Fifty adults cats were subjected to the study to evaluate the role of eicosanoids in cerebral vasopasm. Experimental cerebral vasospasm was produced as follows : Three days after the injection of 3 ml of autologous blood into the cisterna magna, the basilar artery was exposed transclivally and continuously irrigated with the mixture of blood and CSF incubated for 3 days at 37°C. The caliber of basilar artery and rCBF of pontine tegmental region were measured simultaneously by microphotography and heat-and hydrogen clearance method.
Cats were divided into 3 groups : non-treated cats, and cats treated with thromboxane A
2 (TXA
2) antagonists : ONO-3708, ONO-1270, (100 μg/kg/min), and prostacyclin (PGI
2) analogues : OP-41483, (75 ng/kg/min), OP-2507, (100 ng/kg/min). In fifteen nontreated cats, the caliber of basilar artery decreased 29.2 ± 4.4% (mean ± SE) of its original diameter 10 minutes after the irrigation of blood-CSF mixture and remained unchanged as long as it was irrigated. Ten minutes after the irrigation, rCBF was 24.4 ± 1.5 ml/100 g/min and gradually decreased further to the level of 18.6 ± 1.4 ml/100 g/min. In treated cats, basilar artery became spastic as well. The gradual reduction in rCBF, however, could be prevented even in animals with severe cerebral vasospasm. Both TxA
2 antagonists and PGI
2 analogues markedly inhibited platelet aggregation. The adhesion of platelets and red blood cells to the folded luminal surface was also inhibited scanning-electron-microscopically in both treated groups.
These results suggest that the accumulation of TxA
2 or the deficiency of PGI
2 in the cerebral vessel wall, if it should occur after subarachnoid hemorrhage, may not have an important role in the development and progression of cerebral vasospasm in the major vessels but significantly decrease the cerebral blood flow by increasing platelet aggregation.
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