흰쥐의 일과성 전뇌허혈모델에서 허혈성 신경세포손상에 대한 저체온과 고혈당의 동반효과
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Background & Objectives : Hypothermia is used in patients undergoing cardiac surgery to protect the brain. Hyperglycemia aggravates neuronal damage in global and focal cerebral ischemia. However, it is not clear whether it is beneficial or harmful if both hypothermia and hyperglycemia coexist in transient global ischemia. Methods : We used forty male Sprague- Dawley rats. Rats were divided into four groups; 1) normoglycemic, normal temperature (NGNT), 2) normoglycemic, low temperature (NGLT), 3) hyperglycemic, normal temperature (HGNT), and 4) hyperglycemic, low temperature (HGLT). Hyperglycemia was induced by intraperitoneal injection of streptozotocin 3 days before ischemia or intraperitoneal injection of glucose solution 30 minutes before ischemia. Intraischemic body temperature was regulated as 32˚C for hypothermia and 37˚C for normothermia group. Transient global cerebral ischemia was induced by clipping both common carotid arteries and blood exsanguination. Pre- and postischemic blood pressure and preischemic physiologic parameters were measured. The numbers of viable neuron were counted at CA1 sector of hippocampus, 5 or 7 days after ischemia. Results : Mean glucose levels were significantly higher in HGNT and HGLT groups than in NGNT and NGLT groups. The number of viable neurons in NGLT group was significantly higher than that in NGNT group (p = 0.04). No significant differences were recognized between HGLT group and HGNT group (p = 0.71) and between NGNT group and HGLT group (p = 0.55). Conclusions : Hypothermia had protective effect against ischemia in case of normoglycemia, not in hyperglycemia. Our results suggest that avoidance of hyperglycemia is mandatory for the effective neuroprotection by hypothermia and that the harmful effect of hyperglycemia possibly overrides the protective effect of hypothermia in transient global ischemia. Korean Journal of Stroke 2000;2(1): 62~69
Abstract
Background & Objectives : Hypothermia is used in patients undergoing cardiac surgery to protect the brain. Hyperglycemia aggravates neuronal damage in global and focal cerebral ischemia. However, it is not clear whether it is beneficial or harmful if both hypothermia and hyperglycemia coexist in transient global ischemia. Methods : We used forty male Sprague- Dawley rats. Rats were divided into four groups; 1) normoglycemic, normal temperature (NGNT), 2) normoglycemic, low temperature (NGLT), 3) hyperglycemic, normal temperature (HGNT), and 4) hyperglycemic, low temperature (HGLT). Hyperglycemia was induced by intraperitoneal injection of streptozotocin 3 days before ischemia or intraperitoneal injection of glucose solution 30 minutes before ischemia. Intraischemic body temperature was regulated as 32˚C for hypothermia and 37˚C for normothermia group. Transient global cerebral ischemia was induced by clipping both common carotid arteries and blood exsanguination. Pre- and postischemic blood pressure and preischemic physiologic parameters were measured. The numbers of viable neuron were counted at CA1 sector of hippocampus, 5 or 7 days after ischemia. Results : Mean glucose levels were significantly higher in HGNT and HGLT groups than in NGNT and NGLT groups. The number of viable neurons in NGLT group was significantly higher than that in NGNT group (p = 0.04). No significant differences were recognized between HGLT group and HGNT group (p = 0.71) and between NGNT group and HGLT group (p = 0.55). Conclusions : Hypothermia had protective effect against ischemia in case of normoglycemia, not in hyperglycemia. Our results suggest that avoidance of hyperglycemia is mandatory for the effective neuroprotection by hypothermia and that the harmful effect of hyperglycemia possibly overrides the protective effect of hypothermia in transient global ischemia. Korean Journal of Stroke 2000;2(1): 62~69
