[Possible role of microthrombus in the pathogenesis of cerebral vasospasm (author's transl)]

Our previous experimental and clinical studies yielded the following results: CSF flow around the subarachnoid vessels is often interrupted by subarachnoid clots; anaerobical incubation of CSF-blood mixture led to a marked fall in the pH value; the vasocontractility of anaerobically incubated CSF-blood mixtures was greater than that of aerobically incubated samples; vasocontraction induced by anaerobically incubated samples was inhibited to a far greater extent the prostaglandin synthesis inhibitor meclofenamic acid than by phenoxybenzamine; cases of asymptomatic marked angiographical vasospasm or of cerebral ischemia with relatively slight angiographical vasospasm were not rarely encountered. Those results lead us to a hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobical changes of subarachnoid clots may be factor upsetting the balance of the synthesis of TXA2 and PGI2 from PG endoperoxides on the inner surface of cerebral arteries, in favor of TXA2--which plays a role in arterial contraction and in thrombosing with platelet aggregation. On this basis we have been testing the administrations of trapidil, an antagonist and selective synthesis inhibitor of TXA2, in 20 consecutive suitable cases so far, for the prevention of cerebral vasospasm after aneurysmal rupture. Angiographical vasospasm was seen in 9 of the 20 cases, but no signs of cerebral ischemia were detected in 7 of the 9 cases, either clinically or in CT scan. The importance of thrombus formation by platelet aggregation in symptomatic vasospasm are thus suggested.