Abstract
Ultrastructural and histochemical changes in experimental vasospasms were studied in 46 cats. Prolonged vasospasms of the exposed basilar artery were produced by continuous irrigation with a solution of serotonin (1—10 Mg/ml) or calcium gluconate (0.2 M). Vasospasms lasting for less than 10 hours were relieved by topical application of vasodilating agents such as ascorbic acid (25 mg/ml) and methylprednisolone (10 mg/ml). However, spasms continuing for more than 10 hours failed to respond to such treatment.
In the vessels responsive to vasodilators, aggregation of granules and vesicles in extracellular spaces of the media was revealed by electron microscopy. The electron density remained unchanged after treatment by 5-hydroxydopamine, while that of the vesicles in adrenergic terminals increased. The granules and vesicles morphologically resembled the adrenergic vesicles but were biochemically different from them. Necrotic changes in the vessel wall such as fragmentation of myofilaments were observed in the vessels unresponsive to vasodilators.
The potassium pyroantimonate staining technique demonstrated fine deposits within the nucleus, sarcoplasm, sarcoplasmic reticulum and mitochondria, and along the sarcolemma in normal vessels. It was confirmed by X-ray microanalysis and EGTA-chelation that they contained calcium. The deposits along the sarcolemma decreased in number in the lanthanum-loaded vessel walls, and it was confirmed that most of them were present on the outer surface of the sarcolemma.
Calcium deposits somewhat increased in number in the sarcoplasm of spastic vessels responsive to vasodilators, but the deposits along the sarcolemma remained unchanged.
The most characteristic change was that calcium along the sarcolemma disappeared in the spastic vessels unresponsive to vasodilators.
The morphological and functional changes in the arterial smooth muscle cells were discussed in relation to the timing of treatment of cerebral vasospasms.
