The Correlation between Immunological Reaction in the Arterial Wall and the Time Course of the Development of Cerebral Vasospasm in a Primate Model

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Abstract
To investigate the role of immunological reactions in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH);, the authors studied the correlation between immune/inflammatory reactions in the arterial wall and the time course of vasospasm in primates. Twenty monkeys were divided into four groups of 5 animals each: 1); a control group of sham-operated animals, 2); animals subjected to angiography 3 days after the induction of SAH (3-day SAH);, 3); animals subjected to angiography 7 days after SAH (1-week SAH);, and 4); animals subjected to angiography 7 and 14 days after SAH (2-week SAH);. To induce SAH, the main cerebral arteries on the right were dissected free of the arachnoid, and an autologous blood clot was placed around the arteries. To evaluate vasospasm, all animals underwent a baseline angiogram before SAH; angiography was repeated at different intervals in each group, as outlined above. Histopathological changes and the deposition of the immunoglobulin IgG in the arterial wall were evaluated immunohistochemically in each group. The cerebral arteries on the side of the clot showed evidence of mild vasospasm (-24.6% reduction); on the angiogram performed on Day 3, severe vasospasm (-51.7%); on Day 7, and mild vasospasm (-12.8%); on Day 14. The infiltration of inflammatory cells was most marked in the spastic arterial wall in the 1-week SAH group. In the 2-week SAH group, severe myonecrosis and intimal disruption were observed, even in the vessels that showed only mild vasospasm, and the inflammatory reactions had almost abated. Deposition of IgG was observed in the media of the vasospastic artery, and the degree of deposition correlated with the severity and the time course of vasospasm. It is suggested that early damage to the arterial wall after SAH elicits an immunological reaction, and that a local immune complex in the media may play a role in the pathogenesis of vasospasm by activating an effector system, resulting in angionecrosis as part of a chronic inflammatory response.

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