실험적 중대뇌동맥 폐쇄로 인한 급성 뇌경색에 대한 Thiopental 효과 = Effect of the Thiopental in Acute Focal Cerebral Infarction after Experimental Occlusion of the Middle Cerebral Artery

다국어 초록 (Multilingual Abstract)

An experimental ischemic model in cats is described in which we have attempted to produce acute cerebral ischemia by occlusion of the middle cerebral artery (MCA) through the orbit.
The main objectives of this experiment were: to observe the effect of thiopental in the tophographic distribution of infarct; the size of the infarct; histological changes of ischemic nerve ceils following occlusion of a major cerebral artery; to investigate the best timing of the administration and dosage of thiopental after the occlusion.
80 adult cats weighing 2.7 to 4.0kg, were used in this study.
The components of the pathophysiological responses, systemic changes, cerebral infarct size and histopathological ischemic neuronal changes were studied in these groups of animals.
We observed the permanent effect of the thiopental on acute focal cerebral ischemia in 40 cats by effecting permanent occlusion of MCA.
The EEG was monitored continously using bifrontal electrodes from the time of administration of thiopental (10mg/kg).
The animals were divided into 4 groups of 20 cats each.
The 4 different groups were used to investgate the effects of thiopental on focal ischemia according to different time interval.
The time intervals were 6hours, 24hours, 48hours, and 72hours after occlusion of MCA.
Each animal group were divided into two groups, which one was control (n=10) the other, thiopental treated group (n=10).
The results obtained were as follows:
1) Blood gases, artrial pressure, body temperature, and intracranial preosure differed among groups only a s fllows:
(a) Normal blood pressure was maintained but pulse rate was slightly fast in each control group.
(b) Blood pressure and pulse rate in the thiopental treated groups were significantly lower than in the control groups.
In the thiopental treated groups, the value of PaO₂ was significantly higher than control groups, however, PaCO₂, was not significantly higher in the thiopental treated groups as compared to the control group.
2) In the control groups, severe contralateral hemiplegia (grade Ⅲ) developed in the early stage of MCA occlusion, however the neurological deficit progressively improved to the state of abnormal climbing (neurological grade Ⅱ) 48 hours to 72 hours after the occlusion.
In the thiopental treated groups, minimum to mild neurological deficit significantly developed in the early stage of MCA occlusion and in one case walking ability was regained.
3) The size and distribution of the infarct significantly decreased to 60% in the thiopental treated groups (P<0.01).
The vale of the size of the size of the infarct in the thiopental treated groups 72hours after occlusion was minimized to 0.3±0.6% (P<0. 01).
In 80 percent of the control group cases severe extensive ischemic neuronal damage (score 3 or 4), was observed, 70 percent in the thiopental treated groups showed mild ischemic nerve cell changes (score 1 or 2) when the histological examination was given.
Although the severity of the ischemic neuronal damage was gradually improved from 6 hours to 72 hours after occlusion of the MCA in the control, the thiopental treated group was not significantly affected to the time factor.
4) Significant reduction of experimentally induced acute focal cerebral ischemia was associated in the cat model with the administration of thiopental at 5 minute, 30 minute. and one hour postocclusion.
Also we have defined the best barbiturate, best does, and best timing of administration to protect the acute focal ischemia.