Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.

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Abstract
The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.

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