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(Continued from page 95)
by Marshall, et. al., "Journal of Neurosurgery," 1978, 48:560-564, and as late as several weeks as documented by others. We can, therefore, speculate that we can treat vasospasm in traumatic brain injury patients and improve their outcome. According to Neil Martin at UCLA and UCLA Harbor Hospital, they looked at patients over the last five years. With cerebral aneurysms there is massive filling of the subarachnoid space with blood products. The vessels are usually caked with blood and something in the blood induces the morphological change seen in cerebral vasospasm. Pathophysiological and electron microscopy studies suggest that there is a combination of active smooth muscle contraction and possibly a morphological change. This morphological change is due to a cellular proliferation in the vessel wall that causes profound luminal narrowing.
The cause of cerebral vasospasms is not entirely known. Cerebral vasospasm from subarachnoid hemorrhage is refractory to most vasodilators. There is evidence that the mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased potassium conductants and the ability of the potassium channel activators to relax. Dr. Zuccarello, et. al., "Stroke," 1996, 27:311-6, demonstrated that there is relaxation of the basal artery spasms in the rabbit in response to a potassium channel activator, cromakalim, completely, while a protein kinase C antagonist, adenylate cyclase activator and guanylate cyclase activator was less efficacious. In an additional study, Zuccarello, et. al., "Journal of Neurosurgery," 1996, 84:503-7, also demonstrated the use of an oral endothelin A/B receptor antagonist and endothelin A receptor antagonist could also treat vasospasms.
There may be an immune inflammatory response to the blood breakdown products affecting the arterial wall. There is evidence that an intercellular adhesion molecule I, which is a ligand for the leukocyte adhesion receptor from the endothelial and medial layer of the artery on day 2 to 5 following subarachnoid hemorrhage. It has also been shown that nitric oxide synthetase immunoreactivity is virtually absent in the adventitial neurofiber layers of the intracerebral arteries in monkeys with vasospasm. This can be because the nitric oxide synthetase receptors are blocked in the pathogenesis of cerebral vasospasms. Pluta, et. al.,
"Journal of Neurosurgery," 1996, 84:648-54.
There are other studies that look at the decrease of plasma leukocyte intercellular adhesion molecule I, integrins CD18 and CD11B are decreased in traumatized human patients. This decrease may be correlated to the same decrease we see in fibrinogen and other blood coagulation products in a consumptive coagulopathy that is seen in head injury and brain surgery.
Halim, et. al., "Gynecology Obstetrics Investigation," 1995, 39:1-7, demonstrated that endothelin I induced brain edema, EEG changes, ischemia and cerebral vasospasms in rabbits. This is correlated with Seifert, et. al., "Journal of Neurosurgery," 1995, 82:55-62, (Continued on page 97)
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