Effects of vasoactive drugs on platelet aggregation in vivo and in vitro

Based on the generalization that most vasoconstrictor agents promote platelet aggregation while most vasodilator agents inhibit it, experiments were designed to test this premise in the living animal. Platelet aggregates, induced by a laser beam in arterial vessels of the hamster cheek pouch and bat wing, were observed microscopically to determine changes in growth, embolization, and vessel wall adherence in the presence of epinephrine, norepinephrine, phenylephrine, vasopressin, serotonin, isoproterenol, dipyridamole and sodium nitroprusside. Concentrations of the drugs too weak to alter microvessel diameters were used. In vitro responses were determined by inspection of a platelet-rich plasma-drug mixture in a hemocytometer chamber. It was established that drugs which enhanced platelet aggregation in vivo also produced aggregates in platelet-rich plasma from the same animal except for epinephrine and norepinephrine where the results in vitro were not definitive. Phenylephrine and isoproterenol produced changes contrary to expectation. Phenylephrine, an alpha adrenergic stimulator, caused a reduction in the duration of activity of platelets at the site of a laser-induced aggregate. When mixed with platelet-rich plasma, no platelet aggregates were produced. Isoproterenol, a beta adrenergic stimulator, enhanced the duration of activity of the platelet aggregate. When mixed with PRP, small, evenly dispersed aggregates were seen in the hemocytometer chamber.