Background: Risks related to rebleeding of a ruptured intracranial aneurysm have decreased. However, ischemic neurologic deficits related to vasospasm are still the leading causes of mortality and morbidity. It is well known that vasospasm is a dynamic process affected by various factors. The severity of vasospasm in animal models and clinical observations differ from each other. This variability has not been completely explained by blood and blood degradation products. Therefore, metabolites released from the damaged vessel wall during the bleeding are thought to play an important role in vasospasm. Method: To test this hypothesis, we used 46 male Wistar rats that were divided into 7 groups and administered one of the following to cisterna magna: venous blood, arterial blood, arterial wall homogenate, venous wall homogenate, combined mixture of arterial blood and artery wall homogenate, or combined mixture of venous blood and venous wall homogenate. Brainstems of the rats were excised, and the basilar arteries were harvested for morphometric measurements. Result: There were significant differences between the degree of vasospasm caused by arterial and venous blood (P < .0001). The intraluminal area of the basilar artery was significantly narrower after application of arterial blood, artery wall homogenate, or their combination (49% ± 1%) than after venous groups (30% ± 1.9%) (P < .0001). Conclusion: The results of this experiment demonstrated that metabolites from vessel walls play as important roles in the pathophysiology of vasospasm as blood and blood degradation products. Further investigation of these metabolites will improve our understanding of vasospasm, pathophysiology, and its treatment. © 2009 Elsevier Inc. All rights reserved.
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