Reactivity to vasoactive agents of canine basilar arteries exposed to experimental subarachnoid hemorrhage.

Autologous blood was injected into the cisterna magna of mongrel dogs twice with an interval of 48 hours. They were killed 3 days, 1 week, or 4 weeks after the first injection of blood, and helical strips of the basilar artery were prepared. Contractions induced by 5-hydroxytryptamine, noradrenaline, prostaglandin F2 alpha, and oxyhemoglobin were significantly potentiated. Relaxations caused by nicotine, K+, arachidonic acid, and prostaglandin I2 were suppressed, but the relaxant response to calcium ionophore A23187 and substance P did not change significantly. These results suggest that contractions mediated via activation of alpha, 5-hydroxytryptamine, and prostaglandin F2 alpha receptors are potentiated, and relaxations caused by stimulation of vasodilator nerves and by endogenous and exogenous prostaglandin I2 are attenuated in dog basilar arteries exposed to subarachnoid clot. On the other hand, certain relaxations possibly mediated by endothelium-derived relaxing factor do not appear to be significantly influenced.