Intracellular calcium levels in canine basilar artery smooth muscle following experimental subarachnoid hemorrhage: an electron microscopic cytochemical study

Abstract

Changes in intracellular calcium levels in canine basilar arterial smooth muscle were semiquantitatively measured by an electron microscopic cytochemical technique using a combined oxalate-pyroantimonate method. Measurements made after subarachnoid hemorrhage were compared with those made after contraction induced by prostaglandin F2 alpha. Fifteen minutes after topical application of the drug, when the basilar artery was constricted by 20%, 15% of smooth muscle cells contained a large amount of intracellular calcium. One hour later, the diameter of the basilar artery and intracellular calcium precipitation returned almost to control levels. Fifteen minutes after the first intracisternal injection of autologous blood, when acute vasospasm was angiographically evident, 13% of smooth muscle cells contained a large amount of calcium. After 1 h, when acute vasospasm had already abated, the number of smooth muscle cells containing a large amount of calcium markedly increased to 37% and some smooth muscle cells showed early degenerative findings such as intracytoplasmic vacuoles including calcium accumulation. After 48 h, when delayed vasospasm had already started, the calcium deposits and early degenerative changes had decreased significantly. After 49 h and 4 days (1 h and 48 h after the second injection of blood), the change in the amount of calcium was the same as at 1 h and 48 h after the first injection, respectively, but degeneration of smooth muscle cells increased. Therefore, acute vasospasm after subarachnoid hemorrhage may be caused by an initial elevation of intracellular calcium levels, as is the case with drug-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)