[The role of sympathetic nerve and vasoactive amines in experimental cerebral vasospasm in dogs (author's transl)].

In order to study the role of sympathetic nervous system and vasoactive amines in cerebral arterial spasm, the following experiments were performed in dogs. In the first experiment, two weeks after bilateral removal of the superior cervical ganglion subarachnoid hemorrhage was produced by the puncture of the posterior communicating artery in six dogs. Second, the arterial blood of non-reserpinized dog was injected into the cisterna magna of another six reserpinized dogs. Diameter changes of the cerebral basal arteries before and after the experimental subarachnoid hemorrhage were observed utilizing the magnified vertebral angiography. Vasoconstriction 30 minutes after the puncture of the artery in the sympathectomized dogs was milder than that seen in the non-sympathectomized dogs, while vasoconstriction 24 hours after the subarachnoidal hemorrhage was induced similarly in degree in both groups. In reserpinized dogs, vasconstriction 30 minutes after the experimental subarachnoidal hemorrhage was somewhat milder than that seen in control dogs, and angiograms taken 24 hours after the hemorrhage showed that vasoconstriction was remarkably milder than in control dogs. Noradrenergic fluorescence of the arterial wall after the puncture of the posterior communicating artery was examined using Falck's fluorescence histochemical method. Noradrenergic fluorescence in the arterial wall did not disappear 15 minutes, 24 hours and three weeks after the experimental subarachnoid hemorrhage. From these experimental results, it was suggested that the sympathetic innervation to cerebral arteries might contribute to induce early spasm, but not to late spasm. Moreover, it was speculated that vasoactive amines released from the damaged brain tissue might play a role in inducing late spasm.