INCREASED INFLUENCE OF CALCIUM AND NICARDIPINE ON RABBIT BASILAR ARTERY REACTIVITY AFTER BRIEF SUBARACHNOID HEMORRHAGE

We studied the changes in reactivity of basilar arteries immediately after a subarachnoid hemorrhage (SAH) in response to serotonin (5-HT), uridine 5'-triphosphate (UTP), and extracellular Ca2+. Although much evidence suggests that an early phase of vasoconstriction occurs after SAH, no direct data exist on changes in the role of extracellular Ca2+ shortly after in vivo contact with subarachnoid blood. Ten minutes after injection of blood (SAH) or physiologic solution (sham SAH) into the cisterna magna, rabbits were killed and their basilar arteries were removed for isometric tension measurements on 3-mm segments. Responses to UTP, 5-HT, and Ca2+ (with addition of 100 mM K+) were compared between SAH, sham SAH, and control arteries. SAH arteries showed substantially increased responses to all agents as compared with the other two groups. The calcium entry blocker nicardipine (10(-10)-10(-8) M) inhibited all responses to Ca2+ in a concentration-dependent manner; the most sensitive arteries were the SAH arteries. At 10(-9) M nicardipine and 1.5 mM Ca2+, the inhibition attained 52.4% for control, 39.7% for sham SAH, and 70.5% for SAH (p < 0.05, SAH vs. sham SAH). The results suggest that calcium entry into smooth muscle cells is facilitated by SAH, and this might be explained by an increased number of operational calcium channels. This change, in the presence of spasmogens such as the platelet-derived factors we tested, should result in very early large-scale Ca2+ entry, which might contribute to development of the delayed arterial narrowing known as vasospasm which is a major complication of SAH.