Abstract
This experiment determined if the time course of inhibition of arterial relaxation correlates with angiographic vasospasm following subarachnoid hemorrhage (SAH) in dogs. Twenty-two dogs underwent cerebral angiography followed by SAH by 2 injections of blood into the cisterna magna. Dogs had repeated angiography and were sacrificed 4 (n = 5), 7 (n = 4), 10 (n = 4), 14 (n = 5), or 21 (n = 4) days later. Four dogs served as controls and underwent angiography only, followed by sacrifice. The basilar arteries were removed and studied under isometric tension to determine relaxations to acetylcholine and sodium nitroprusside. There was significant reduction in basilar artery diameter at each time after SAH (day 4: -52% +/- 10%, day 7: -37% +/- 10%, day 10: -54% +/- 10%, day 14: -37% +/- 10%, and day 21: -26% +/- 18%, p < 0.05, analysis of variance), although there were no pairwise differences in the degree of vasospasm over time. Relaxations to acetylcholine were significantly reduced at all times after SAH (p < 0.05, analysis of variance). Relaxations to sodium nitroprusside were significantly reduced 7 days after SAH. There was a significant linear correlation between increasing time after SAH and decreasing relaxation to acetylcholine. There was no correlation in univariate or multivariate analysis, between the time after SAH, the degree of vasospasm and the relaxation to acetylcholine or sodium nitroprusside. It is concluded that inhibition of arterial relaxation depends on the relaxant used and does not correlate with vasospasm. The lack of correlation between angiographic vasospasm and relaxation suggests that while the latter occurs after SAH, contractile processes may be more important in the pathogenesis of vasospasm.
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