Cerebral vasospasm is one of the most important factors influencing morbidity and mortality of intracranial operations or diseases. Platelet aggregation and adhesion is increased in spastic vessels. Degradation of platelets liberates mediators, which in turn increase vasospasm, thus creating a vicious cycle. Healthy vessels cope with this by increasing the synthesis of prostacyclin. The purpose of this study was to increase experimentally the levels of arterial prostacyclin and adenosine triphosphate (ATP) in animals through intraarterial injection of these substances because they are lower in spastic vessels. Prostacyclin promotes antiaggregation and dilatation, increases blood flow, inhibits thromboxane A2, and prevents synthesis of angiotensin II. Most of these effects were done by increasing cyclic adenosine monophosphate (cAMP). After injecting autogenous blood into the cisterna magna of male dogs, both the acute and chronic phases of vasospasm and the degenerative changes in the arterial wall were observed. Injecting ATP increased the severity of vasospasm. During vasospasm it was found that when prostacyclin is used intraarterially, vasodilatation began, but degeneration of the arterial wall could not be prevented. In the group of animals in which both ATP and prostacyclin were used, there was no degeneration of the arterial wall and the basilar artery was seen to be normal when viewed under the electron microscope.