The role of endothelium in cerebral vasospasm

Following subarachnoid hemorrhage, the smooth muscle cells of the major cerebral arteries are exposed to a variety of vasoconstrictor substances, including those liberated from subarachnoid clots in the plasma, released from activated platelets adherent to the damaged endothelium, and released from the injured endothelium. There is no doubt that these vasoconstrictor substances induce the long-lasting contraction of the cerebral arteries. In this article, we discussed supplement mechanisms associated with endothelial damage in the major cerebral arteries with regard to the pathogenesis of vasospasm. Increased permeability in the major cerebral arteries after subarachnoid hemorrhage may allow access of vasoconstrictor and mitogenic substances to the media. These substances may augment the contraction of smooth muscle cells, produce the subendothelial thickening, or both. In addition, the impairment of vasodilatory properties in the major cerebral arteries, including the diminished synthesis of PGI2 and EDRF, as well as the inhibition of EDRF and neurogenic vasodilation by hemoglobin, probably augment the contraction triggered by a variety of vasoconstrictor substances. Furthermore, the impairment of antithrombogenic properties after subarachnoid hemorrhage could participate in the disturbance of cerebral microcirculation and the development of cerebral ischemic symptoms.