[Experimental Subarachnoid hemmorrhage in dogs--effect of various drugs and sympathectomy on cerebral arterial spasm (author's transl)].

Adult mongrel dogs were used. The posterior communicating artery was punctured with a fine needle and subarachnoid hemorrhage was produced, which simulated aneurysmal rupture in human. The cerebral basal arteries were constricted remarkably after the puncture. However this vasospasm disappeared in about 60-120 minutes. After this restoration, the vessels began to be constricted again and reduced their diameter in greater degree with lapse of time. Effect of various drugs and sympathectomy on the experimental spasm induced by this method were studied utilizing the magnified vertebral angiography. The drugs used were papverine, isoxuprine, methysergide, phentolamine and propranolol. One of these drugs was given to each dog into the vertebral artery 15 minutes after the puncture of the artery for study of the early spasm, and the same procedure was carried out 24 hours after the late spasm. Vertebral arteriograms were taken immediately after and at 5, 10 and 30 minutes after injection of the drug. Diameter changes of the cerebral basal arteries were measured on the film. Smooth muscle relaxtants, papaverine and isoxsuprine, were effective on relieving the early and the late spasm. An antiserotonin agent, methysergide, relieved slightly the early spasm, but it had no effect on the late spasm. Phentolamine, that is an adrenergic blocking agent, relieved the early spam remarkably, but it was less effective on the late spam. A beta adrenergic blocking agent, propranolol, was effective on relieving neither the early nor the late spasm. Two weeks after the removal of the bilateral upper cervical ganglia, subarachnoid hemorrhage was produced by the smae method as mentioned above in four dogs. Arteriograms taken 24 hours after puncture of the posterior communicating artery in these dogs showed vasoconstriction as same as in the non-sympathectomized dogs. From these experimental results, it was suggested that an etiological difference in the early and the late spasm may exist, and that the occurence of the late spasm may not be influenced by the sympathetic system.