Propagated constriction in mouse pial arterioles: possible role of endothelium in transmitting the propagated response.

Two lines of evidence are presented demonstrating propagated constriction in mouse pial arterioles. First, a 2 second microapplication from a 6 micron pipette tip of approximately 12 nanoliters of BaCl2 or uridine triphosphate produced constrictions which spread to points 300 microns or more upstream from the point of application. Second, constrictions were elicited between 2 points of endothelial injury, each made with a focused laser beam 18 microns wide. A helium-neon laser was used in the presence of intravascular Evans blue. The constrictions were produced when a very brief exposure at a downstream site was followed by a more prolonged exposure at an upstream site 300 to 1100 microns from the downstream injury. In approximately half the cases the upstream damage elicited a local platelet aggregate. Therefore, vasoconstrictors released by aggregating platelets may have played a role in initiating constriction. Constriction was limited to the segment between the two endothelial injuries. The necessity for 2 injuries, rather than one, suggests that local losses of endothelium derived vasodilators also played a role in initiating constriction and/or permitting its propagation. Abrupt cessation of constriction at the sites of endothelial damage suggests that endothelium plays a role in propagation of constriction. Propagated constriction may play a role in amplifying the spasmotic effects of local subarachnoid hemorrhage or in the spread of constriction beyond local areas of reduced metabolic demand.