Abstract
Experimental vasospasm of the cerbral arteries was produced in dogs by the double injection method. Somatosensory evoked potentials were recorded epidurally on the cerebral cortex and the second cervical vertebrae. Cerebral blood flow was measured by H2 clearance technique. Angiography, taken periodically, revealed diffuse vasospasm of about 50% of the control vascular diameter at 48 hours after the second blood injection. However there was no significant delay of the central conduction time after the appearance of vasospasm. Regional cerebral blood flow was reduced to 33.1 ± 12.9 ml/100 g/min, nearly 70% of control blood flow, just after the first injection of autologous blood into the subarachnoid space. Then 20% flow reduction was observed at 48 hours after the second injection of autologous blood.
Our results confirmed that cisternal blood injection alone did not reduce the cerebral blood flow significantly despite the presence of angiographic vasospasm. Furthermore, it did not affect the central conduction time. This suggests that the vasospasm produced by cisternal blood injection does not induce a critical level of cerebral ischemia, which is frequently induced following ruptured cerebral aneurysm in clinical cases.
There is no argument that vasoactive substances derived from the extravasated blood induce vasospasm; however, vasospasm alone does not produce such severe cerebral ischemia. We would like to stress that initial brain damage induced by subarachnoid hemorrhage together with vascular tearing might be importatant for the occurrence of symptomatic vasospasm.
