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These results consisted with the reports showing that oxyhemoglobin is a major causative component of blood clot for cerebral vasospasm following SAH [ 26] and that ET-1 potentiates the oxyhemoglobin-induced cerebrovascular smooth muscle contraction via the rhoA/rho kinase and PKC pathways [ 28, 29].
These results are consistent with the reports showing that oxyhemoglobin is a major causative component of blood clot for cerebral vasospasm following SAH [ 30, 31] and that ET-1 potentiates the oxyhemoglobin-induced cerebrovascular smooth muscle contraction via the rhoA/rho kinase and PKC pathways [ 11].
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