Deterimental effect of prolonged hypothermia in cats and monkeys with and without regional cerebral ischemia.

Steen, Petter Andreas; Soule, Edward H.; Michenfelder, John D.

doi:10.1161/01.str.10.5.522

Cited by 123 publications

(46 citation statements)

References 31 publications

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“…In animal studies, it was reported that toxicity from moderate hypothermia increases as the temperature is further decreased and as the duration of hypothermia is increased. 38,39 In this study, we could not observe a significant increase in the occurrence of side effects between patients cooled for 48 hours and those treated for 72 hours. Hypothermia affects virtually every organ system.…”

Section: Discussioncontrasting

confidence: 68%

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Schwab

Schwarz

Spranger

et al. 1998

Stroke

599

351

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Background and Purpose-Animal research and clinical studies in head trauma patients suggest that moderate hypothermia may improve outcome by attenuating the deleterious metabolic processes in neuronal injury. Clinical studies on moderate hypothermia in the treatment of acute ischemic stroke patients are still lacking. Methods-Moderate hypothermia was induced in 25 patients with severe ischemic stroke in the middle cerebral artery (MCA) territory for therapy of postischemic brain edema. Hypothermia was induced within 14Ϯ7 hours after stroke onset and achieved by external cooling with cooling blankets, cold infusions, and cold washing. Patients were kept at 33°C body-core temperature for 48 to 72 hours, and intracranial pressure (ICP), cerebral perfusion pressure, and brain temperature were monitored continuously. Outcome at 4 weeks and 3 months after the stroke was analyzed with the Scandinavian Stroke Scale (SSS) and Barthel index. The side effects of induced moderate hypothermia were analyzed. Results-Fourteen patients survived the hemispheric stroke (56%). Neurological outcome according to the SSS score was 29 (range, 25 to 37) 4 weeks after stroke and 38 (range 28 to 48) 3 months after stroke. During hypothermia, elevated ICP values could be significantly reduced. Herniation caused by a secondary rise in ICP after rewarming was the cause of death in all remaining patients. The most frequent complication of moderate hypothermia was pneumonia in 10 of the 25 patients (40%). Other severe side effects of hypothermia could not be detected. Conclusions-Moderate hypothermia in the treatment of severe cerebral ischemia is not associated with severe side effects.Moderate hypothermia can help to control critically elevated ICP values in severe space-occupying edema after MCA stroke and may improve clinical outcome in these patients. (Stroke. 1998;29:2461-2466.)

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Section: Discussioncontrasting

confidence: 68%

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Schwab

Schwarz

Spranger

et al. 1998

Stroke

599

351

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“…In experiments in which brain tempera ture is not monitored, there is a potential for a vari able brain temperature response during ischemia, which would be expected to result in variable histo pathological consequences. The detrimental effects associated with prolonged body hypothermia have been previously discussed (Michenfelder and Milde, 1977;Steen et al, 1979). The present findings are therefore of clinical importance in that the beneficial effects of hypothermia were seen without lowering overall body temperature.…”

Section: Discussionsupporting

confidence: 66%

Small Differences in Intraischemic Brain Temperature Critically Determine the Extent of Ischemic Neuronal Injury

Busto

Dietrich

Globus

et al. 1987

J Cereb Blood Flow Metab

1,706

614

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Summary:We have tested whether small intraischemic variations in brain temperature influence the outcome of transient ischemia. To measure brain temperature, a ther mocouple probe was placed stereotaxically into the left dorsolateral striatum of rats prior to 20 min of four-vessel occlusion. Rectal temperature was maintained at 36-37°C by a heating lamp, and striatal temperature prior to ischemia was 36°C in all animals. Six animal subgroups were investigated, including rats whose intraischemic striatal brain temperature was not regulated, or was maintained at 33, 34, 36, or 39°C. Postischemic brain tem perature was regulated at 36°C, except for one group in which brain temperature was lowered from 36°C to 33°C during the first hour of recirculation. Energy metabolites were measured at the end of the ischemic insult, and his topathological evaluation was carried out at 3 days after ischemia. Intraischemic variations in brain temperature had no significant influence on energy metabolite levels measured at the conclusion of ischemia: Severe depletion of brain ATP, phosphocreatine, glucose, and glycogen and elevation of lactate were observed to a similar degree in all experimental groups. The histopathological conse quences of ischemia, however, were markedly influenced by variations in intraischemic brain temperature. In the Despite the utility of small animal models of global ischemia, several groups have noted vari ability of outcome from animal to animal (Payan et aI., 1965;Furlow, 1982; Blomqvist et aI., 1984; Harrison et aI., 1985; Vibulsresth et aI., 1987). Al though these variations, in part, may be the conse quence of differences in the severity of ischemia it- 729hippocampus, CA I neurons were consistently damaged at 36°C, but not at 34°C. Within the dorsolateral striatum, ischemic cell change was present in 100% of the hemi spheres at 36°C, but in only 50% at 34°C. Ischemic neu rons within the central zone of striatum were not ob served in any rats at 34°C, but in all rats at 36°C. In rats whose striatal temperature was not controlled, brain tem perature fell from 36 to 30-31°C during the ischemic in sult. In this group, no ischemic cell change was seen within striatal areas and was only inconsistently docu mented within the CAl hippocampal region. These re sults demonstrate that (a) rectal temperature unreliably reflects brain temperature during ischemia; (b) despite severe depletion of brain energy metabolites during isch emia at all temperatures, small increments of intra ischemic brain temperature markedly accentuate histo pathological changes following 3-day survival; and (c) brain temperature must be controlled above 33°C in order to ensure a consistent histopathological outcome. Low ering of the brain temperature by only a few degrees during ischemia confers a marked protective effect. Key Words: Ischemia-Brain temperature-Rats-Hypo thermia.self, other factors not directly related to the pri mary insult may also play an important role in determining the ultimate histopathological out come.Recen...

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“…This finding in the rat contrasts with early studies in cat and monkey MCAo models where 48 h of 29°C hypothermia was frequently lethal (30,40). While these strikingly different outcomes may represent a species effect, these early failures are more likely due to the greater prevalence of side-effects of moderate (i.e., Ͻ30°C) hypothermia (35).…”

Section: Discussioncontrasting

confidence: 57%

Persistent Neuroprotection with Prolonged Postischemic Hypothermia in Adult Rats Subjected to Transient Middle Cerebral Artery Occlusion

Corbett

Hamilton

Colbourne

2000

Experimental Neurology

147

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Deterimental effect of prolonged hypothermia in cats and monkeys with and without regional cerebral ischemia.

Cited by 123 publications

References 31 publications

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Small Differences in Intraischemic Brain Temperature Critically Determine the Extent of Ischemic Neuronal Injury

Persistent Neuroprotection with Prolonged Postischemic Hypothermia in Adult Rats Subjected to Transient Middle Cerebral Artery Occlusion

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