Impaired Calcium Regulation of Smooth Muscle during Chronic Vasospasm following Subarachnoid Hemorrhage

Abstract

The intracellular calcium level was determined in the canine basilar artery to investigate whether Ca2+regulation of its smooth muscle is altered during chronic vasospasm following subarachnoid hemorrhage. A double-hemorrhage model was used. The occurrence of vasospasm was confirmed angiographically 7 days after initial hemorrhage. The intracellular calcium concentration ([Ca2+]i) of smooth muscle was measured using Fura-2. Fluorescence to excitation at 340 and 356 nm was monitored and the ratio R340/356was used as the indicator of [Ca2+]i. When the extracellular calcium concentration ([Ca2+]e) was increased from pCa 8 to 2, [Ca2+]ialso increased. In the spastic arteries, the [Ca2+]e− [Ca2+]icurve was elevated as compared with the normal arteries. Treatment with ionomycin elevated the curve in the normal group, but it had little effect in the spastic arteries. Values of [Ca2+]i, calculated in multiples of Kd, were greater in the spastic arteries. Diltiazem (10;−5mol/L) partially suppressed the augmented [Ca2+]isignal in the spastic arteries, whereas it did not affect the curve in the control group. These results indicate that calcium regulation of smooth muscle is impaired after subarachnoid hemorrhage, which may contribute to the pathogenesis of chronic vasospasm.