For making an experimental subarachnoid homorrhage that closely simulates human aneurysmal rupture, a needle previously inserted into the posterior communicating artery is subsepuently withdrawh by traction on a thread. Biphasic sqasm is revealed by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lastsd 60 minutes and the late spasm begins 3 or 4 hours after subarachnoid hemorrhage and continues for several days.
Effects of vasoactive drugs and sympathectomy on the early and late spasm are studied utilizing vertebral angiography. Papaverine and isoxsurprine injections into the vertebral artery release both early and late spasm, which suggest these spasm are a manifestation of the local muscle contraction. The antiserotonin agent, methysergide, releases the early spasm, while it does not relax the late spasm. The alpha blocking agent, phentolamine, releases the early spasm, but it scarcely relaxes the late spasm. In sympathectomized dogs, the early spasm is revealed milder than in the untreated dogs. However, the late spasm is demonstrated to the similar extent as seen in the untreated dogs. The authors emphasize an etiological difference in the early and late spasm.
The study on microcirculation in the hypothalamus using perfusion technique with colloidal carbon after rupture of the artery reveales that spasm is induced with ischemic changes in the hypothalamus. Aside from blood chemicals, the authors speculate that changes in sensitivities of the cerebral blood vessels which might be influenced by the vasomotor center in the hypothalamus should play an important role in producing vasospasm.