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

Selective neuronal cell death in the CA1 pyramidal cells of the hippocampus and neurons of the dorsolateral striatum as a consequence of brain ischemia/reperfusion (IR) can be ameliorated with brain hypothermia. Since postischemic injury is mediated partially by chemical production of reactive oxygen species (ROS), decreased ROS production may be one of the mechanisms responsible for cerebral protection by hypothermia. To determine if ischemic brain temperature alters ROS production, reversible IR was produced in rats by occlusion of both carotid arteries with hemorrhagic hypotension. After 15 min of ischemia, circulation was restored for 60 min. Brain temperature was maintained during ischemia at either 30, 36, or 39 degrees C and kept at 36-37 degrees C after reperfusion. Using cerebral microdialysis, we measured nonenzymatic hydroxylation of salicylate by HPLC with electrochemical detection in the hippocampus. CBF was also compared among the groups during IR. The results were that normothermic animals during reperfusion had persistently increased levels of the salicylate hydroxylation product, 2,3-dihydroxybenzoic acid (2,3-DHBA), reaching 251% of control at 60 min. This increase in 2,3-DHBA production was potentiated after 60 min of reperfusion (406% of control) with ischemic hyperthermia. In hypothermic ischemia, 2,3-DHBA production at 60 min was attenuated to 160% of control. CBF decreased to approximately 5% of baseline value during ischemia, but increased three- to four-fold relative to control in all three groups. Therefore, the effects of ischemic brain temperature on 2,3-DHBA production did not correlate with changes in CBF during IR. We conclude that brain-temperature-related changes in OH.production are readily detected in the rat and decreased ROS generation may contribute to cerebral protection afforded by hypothermia during brain ischemia.
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PMID:Brain temperature alters hydroxyl radical production during cerebral ischemia/reperfusion in rats. 853 May 42

Patients with untreated giant intracranial aneurysms have a dismal prognosis as a result of hemorrhage, cerebral compression, and thromboembolism. Therefore, giant aneurysms should be treated. The operative approach is chosen to maximize exposure of the aneurysm. Direct clipping of the aneurysm neck, with preservation of the parent and branch vessels, is the preferred method of occlusion. Hypothermic circulatory arrest may facilitate clipping in selected patients. Alternative techniques for unclippable aneurysms can be utilized, but they compromise parent arteries and require revascularization to maintain CBF. Because mass effect is an important cause of patient morbidity, giant aneurysms are usually debulked after they have been eliminated completely from the circulation. Giant aneurysms are complex lesions that demand thorough surgical planning, individualized strategies, and a multidisciplinary effort.
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PMID:Surgical management of giant intracranial aneurysms: experience with 171 patients. 884 96

This study investigates changes of jugular bulb oxygen saturation (SjO2) measured by fiberoptic jugular bulb oximetry and changes of intracranial hemodynamics using transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG) in 17 ASA III patients. Anesthesia was maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. SjO2 (%) was measured by a fiberoptic catheter (Opticath F 5.5; Abbott Critical Care Systems) placed in the right jugular bulb via the right internal jugular vein. Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (Transpect, Medasonics). Data were recorded continuously from the beginning to the end of the CPB. During cooling and hypothermia (27 degrees C); SjO2 and Vmean did not change compared with values at the start of CPB. However, with the beginning of rewarming, Vmean was increased 65% compared with stable hypothermia (27 degrees C). This increase in Vmean was associated with a 25% decrease in SjO2. Maximum desaturation occurred at a 36 degrees C jugular bulb temperature. During cooling and stable hypothermia, global oxygen balance and intracerebral perfusion seemed to be maintained. However, a major alteration in the balance of the cerebral oxygen supply and demand may occur in response to rewarming despite increases in Vmean. Findings suggest inadequate increases in CBF to meet cerebral metabolic demand. Further investigations need to validate these findings with biochemical techniques and neuropsychological tests.
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PMID:Jugular bulb oxygen saturation and middle cerebral blood flow velocity during cardiopulmonary bypass. 910 Jan 81

The effects of mild (34 degrees C) and moderate (31 degrees C) hypothermia on the electroencephalogram, cerebral blood flow and outcome from incomplete brain ischemia were compared to normothermia (37 degrees C) in the rat. Rats were anesthetized with fentanyl (25 mu g kg(-1) h(-1)) and 70 percent nitrous oxide in oxygen. Ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 25 mmHg for 30 min. CBF was measured in the right parietal cortex by laser Doppler. Neurologic outcome was measured daily for 3 days after ischemia and histopathology determined at the end of the study. Before ischemia, neither EEG nor CBF were changed by hypothermia compared to normothermic controls. Total EEG and beta EEG (12.5-32 Hz) were abolished and CBF decreased by 70 percent during ischemia. During a 2.5 h recovery period total EEG and beta EEG activity recovered better with moderate hypothermia compared to normothermia. Recovery of cerebral blood flow was not significantly different between the treatment groups. Neurologic and histopathologic outcome were improved in rats receiving moderate hypothermia compared to normothermic controls. These results show that during severe incomplete ischemia, hypothermia has a graded effect on outcome which is consistent with its effects on brain metabolism.
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PMID:Effects of graded hypothermia on outcome from brain ischemia. 916 76

The effects of mild hypothermia on regional CBF (rCBF) and autoregulation were investigated in 60 awake and spontaneously breathing Wistar rats. They were divided into normothermic (rectal and brain temperatures: 37.0 +/- 0.5 degrees C) and mildly hypothermic (33.0 +/- 0.5 degrees C) groups the temperature of the latter group was controlled by cooling a lead cast around each rat with ice-cold water. rCBF was measured by means of an autoradiographic technique with 14C-iodoantipyrine. In normothermia, rCBF in most of the supratentorial cortical regions was maintained down to a mean arterial blood pressure (MABP) of 50 mmHg, produced by exsanguination, while rCBF in most of the brain stem regions showed a tendency to increase despite this reduction of MABP (predysautoregulatory overshoot of CBF). In the mildly hypothermic group, pre-exsanguination rCBF values were lower than those in normothermia, and rCBF in all brain regions declined significantly in proportion to decreasing MABP, produced by exsanguination. It is, therefore, concluded that mild hypothermia disturbs cerebrovascular autoregulation in awake rats.
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PMID:Mild hypothermia disturbs regional cerebrovascular autoregulation in awake rats. 960 65

The effects of hypothermia on production of nitric oxide (NO) in ischemic brain were investigated by using in vivo microdialysis. Male Wistar rats were randomly divided into three groups; saline-treated normothermic group (37 degreesC, n=6), 30 mg/kg N-nitro-l-arginine methyl ester(l-NAME)-treated normothermic group (n=6), and saline-treated hypothermic group (30 degreesC, n=6). Transient forebrain ischemia was produced by bilateral common carotid artery occlusion combined with hypotension (MABP=50 mmHg). Saline-treated normothermic animals resulted in a reduction of LCBF to 9% of baseline. Saline-treated hypothermic rats revealed the similar changes of LCBF. In contrast, l-NAME administration reduced the basal CBF to 85% of saline-treated group and to 8% after ischemia. NO products were decreased during ischemia and transiently increased after reperfusion in saline-treated groups. However, the increase of NO products after reperfusion was less significant in the hypothermia. l-NAME-treated group showed a constant reduction of NO production during ischemia and after reperfusion.
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PMID:Consecutive in vivo measurement of nitric oxide in transient forebrain ischemic rat under normothermia and hypothermia. 976 79

The hippocampal CA1 sector is selectively vulnerable to forebrain ischemia but protected by mild hypothermia. However, the consequence of intraischemic hypothermia on CA1 blood flow during the insult has not been adequately characterized. The effects of mild intraischemic hypothermia on relative changes in regional hippocampal CA1 blood flow were recorded continuously using laser Doppler flowmetry (LDF) during and 30 min after 6 min of forebrain ischemia. Six experimental groups (n=6/group) of fasted male Wistar rats were compared. Groups 1, 3 and 5 consisted of normothermic rats that underwent either 6 (for CBF measurements) and 6 or 10 (for 7 day survival-CA1 neuronal death measurements) min of transient forebrain ischemia using bilateral carotid clamping and hemorrhagic hypotension. Groups 2, 4 and 6 rats were subjected to mild hypothermia (34 degrees C) before, during, and 30 min after 6 (for CBF measurements) and 6 or 10 (for 7 day survival-CA1 neuronal death measurements) min of transient forebrain ischemia. CA1 blood flow and electroencephalogram (EEG) were continuously recorded. During the ischemic insult there were intergroup differences in the magnitude of CBF decreases in the CA1 region. In both groups 1 and 2, CBF returned to preischemic values within 1 min of reperfusion but hypothermic rats had more sustained hyperemia. Hypothermic rats had a quicker recovery of EEG activity and less delayed CA1 neuronal death (group 2 versus 4). These data suggest ischemic blood flow to the CA1 sector was altered by intraischemic mild hypothermia which may contribute to the greater benefit of intraischemic hypothermic neuroprotection.
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PMID:Intraischemic mild hypothermia increases hippocampal CA1 blood flow during forebrain ischemia. 1116 63

This study evaluated the cerebral ischemic parameters during the rewarming period after therapeutic hypothermia to determine the critical cerebral perfusion pressure (CPP) threshold to avoid ischemic deterioration. Cat experimental head injury was induced by inflation of an epidural rubber balloon to maintain intracranial pressure at 30 mmHg under hypothermia. During the rewarming period, CPP was maintained at > or = 120 mmHg, 90 mmHg, and 60 mmHg by controlling the blood pressure. CBF, CMRO2, AVDO2, and cerebral venous oxygen saturation (ScvO2) were measured. Brain extracellular glutamate concentrations were also measured by a dialysis electrode. Histological preparations of all brains were examined under an electron microscope. The cerebral metabolic parameters in animals with CPP of more than 90 mmHg returned to the base values after rewarming. However, ScvO2 was significantly lower (27 +/- 6%) and AVDO2 was significantly higher (9.4 +/- 1.8 ml/100 g/min) after rewarming in the animals with CPP = 60 mmHg, which indicated misery perfusion. Animals with CPP = 60 mmHg also showed increased extracellular glutamate concentration and histological ischemic damage (mitochondrial swelling). CPP of 60 mmHg during the rewarming period is associated with irreversible ischemia, which indicates continuation of cerebral vasoconstriction. Therefore, a CPP of greater than 90 mmHg is required to avoid cerebral ischemia.
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PMID:Appropriate cerebral perfusion pressure during rewarming after therapeutic hypothermia. 1216 14

Unfortunately no specific pharmacologic therapies are available for the treatment of TBI in patients. Current investigation of contemporary therapies for the treatment of TBI consists of recycling of previously tested therapies in the era of contemporary neurointensive care. These therapies include hypothermia, decompressive craniectomy, osmotherapy, and controlled hyperventilation. It is hoped that more detailed knowledge regarding the dominant pathophysiologic mechanisms associated with TBI-excitotoxicity, CBF dysregulation, oxidative stress, and programmed cell death-will catapult an efficacious intervention from the laboratory bench to the bedside. This intervention may be a potent agent targeting a single dominant pathway, a broad-spectrum intervention such as hypothermia, or, more likely, a combination of therapies. Meanwhile, practitioners must offer meticulous supportive neurointensive care using clinically proven therapies aimed at minimizing cerebral swelling for the management of pediatric patients who are victims of TBI.
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PMID:Traumatic brain injury in infants and children: mechanisms of secondary damage and treatment in the intensive care unit. 1284 19

Cerebral ischemia results in a rapid depletion of energy stores that triggers a complex cascade of cellular events such as cellular depolarization and Ca2+ influx, resulting in excitotoxic cell death. The critical determinant of severity of brain injury is the duration and severity of the ischemic insult and early restoration of CBF. Induced therapeutic hypothermia following CA is the only strategy that has demonstrated improvement in outcomes in prospective, randomized clinical trials. Although pharmacologic neuro-protection has been disappointing thus far in a variety of experimental animal models, further research efforts are directed at using some agents that demonstrate marginal or moderate efficacy in combination with hypothermia. Although the signal transduction pathways and intracellular molecular events during cerebral ischemia and reperfusion are complex, potential therapeutic neuroprotective strategies hold promise for the future.
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PMID:Mechanisms of brain injury after global cerebral ischemia. 1644 27


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