• Aya Aoki, Kentaro Mori, and Minoru Maeda.
• Department of Neurosurgery, Juntendo University, Izunagaoka Hospital, Shizuoka, Japan. aya@med.juntendo.ac.jp
• Neurol. Res. 2002 Apr 1; 24 (3): 271-80.

AbstractIschemic deterioration during rewarming is one of the most notable clinical complications after successful therapeutic cerebral hypothermia, but the mechanism is not completely understood. Hypothermia may cause vasoconstriction and relative ischemia, especially with insufficient cerebral perfusion pressure (CPP). Various parameters were evaluated to determine the critical CPP threshold to avoid ischemia during rewarming. Cat experimental head injury was induced by inflating an epidural rubber balloon, and intracranial pressure was maintained at 30 mmHg. During rewarming after cerebral hypothermia, CPP was maintained at >120 mmHg (n = 16), 90 mmHg (n = 11), 60 mmHg (n = 11), and 40 mmHg (n=4) by controlling the blood pressure. Cerebral blood flow, cerebral metabolic rate for oxygen, arteriovenous difference of oxygen (AVDO2), cerebral venous oxygen saturation (ScvO2), and extracellular glutamate concentrations were monitored by glutamate oxidase electrode. After rewarming, the cerebral metabolic parameters were almost restored to the pre-injury level in animals with CPP of more than 90mmHg. However, in the animals with CPP= 60 mmHg, all parameters significantly deteriorated and indicated misery perfusion; ScvO2 was low (29.5+/-1.1%), AVDO2 was significantly high (9.9+/-0.8 ml 100 g(-1) min(-1)) (one-way analysis of variance, p<0.05), and electron microscopic features showed subcellular ischemic change. Extracellular glutamate significantly increased during the rewarming period only in the CPP= 40 mmHg group. CPP less than 60 mmHg during rewarming causes secondary ischemic insult, which might indicate continuation of cerebral vasoconstriction in hypothermia. CPP higher than 90 mmHg is required to avoid the potential risk of relative ischemia after hypothermia.

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