IMPAIRED CALCIUM REGULATION OF SMOOTH-MUSCLE DURING CHRONIC VASOSPASMFOLLOWING SUBARACHNOID HEMORRHAGE

The intracellular calcium level was determined in the canine basilar a rtery to investigate whether Ca2+ regulation of its smooth muscle is a ltered during chronic vasospasm following subarachnoid hemorrhage. A d ouble-hemorrhage model was used. The occurrence of vasospasm was confi rmed angiographically 7 days after initial hemorrhage. The intracellul ar calcium concentration ([Ca2+](i)) of smooth muscle was measured usi ng Fura-2. Fluorescence to excitation at 340 and 356 nm was monitored and the ratio R(340/356) was used as the indicator of [Ca2+](i). When the extracellular calcium concentration ([Ca2+](e)) was increased from pCa 8 to 2, [Ca2+](i) also increased. In the spastic arteries, the [C a2+](e) - [Ca2+](i) curve was elevated as compared with the normal art eries. 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 K-d, were greater in the spastic arterie s. Diltiazem (10(-5) mol/L) partially suppressed the augmented [Ca2+]( i) signal 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.