Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.


新井 達潤 岡山大学医学部麻酔学教室
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Ventricular fibrillation was induced in fifteen monkeys by electric stimulation using a bipolar intracardiac pacemaker electrode which was inserted through a femoral vein. The monkeys were defibrillated and resuscitated after several minutes. Cerebral blood flow (CBF), intracranial pressure (ICP) and EEG were monitored continuously. CBF autoregulation was checked regularly before and after ventricular fibrillation to study the relation between it and other parameters such as CBF, ICP, EEG. Fifteen monkeys were divided into two groups, a burr-hole group and a no burr-hole group. ICP was measured in the burr-hole group (10 monkeys). The purpose of having two groups was to ascertain the effect of a burr-hole (artificial injury in the skull and dura) on the parameters CBF, EEG and autoregulation. CBF was measured with electromagnetic flowmeter at internal carotid artery. The conclusion of the experiment was as follows; (1) Autoregulation was lost in all monkeys after resuscitation. In the monkeys which had had autoregulation before cardiac arrest, the autoregulation recovered in three (no burr-hole group) to five (burr-hole group) hours after resuscitation, if resuscitation took place within five minutes. In the monkeys whose autoregulation had already been lost before cardiac arrest, it did not return despite successful cardiac resuscitation. (2) Immediately after resuscitation, BP, ICP and CBF increased for 20-60 minutes. In the monkeys who had no recovery of autoregulation after resuscitation, the rate of increase of ICP was much larger than those whose autoregulation recovered, and at the peak of ICP, the CBF decreased. Impairment of autoregulation itself, indicates that the ballance of circulatory dynamics of the brain is easily impaired by noxious stimulation such as hypoxia. (3) In the monkeys with recovery of autoregulation, general status was good after resuscitation but in the monkeys without recoverey, symptomes of increased ICP were seen and the prognosis was poor. (4) Six minutes of cardiac arrest would appear to be the upper limit for monkeys to survive after resuscitation. (5) Before ventricular fibrillation, corresponding changes in the CBF and the frequency of the EEG wave recorded, but after resuscitation the frequency of the EEG wave decreased despite an increase in CBF. This is probably the same mechanism as occures in the "luxury perfusion syndrome". There was no, relation between EEG and autoregulation, but when EEG showed dominant slow or flat waves, there was no autoregulation.