ischaemia or to prevent it. In the submitted paper some methods of neuroprotection are described and their potential or actual applicability in clinical neurosurgery are discussed. In addition to influencing the brain cell and pretentious methods in the sphere of molecular biology and genetics the induction of systemic hypertension supplemented alternatively by other methods such as hypothermia, the use of mannitol, haemodilution and hypervolaemia seem natural. A higher blood pressure helps to make leptomeningeal and cortical anastomoses patent and strengthens the collateral circulation from marginal zones of ischaemia, penumbra to the ischaemic centre and to prevent thus cerebral infarction.
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PMID:[Cerebral ischemia and neuroprotection from the viewpoint of the neurosurgeon]. 1074 19

Recent studies suggest that mild hypothermia significantly alleviate damage following cerebral ischemia though the precise mechanism is poorly defined. In the present study, middle cerebral artery occlusion (MCAo) was induced in Sprague-Dawley (SD) rats for 1 h followed by varying periods of reperfusion. Cerebral infarcts identified by hematoxylin & eosin (H&E) staining revealed extensive lesion in normothermic (NT) 37 degrees C and small lesion in hypothermic (HT) 33 degrees C group of rats. Immunohistochemical analysis revealed Bcl-2 was induced in many neurons of HT group, while Bax and cytochrome c was induced in few neurons. In situ detection of DNA fragmentation using 3'-OH end labeling method (terminal dUTP nick-end labelling (TUNEL)) indicated, higher number of TUNEL-positive cells in NT group, but significantly decreased in HT group. The expression pattern revealed many neurons at the penumbra region could survive in HT group whereas, many neurons are committed to die in NT group. Our results suggest that hypothermia is selectively interfering at more than one place and providing protection.
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PMID:Immunohistochemical expression of Bcl-2, Bax and cytochrome c following focal cerebral ischemia and effect of hypothermia in rat. 1098 40


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