ABSTRACT
It is well documented that elevation of intracranial pressure is accompanied by arterial blood pressure(cushing response) in laboratory animals as well as in human. When the elevation of intracranial pressure(ICP) was repeated in a rabbit at an interval of 30-60 min, the blood pressure increased more promtly than in the first elevation of ICP, suggesting that mechanism involved in the pressure might be different. Therefore, this study was undertaken to clarify the pharmacological characteristics of the response to the first and repeated(second) elevation of ICP in urethane anesthetized rabbits. Increasing ICP, induced by infusion of saline into a ballooned in the epidural space, produced arise of the arterial blood pressure. When the blood pressure reached a peak, the balloon was suddenly deflated to reduced the ICP and blood pressure declined (the first ICP elevation experiment). After 30-60 min the same procedure was repeated (the second ICP-elevation experiment) Results are summarized as follows; 1) In the first ICP elevation experiment, the arise of ICP was relatively slow at the beginning of the infusion but became sharp as the infusion proceeded. When ICP increased sharply BP also increased abruptly and heart rate decreased. 2) In the second ICP elevation experiment, the slight decrease in BP which appeard at the beginning of the first ICP elevation experiment rat observed, so that only an abrupt arise of BP was seen. 3) Intravenous chlorisondamine inhibited the pressure responses in the second ICP elevation experiment. 4) Intraventricular corynanthine had little effect on the pressure response to the first ICP elevation but inhibited the pressure response to the second ICP elevation. 5) Intraventricular clonidine, yohimbine and prazosin little effect on the pressure response to the second ICP elevation. From this results that functional integrity of central alpha 2-adrenoceptor which took part in the pressure response to the first ICP elevation might have deranged in the second ICP elevation and that central alpha 1-adrenoceptors play a dominant role in the pressure response to the second ICP elevation.