Why Experimental Vasospasm Resolves

Abstract

P112 It has been suggested that changes in the arterial wall contribute to the maintenance and resolution of vasospasm after subarachnoid hemorrhage (SAH). This study determined if such changes contribute to the resolution of vasosapsm after SAH, if vasospasm resolves because of loss of subarachnoid blood clot or if a combination of these mechanisms is involved. 27 monkeys underwent baseline angiography and unilateral (n = 17) or bilateral (n = 8) SAH. Animals with bilateral SAH underwent angiography 1, 3, 5 and 7 days later followed by euthanasia. Animals with unilateral SAH had angiography 7 days later. The clot then was removed in these animals and replaced with fresh clot (n = 7) or removed and not replaced (n = 5). The removed clot was placed on the left side (n = 12). Controls did not have clot removal (n = 5) and/or had fresh clot placed on the left on day 7 (n = 5). Angiography was repeated every 2 days until euthanasia on day 14. SAH caused significant middle cerebral artery vasospasm on day 7 that slowly resolved by day 14. Removal of clot on day 7 resulted in more rapid reversal of vasospasm suggesting that vasospasm depended on continued presence of subarachnoid clot rather than on or in addition to structural changes in the artery. Placing fresh clot on the right side on day 7 produced vasospasm that persisted without resolving suggesting that there is no preconditioning response in the artery that prevents or conributes to reversal of vasospasm. On the other hand, placing 7-day-old clot from the right onto the left caused significantly more rapid onset of severe vasospasm than placing fresh clot from animals 7 days after SAH, suggesting that breaking up the clot to replace it on the left increases release of spasmogens or that there is a negative adaptive response that exacerbates vasospasm. In conclusion, vasospasm resolves because of loss of subarachnoid clot. There is no evidence for a preconditioning response in cerebral arteries that renders them less responsive to subarachnoid clot. Spasmogen release from clot 7 days after SAH may be reduced in this model so that breaking up the clot increases spasmogen release resulting in rapid onset of severe vasospasm and/or that there is a negative adaptive response 7 days after SAH that worsens vasospasm.