Does dopamine D2-receptor-mediated increase in vascular and endothelial NOS activity ameliorate cerebral vasospasm after subarachnoid hemorrhage in vitro?
Cerebral vasospasm is significantly reversed in a functional measure of vasospasm in vitro by dopamine, via a D(2)R-mediated pathway. The increase in NOS protein seen in both the endothelium and vascular smooth muscle in response to CSF(V) is enhanced by dopamine, also in a D(2)R-dependent mechanism.
Pulmonary vascular dysfunction is common in ALI, and is independently associated with poor outcomes. Future trials targeting pulmonary vascular dysfunction may be indicated.