Abstract
Experimental subarachnoid hemorrhage was produced by an intracisternal injection of fresh autologous arterial blood in 33 cats. Three days later the basilar artery was exposed transclivally and further advanced prolonged vasospasm was produced by topical application of blood-CSF mixture incubated at 37°C for three days. Regional cerebral blood flow (rCBF) in the brain stem was measured by means of heat clearance method. Arterial blood pressure in the femoral artery was also monitored continuously. Intravenous administration of either PGI2 or OKY-1581 (a specific inhibitor of thromboxane A2 synthetase) produced a decrease of arterial blood pressure. The changes of rCBF were divided into three types: Type A consisted of those with no changes. Type B was related to the arterial blood pressure. Type C showed increase in rCBF despite of systemic hypotension.
Type A or B in rCBF was observed in 17 out of 19 cats in which PGI2 was administered intravenously, and Type C was observed in only 2 cats. Comparative study was done in 13 control cats in which had neither subarachnoid hemorrhage nor topical application of blood-CSF mixture. Type A or B was shown in 12 and Type C was in only one cat. From these results, PGI2 was likely to dilate extracranial rather than intracranial vessels regardless of cerebral vasospasm.
OKY-1581 was administered in 14 cats with cerebral vasospasm and in 10 control cats. Type C pattern was demonstrated in 10 cats with vasospasm and in 7 of the control cats.
Though OKY-1581 produced the increase of rCBF in most of normal cats and those with cerebral vasospasm, its action did not seem to be due to the increase of PGI2 synthesis by inhibition of TXA2. synthesis. OKY-1581 might be useful in prophylaxis and treatment of ischemic syndrome due to cerebral vasospasm.
