SCOPUS
SCIE
KCI등재
급성 허혈성 뇌병소에 대한 혈압강하의 영향에 관한 실험적 연구 = An Experimental Study for Effect of Controlled Hypotension on Acute Ischemic Brain Lesion
Controlled hypotension and temporary clip of feeding artery are used to reduce bleeding and to facilitate the neurosurgical operations, especially in intracranial aneurysm surgery, but the microvasculature of acute ischemic brain from impaired blood flow is quite susceptible to decrease in blood pressure and blood volume.
The reversibility of brain damage following an ischemic brain lesion depends on the amount of regional cerebral blood flow as well as the severity of ischemia.
The present study was designed to elucidate the effect of controlled hypotension on cerebral blood flow, cerebrovascular resistance, and pathological changes in acute ischemic brain lesion. Cerebral ischemia was induced in cats by middle cerebral artery occlusion for 6 hours through the transorbital appraoch.
Forty-nine cats were divided into 3 groups, namely control group with mean blood pressure maintained at normal after right middle cerebral artery occlusion, hemorrhagic hypotension group with mean blood pressure decreased to 80, 60, and 40 ㎜Hg by with drawing of blood after right middle cerebral artery occlusion and drug-induced hypotension group with mean blood pressure decreased to 80, 60, and 40 ㎜Hg with arfonad infusion after right middle cerebral artery occlusion
Regional cerebral blood flow was measured by the hydrogen clearance method following middle cerebral artery clipping and gradual decreasing mean blood pressure. Cerebrovascular resistance was calculated after regional cerebral blood flow was measured and size of infarct were examined in each groups after the experiment was completed.
Results were as follows:
1) In control group, regional cerebral blood flow and cerebrovascular resistance of the right parietal area with mean blood pressure maintained at normal after right middle cerebral artery occlusion were 19.4±2.1㎖/2.1㎖/100g/min and 5.5±0.4㎜Hg/㎖/100g/min. The size of cerebral infarct was minimal in 71% of the control group.
2) In hemorrhagic hypotension group, regional cerebral blood flow of the right parietal area with mean blood pressure decreased to 80, 60, and 40 ㎜Hg was 17.6 ±1.5, 15.4±3.8, and 7.8±2.9㎖/100g/min respectively, thus 6, 25, and 57% lower than the control group. Cerebrovascular resistance of the right parietal area with mean blood pressure at 80 and 60㎜Hg was 4.7±0.1 and 4.5±0.3㎜Hg/㎖/100g/min respectively, thus showing a gradual decrease in relation to the decreasing mean blood pressure. With mean blood pressure reduced to 40 ㎜Hg, the cerebrovascular resistance drastically increased to 5.1±0.5㎜Hg/㎖/100g/min. When mean blood pressure was reduced to 60 and 40 ㎜Hg, the size of infarct was marked in 57 and 85% of the hemorrhagic hypotension group.
3) In drug-induced hypotension group, regional cerebral blood flow of the right parietal area with mean blood pressure reduced to 80, 60, and 40 ㎜Hg was 19.1±2.3, 17.8±3.1, and 7.4±2.7㎖/100g/min respectively, thus 2, 10, and 38% lower than the control group. The regional cerebral blood flow of the right parietal area in the drug-induced hypotension group was slightly higher than the hemorrhagic hypotension group when mean blood pressure was reduced to 80 or 60㎜Hg, while there was no significant difference of regional cerebral blood flow in the both groups when mean blood pressure was reduced to 40㎜Hg. Cerebrovascular resistance of the right parietal area with mean blood pressure at 80 and 60 ㎜Hg was 4.1±0.3 and 3.1±0.2㎜Hg/㎖/100g/min respectively, thus showing a gradual decrease in relation to decreasing mean blood pressure. With mean blood pressure reduced to 40㎜Hg, the cerebrovascular resistance was 5.6±0.9㎜Hg/㎖/100g/min, thus higher than the hemorrhagic hypotension group.
When mean blood pressure was decreased to 60 and 40 ㎜Hg, the size of infarct was marked in 42 and 85% of the drug-induced hypotension group. The extent of cerebral infarct was more extensive in the hemorrhagic hypotension group than in the drug-induced hypotension.
4) In the contralateral hemisphere of the infarct, there was no change in regional cerebral blood flow when the mean blood pressure was decreased to 80 and 60㎜Hg but when the mean blood pressure decreased to 40㎜Hg, the regional cerebral blood flow was markedly reduced in all groups. When the mean blood pressure decreased to 60 ㎜Hg there was no change in cerebrovascular resistance, however when the mean blood pressure was at 40 ㎜Hg, there was a drastic increase in cerebrovascular resistance in all groups.
Due to loss of autoregulation in the ischemic brain lesion, the regional cerebral blood flow depends on the brain perfusion pressure and accordingly when there is ischemic brain lesion., the hemorrhagic hypotension produces serious brain infarction and edema than drug-induced hypotension.
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