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 ration R340/356 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 [Ca2+]e - [Ca2+]i curve 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(-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 the
calcium regulation of smooth muscle is impaired after
subarachnoid hemorrhage, which may contribute to the pathogenesis of chronic vasospasm.