Author:
Nakagomi Tadayoshi,Kassell Neal F.,Sasaki Tomio,Fujiwara Shigeru,Lehman R. Michael,Johshita Hiroo,Nazar Gregory B.,Torner James C.
Abstract
✓ The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. The SAH was induced by injecting 5 ml of fresh arterial blood into the cisterna magna. Sixty-two rabbits were separated into four groups according to the timing of sacrifice: control rabbits, and operated rabbits sacrificed on Days 2, 4, and 6 after SAH. Acetylcholine (ACh) (10−7 M to 10−4 M) and adenosine triphosphate (ATP) (10−7 M to 10−4 M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10−6 M serotonin (5-HT). There were no significant differences in the vasodilatory response to ACh among these four groups. Relaxation to approximately 84% of the initial contractile tone occurred with 10−4 M ACh. On the other hand, the vasodilatory response to ATP was suppressed in the animals sacrificed 2 days after SAH; the relaxation of this group was approximately 52% at 10−4 M ATP, compared to a relaxation of 87% observed in the other groups of animals. One of the major causes of the impairment of endothelium-dependent vasodilation seems to be an inhibition of the production of endothelium-derived relaxing factor by endothelial cells.
After the relaxation studies, the dose-response curves for 5-HT were obtained. Serotonin caused significantly more contraction in the animals sacrificed 2 days after SAH than in the other groups. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH, together with the potentiation of the contractile response to vasoactive agents in cerebral arteries, may play an important role in the pathogenesis of vasospasm.
Publisher
Journal of Neurosurgery Publishing Group (JNSPG)
Cited by
83 articles.
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