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

Corbett, Dale; Hamilton, Mark G.; Colbourne, Frederick

doi:10.1006/exnr.2000.7369

Cited by 146 publications

(68 citation statements)

References 48 publications

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“…A significant difference in infarct size was noted between the 37°C and the 34°C and 33°C groups (203Ϯ30, 119Ϯ19, and 114Ϯ26 mm 3 , respectively, both PϽ0.05, ANOVA). Differences between the 33°C and 34°C groups were not significant.…”

Section: Infarct Sizementioning

confidence: 87%

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Different Degrees of Hypothermia After Experimental Stroke

Kollmar

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Han

et al. 2007

Stroke

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Background and Purpose-The neuroprotective role of mild therapeutic hypothermia was established in animal models of cerebral ischemia. Still, several issues, including optimal target temperature, remain unclear. The optimal depth of hypothermia in a rat model of focal cerebral ischemia was investigated. Methods-Eighty-four male Wistar rats (nϭ84) were subjected to filament occlusion of the middle cerebral artery for 90 minutes. Sixty animals were equally split into 6 groups kept at core temperatures of 37°C, 36°C, 35°C, 34°C, 33°C, and 32°C over a period of 4 hours starting 90 minutes after middle cerebral artery occlusion. Twenty-four hours later, after performing a neuroscore, animals were killed and brains examined for infarct size, edema, and invasion of leukocytes.In the second part, 24 animals (8 per group) were kept at 33°C, 34°C, and 37°C for 4 hours, allowed to survive for 5 days, and underwent additional investigation of transferase dUTP nick-end labeling. Results-In the first part, one animal in each treatment group and 2 animals in group 37°C died. The infarct size and edema were smaller for 34°C and 33°C compared with all other groups (PϽ0.05) over 24 hours. These animals also had better functional outcome (PϽ0.05) with an advantage for 34°C versus 33°C (PϽ0.05). Leukocyte count was lower for 34°C and 33°C as compared with the 37°C group. Similar results were obtained in the second part of the study with an advantage for 34°C versus 33°C. Conclusion-Our results suggest that the optimal depth of therapeutic hypothermia in temporary middle cerebral artery occlusion is 34°C.

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Section: Infarct Sizementioning

confidence: 87%

“…[1][2][3][4][5] Still, some issues concerning its appropriate use remain unsolved. The optimal depth is probably the most important factor.…”

mentioning

confidence: 99%

Different Degrees of Hypothermia After Experimental Stroke

Kollmar

Blank

Han

et al. 2007

Stroke

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“…schaller and Graf 3 , reviewed the pathophysiological background for the neuroprotective effect of hypothermia on stroke and the main findings were: decrease in the synthesis, release and recovery of neurotransmitters, specially the extracellular glutamate, reduction of postischemic changes in cerebral perfusion, decrease of the blood-brain barrier permeability, reduction in the brain metabolic rate, in the release of free radicals, and in the intracellular acidosis; resynthesis of ubiquitin; inhibition of protein kinases, and recuperation of the synthesis of proteins 4,15,[20][21][22][23][24][25] . According to Huh et al 20 , the mechanisms of injury improved by mild/moderated hypothermia were: release of excitatory neurotransmitters; activation of the protein kinases; decrease of brain-barrier permeability; production of oxygen radical with peroxidative damage to the lipids, protein or deoxyribonucleic acid; change in gene expression; ischemic depolarizations; cytoskeletal breakdown, microglial activation, and reduction in the brain metabolic rate.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of mild hypothermia in the temporary brain ischemia in cats

Nakano

Colli

Lopes

2007

Arq. Neuro-Psiquiatr.

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-Objective: to evaluate the neuroprotective effect of mild hypothermia during temporary focal ischemia in cats. Method: 20 cats underwent middle cerebral artery 60 minutes occlusion and 24 hours reperfusion: 10 under normothermia and 10 under mild hypothermia (32º c). Brain coronal sections 2mm thick were stained with 2,3,5-triphenyltetrazolium hydrochloride, photographed and evaluated with software for volume calculation. Results: cortical ischemia was found in 7 and basal ganglia ischemia in 8 animals of group 1 and in both regions in 5 animals of group 2 (no difference: p=0.6499 for cortical; p=0.3498 for basal ganglia). No ischemia was found in 5 animals of group 2 and in none of group 1 (significant difference, p=0.0325). the infarct volume was greater in group 1 than 2 (p=0.0433). Conclusion: Mild hypothermia did not interfere with location of ischemia, but it was effective for reducing the infarct volume.Key words: cats, focal cerebral ischemia, mild hypothermia, neuroprotection.Efeito neuroprotetor da hipotermia leve na isquemia cerebral focal temporária em gatos resuMo -Objetivo: Avaliar o efeito neuroprotetor da hipotermia leve na isquemia cerebral focal temporária em gatos. Método: oclusão da artéria cerebral média durante 60 minutos e 24 horas de reperfusão em 10 gatos sob normotermia e 10 sob hipotermia leve (32º c). secções cerebrais coronais de 2 mm coradas com 2,3,5-cloreto de trifeniltetrazolio, fotografadas e cálculos volumétricos (hemisférios/áreas isquêmi-cas) com programa específico. Resultados: Isquemia cortical em 7 e nos gânglios da base em 8 animais do grupo 1 e em ambas as regiões em 5 animais do grupo 2 (sem diferença: p=0,6499 cortical; p=0,3498 gân-glios da base). cinco animais do grupo 2 e nenhum do grupo 1 não apresentaram isquemia (diferença significante, p=0,0325). o volume do infarto foi maior no grupo 1 (p=0,0433). Conclusão: Hipotermia leve não interferiu com a localização da isquemia mas foi eficaz para reduzir o volume do infarto.PAlAvrAs-cHAve: gatos, isquemia cerebral focal, hipotermia leve, neuroproteção. Dr. Benedicto Oscar Colli -Departamento de Cirurgia / HCFMRP -Campus Universitário USP -14048-900 Ribeirão Preto SP -Brasil. E-mail: bocolli@fmrp.usp.brBrain ischemia is common found in arterial vasospasm secondary to subarachnoid hemorrhage, by brain injury and during temporary occlusion of arteries during neurovascular procedures. despite attempts of using many strategies, the results of treatment for cerebral stroke are not ever satisfactory. the severity of brain lesion depends on the duration of ischemia, on the vessel occluded and on collateral circulation. several studies aiming better understanding of the ischemia/reperfusion pathophysiology and the improvement of brain protection in these phenomena have been done. In human being, these studies are generally clinical evaluations and image examinations that not allow detection of early cellular phenomena secondary to ischemia/reperfusion. experimental models have the advantage of better control of biolog...

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“…The use of brain probes is more difficult in the clip-occlusion MCAO model in rat due to the need to estimate blood flow near the brain probe assembly. Brain probes can easily be used in the intraluminal suture occlusion MCAO model, a method usually applied in rats [21]. The mouse is the species used in knockout gene experiments.…”

Section: Application Of Radiotelemetry In Ischemia Researchmentioning

confidence: 99%

“…This has not been consistently found, however, with rectal temperature measurements [19]. Furthermore, recent studies with distal middle cerebral artery occlusion (MCAO) via clip occlusion [20] and intraluminal MCAO ( [21]; Oryu, Colbourne, and Auer, unpublished data) did not substantiate the occurrence of any postischemic hyperthermia. Such differences are likely due to model differences (e.g., involvement of hypothalamus), but may also, in part, be related to the method of measuring temperature.…”

Section: Introductionmentioning

confidence: 96%