A model for producing chronic cerebral vasospasm in monkeys by injecting autologous blood into the basal cistern is described. Spasm/narrowing was observed by angiography one hour after SAH in 8 out of 10 monkeys and in 5 of these 8, spasm was observed both one and two weeks later. No narrowing of the vessels was observed in the control cases. In monkeys that showed spasm one week after SAH, narrowing of the extracranial vertebral arteries was also observed. Repeated injections of blood at intervals of one and two weeks caused intensification of spasm in the intracranial portion of vertebral arteries and the basilar arteries. It is suggested that cerebral vasospasm following SAH may in part be mediated by a central control mechanism acting through the sympathetic nervous system in that extracranial vessels remote from direct contact with blood showed reactive narrowing. Stroke, Vol 13. No 4. 1982 CEREBRAL ARTERIAL SPASM following sub-arachnoid hemorrhage (SAH) is a most important un-resolved problem in neurosurgery. 1 Clinically, it is reported that cerebral arterial spasm occurs about the 4th to 10th days after SAH; therefore surgery during this period is usually avoided by most people. 2 3 Many unsuccessful attempts have been made to relieve the symptoms or relax the vasospasm but there is still incomplete understanding of the pathogenesis of the condition. For this reason, we initiated this study of SAH in monkeys and observed the changes in the intracranial pressure (ICP), systemic blood pressure (BP) and cerebral angiography with a view to a better understanding of the mechanisms of vasospasm. Methods Fifteen Macaque fascicularis monkeys, weighing between 2.3 kg and 3.2 kg, were used in this study. Three of them were excluded from the data due to technical errors with the radiological and surgical procedures. SAH was created in ten of the remaining animals by injecting fresh autologous arterial blood into the subarachnoid space by means of cisternal puncture. The other two were injected with Elliot's B-solution to serve as controls. The monkeys were given atropine sulphate (0.05 mg/kg), followed by 5-10 mg/ kg of ketamine hydrochloride (IP). After intubation, angiography was carried out. The animals were placed in a supine position with the head fixed such that the orbito-meatal line was horizontal. Bilateral retrograde brachial arteriography was carried out using Conray 60 administered via a mechanical pressure injector at the rate of 2 cc/sec through a Y-connector. Double magnification angiogram films were taken in the basal projection at the rate of 2 films per second for 5 seconds, then 1 film per second for the next 5 seconds. PC0 2 was measured at the time of angiography. After performing baseline angiography prior to the From the Division of Neurosurgery, induced SAH, each monkey was placed on the experimental stand in prone position with head down. The body was tilted 15 degrees forward so that the orbito-meatal line was vertical. Two 22-gauge lumbar needles were inserted into the monkey's basal cis...