The effect on the development of cerebral vasospasm in the rat of lesioning of the peripheral and central catecholamine systems.

An experimental SAH was produced in the rat by the intracisternal injection of blood. The animals were examined with bilateral vertebral angiography or autoradiographic CBF- and CMRgI-studies. A biphasic vasospasm was seen with a maximal acute spasm at ten minutes and a maximal late spasm at two days post SAH. On day two post SAH, CBF studies demonstrated focal low flow areas in the cortex and caudate-putamen. The CMRgI examinations revealed focal areas with deoxyglucose accumulation corresponding to the low flow areas, suggesting an anaerobic glycolysis. Adrenal demedullation did not change the degree of spasm. Cranial sympathectomy reduced the degree of late spasm by about 50%. Lesioning of the ascending CA pathways in the mesencephalon prior to the SAH, prevented the development of both the acute and the late spasm. It also prevented the development of the focal CBF and CMRgI changes.