Biochemical Assessments of Cerebral Vasospasm: Measurement of cGMP, PKC, and PTK in Cerebral Arteries

Cerebral arterial tone is regulated by a concert of contractile signals [e.g., increased intracellular Ca²⁺ , protein kinase C (PKC) activation], and vasodilatory signals [e.g., increased cyclic guanosine monophosphate (cGMP)] in arterial smooth muscle cells. After subarachnoid hemorrhage (SAH), a variety of molecules are released into subarachnoid space and stimulate arterial cells to enhance contractile signals and/or attenuate vasodilatory signals, resulting in a severe constriction in cerebral arteries called cerebral vasospasm. Previous studies suggest increased PKC and protein tyrosine kinase (PTK) activity as well as decreased cGMP signaling may contribute to the development of cerebral vasospasm following SAH. Here, we describe approaches to examine these intracellular signaling molecules, PKC (isoforms), PTK, and cGMP, in cerebral arteries from a dog SAH model.