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

The effects of deep hypothermia on ischemic neuronal injury were examined using a permanent middle cerebral artery occlusion model in the rat. Animals were maintained at temporalis temperatures of either 24 degrees C or 36 degrees C and killed 6 hours after arterial occlusion. Normothermic rats displayed an average infarct volume of 25.1% +/- 1.6% of the right hemisphere, whereas hypothermic rats had an average infarct volume of 4.1% +/- 1.3% (p less than 0.001). The right/left hemispheric ratio was 1.05 +/- 0.02 in the normothermic group and 1.00 +/- 0.02 in the hypothermic group (p less than 0.05). These results suggest that hypothermia to 24 degrees C may reduce cerebral infarction and edema formation following middle cerebral artery occlusion in the rat.
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PMID:Hypothermic protection following middle cerebral artery occlusion in the rat. 187 67

The effect of transient hypothermia on focal cerebral ischemia was evaluated using a rat model of permanent middle cerebral artery (MCA) occlusion. MCA occlusion was performed on 10 rats at a temporalis muscle temperature of 24 degrees C (hypothermic group) and on 10 rats at 36 degrees C (normothermic group). Rats in the hypothermic group were maintained at 24 degrees C for 1 hour after MCA occlusion and then allowed to rewarm to 36 degrees C over the next 2 hours. Animals in both groups were killed 24 hours after MCA occlusion. Cerebral infarcts were visualized by staining of coronal brain sections with 2,3,5-triphenyltetrazolium chloride. Normothermic rats displayed an average infarct volume of 233.1 +/- 13.2 mm3 (standard error of the mean), whereas hypothermic rats had an average infarct volume of 166.2 +/- 22.8 mm3 (P less than 0.01). Expressed as a percentage of the volume of the right hemisphere, the normothermic group had an infarct volume of 22.1 +/- 1.5% and the hypothermic group an infarct volume of 16.0 +/- 2.2% (P less than 0.05). These results demonstrate that transient hypothermia to a temporalis muscle temperature of 24 degrees C significantly reduces subsequent infarct size in an experimental model of permanent arterial occlusion.
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PMID:Transient hypothermia reduces focal ischemic brain injury in the rat. 192 3

A balloon catheter was utilized to occlude the distal aorta during prosthetic replacement of an aortic arch aneurysm in 4 consecutive patients under conditions of separate cerebral and peripheral perfusion and deep hypothermia. All patients survived the procedure, and 3 were doing well 1 to 1.5 years following operation. One patient sustained a cerebral infarction and recovered with some sequent disability. The use of a balloon occlusion catheter allowed us to perform the operation through a median sternotomy only, and eliminated the procedure of pulmonary dissection for distal clamping and the risk of emboli. In addition, its use provided a relatively bloodless field and sufficient protection for organs in the lower body through adequate perfusion, even when their function was poor or when the distal anastomosis was prolonged. We realized improved surgical results in the treatment of aneurysms of the aortic arch.
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PMID:Use of the balloon catheter for distal occlusion of the aorta in prosthetic replacement of aortic arch aneurysms. 400 94

Among 172 cases of coronary artery bypass grafting, 9 cases (5%) revealed severely atherosclerotic ascending aorta. In 3 of the 9 cases, total aortic cross-clamping in the distal anastomoses of saphenous vein graft (SVG) and partial aortic clamp in the proximal anastomoses of SVG were performed. In 1 case with this technique, cerebral infarction was occurred. In 4 cases, total aortic cross-clamping in the distal and proximal anastomoses of SVG was performed. In 2 of these cases with this technique, cerebral infarctions were occurred. Hypothermic circulatory arrest was performed in 2 of the rest. In one case that was predicted to have atherosclerosis of ascending aorta prior to operation, the left internal thoracic artery was anastomosed to the left anterior descending, and SVG to the right coronary artery with hypothermia and ventricular fibrillation. And during the proximal anastomoses of SVG, hypothermic circulatory arrest without aortic clamping was initiated. In another case, atherosclerosis of ascending aorta was noted after aortic cross-clamping. Then the aorta was declamped, hypothermic circulatory arrest was established, the aorta was opened, the diseased segment was resected, and proximal anastomoses of SVG was performed to Dacron patch which was implanted for aortic wall. There were no cerebral infarction in last two patients.
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PMID:[Coronary artery bypass grafting in cases with the atherosclerotic ascending aorta]. 756 18

In ten patients we treated with distal arch aneurysms exposed through left posterolateral incisions, we induced profound hypothermia and circulatory arrest. Before circulatory arrest, thiopental, nicardipine and glycerol were used to protect the brain. The brain function was objectively evaluated through continuous recording of EEG and PO2 tension of the internal jugular vein. A cardiopulmonary bypass was introduced via the left atrium, pulmonary artery and left femoral artery cannulation. After proximal anastomosis between the graft and transverse aorta, graft cannulation was added. The distal aortic arch was replaced in all patients, with the entire descending thoracic aorta additionally replaced in two. No patients died in hospital. Two suffered neurological deficit, i.e., one having slight memory impairment and the other having a left-sided stroke due to right cerebral infarction, but recovering completely within a week. Our results indicate that profound hypothermia and circulatory arrest can be implemented safely when treating patients with distal arch aneurysm.
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PMID:[The treatment of patients with distal arch aneurysms--hypothermic circulatory arrest and left posterolateral exposure]. 759 44

The effect of thrombolytic therapy is well-documented in acute myocardial infarction. In acute cerebral infarction, thrombolytic therapy has been evaluated in small series of patients. The point of thrombolytic therapy is to avoid or reduce ischemic damage of neuronal tissue by rapid arterial recanalization. In thrombolytic therapy of cerebral vascular occlusion, the pathophysiology of reperfusion needs further investigation and documentation. This review describes studies of thrombolysis in embolic stroke using animals embolized by intracarotid injections of blood clots. Vascular occlusion was demonstrated by angiography and measurement of cerebral blood flow. Thrombolytic therapy with recombinant tissue-type plasminogen activator was initiated after varying periods of time. Reperfusion, cellular function, and brain damage were examined by angiography and by clinical and pathoanatomical examination. Based mainly on results from our own investigations, the following theses concerning ischemic stroke were made: (a) Cerebral infarction caused by arterial occlusion is due to delayed, incomplete, or no reperfusion. Spasms, or hemodynamic mechanisms, seem to be of only minor importance. (b) Early thrombolytic therapy in animal models increases the degree of reperfusion and reduces brain damage, clinical deficits, and mortality. (c) Early arterial reperfusion reduces cerebral infarction and related edema. With early reperfusion, the extent of brain damage correlates to the length of the delay from onset of ischemia. (d) Cerebral stunning is caused by arterial occlusion followed by very early spontaneous or induced reperfusion, as neurons temporarily lose their functional capabilities without dying. (e) Multiple embolic microclots in experimental stroke result in more brain damage than a single macroclot, and with clots the extent of brain damage is dependent on the structural composition and volume of emboli. (f) The ability to recanalization in experimental embolic stroke is related to the amount of red cells in the emboli and inversely related to the volume of emboli and to the fibrin content and density of the clots. (g) Infarct-limiting effects in experimental stroke can be obtained by ischemic neuroprotectants or by hypothermia, either alone or with thrombolytic therapy, which then reduces brain damage further.
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PMID:Thrombolytic therapy in experimental embolic stroke. 781 66

A 75-year-old female with a history of cerebral infarction fell into sudden hypotension (mean blood pressure of around 46 mmHg) and severe anemia (hematocrit < or = 10%; minimum hemoglobin concentration of 2.0 g.dl-1) of approximately one hour due to massive hemorrhage during surgical removal of pheochromocytoma originated in the right adrenal gland. Nevertheless, she recovered from the unconsciousness after over 9 hours postoperatively. It is suggested that major reasons for her escaping from the brain damage, in spite of the low cerebral perfusion pressure, might be the decreased cerebral oxygen consumption due to the intraoperative mild hypothermia (31.5 degrees C) and the avoidance due to hemodilution of the extremely low cerebral blood flow.
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PMID:[Recovery from unconsciousness following severe hemodilution and hypotension caused by intraoperative massive hemorrhage: a case report]. 793 80

Does the use of warm-body perfusion in elderly patients with severe cerebrovascular disease lead to a higher incidence of stroke, due to hypotension secondary to low systemic vascular resistance? Two thousand, three hundred eighty-three (2,383) consecutive myocardial revascularizations were performed (1987-1992) using warm-body (perfusion 37 degrees C), cold-heart surgery (cold cardioplegic arrest). The perfusion pressure was maintained between 50-70 torr; hematocrit was kept around 20%. Prospective data during hospitalization revealed 23 operative deaths (1%), and 24 patients (1%) who developed new neurological signs after surgery. The latter formed three groups: Group I consisted of six patients with severe neurological deficits, who never regained consciousness and died after support systems withdrawal. Group II included 14 patients with postoperative clinical evidence of focal cerebral infarction (9 had hemiplegia, 2 had visual disturbance, and 3 showed alteration of memory), all of whom had residual defects at discharge; Group III was composed of four patients with minor neurological deficits after surgery (hemiparesis, gait disturbance, mental changes) which had cleared up by discharge. These data were compared retrospectively with 1605 patients (1980-1986) undergoing myocardial revascularization with moderate (25-30 degrees C) hypothermia and the same surgical team and operative techniques. Both groups had similar preoperative demographics except the warm group included more elderly patients, higher numbers with unstable angina and poor ejection fraction, and more frequent use of a mammary artery conduit. Neurological complications were 1% and 1.3% for the normothermic and hypothermic perfusion groups respectively. Incremental risk factors of stroke remain: age over 70 years, diffuse atherosclerosis of the aorta, carotid occlusive disease, and severe hypotension during perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurological complications during myocardial revascularization using warm-body, cold-heart surgery. 804 89

Experimentally, focal and global cerebral ischemia are markedly affected by small changes in brain temperature. Mild hypothermia greatly ameliorates and mild hyperthermia markedly exacerbates ischemic-induced neuronal injury. Mild hypothermia not only protects against neuronal injury but also improves clinical outcome. This effect depends on the temperature of the brain both during and after the ischemic episode. Clinical and laboratory evidence concerning the value of hypothermia and the danger of hyperthermia in acute ischemia are presented. Potential mechanisms of action of hypo- and hyperthermia in ischemic injury are also addressed. The need to treat fever in acute cerebral ischemia, even if evidence is only empiric, and the intriguing possibility of using mild hypothermia to treat acute cerebral infarction are discussed.
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PMID:Hypothermia as a potential treatment for cerebral ischemia. 811 May 95

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


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