Debdi M, Seylaz J, Sercombe R
Laboratoire de Recherches Cérébrovasculaires, CNRS U.A. 641, Faculté de Médecine Lariboisière-Saint Louis, Paris, France.
J Cardiovasc Pharmacol. 1993 May;21(5):754-9. doi: 10.1097/00005344-199305000-00010.
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.
我们研究了蛛网膜下腔出血（SAH）后基底动脉对血清素（5-HT）、尿苷5'-三磷酸（UTP）和细胞外Ca2+反应性的变化。尽管有很多证据表明SAH后会出现早期血管收缩阶段，但关于体内与蛛网膜下腔血液接触后不久细胞外Ca2+作用变化的直接数据并不存在。向枕大池注射血液（SAH）或生理溶液（假SAH）10分钟后，处死兔子并取出其基底动脉，用于对3毫米节段进行等长张力测量。比较了SAH组、假SAH组和对照组动脉对UTP、5-HT和Ca2+（添加100 mM K+）的反应。与其他两组相比，SAH组动脉对所有试剂的反应均显著增强。钙通道阻滞剂尼卡地平（10(-10)-10(-8) M）以浓度依赖性方式抑制对Ca2+的所有反应；最敏感的动脉是SAH组动脉。在10(-9) M尼卡地平和1.5 mM Ca2+时，对照组的抑制率达到52.4%，假SAH组为39.7%，SAH组为70.5%（p < 0.05，SAH组与假SAH组相比）。结果表明，SAH促进了钙进入平滑肌细胞，这可能是由于可操作钙通道数量增加所致。在我们测试的诸如血小板衍生因子等致痉剂存在的情况下，这种变化应导致非常早期的大规模Ca2+内流，这可能有助于SAH的主要并发症——称为血管痉挛的延迟性动脉狭窄的发展。
