[Cerebral vasospasm: molecular analysis].
Calcium concentration modifications in endothelial and smooth muscle cells, represent a key element in the pathogenesis of cerebral basilar artery vasospasm, induced by subarachnoid hemorrhage (SAH). These calcium concentration modifications induce, in turn activation of calcium-dependent PKCS. However, calcium antagonists, including nimodipine, exhibit weak clinical efficiency in this disease. Our data show that SAH-induced-cerebral vasospasm in a rat experimental model is accompanied not only by marked concentration modifications of several calcium-dependent PKCS, but also by marked concentration modifications of calcium-independent PKCS. Our data also evidence the fact that another group of calcium-dependent proteins, i.e. S100 proteins, exhibit marked modifications in their concentrations in the above mentioned rat model of cerebral vsospasm. All these data suggest that S100 proteins could represent a link by which calcium activates calcium-dependent as well as calcium-independent PKCS.