Vrints C J, Bult H, Bosmans J, Herman A G, Snoeck J P
Department of Cardiology, University Hospital of Antwerp, Belgium.
Eur Heart J. 1992 Jun;13(6):824-31. doi: 10.1093/oxfordjournals.eurheartj.a060264.
In experimental atherosclerosis, impairment of endothelium-dependent vasodilation results in an unmasking of potent vasoconstrictor responses to serotonin, a substance released by aggregating platelets. To determine whether similar changes occur in diseased human coronary arteries, the responses to selective intracoronary infusions of acetylcholine and serotonin (both endothelium-dependent vasodilators) and to isosorbide dinitrate (a dilator directly acting on the smooth muscle) were assessed by quantitative coronary arteriography in 16 patients with angiographically normal coronary arteries, in 10 patients with minimal (less than 30% narrowing) and in five patients with more advanced (greater than 50% narrowing) coronary atherosclerosis. Acetylcholine induced constriction in diseased coronary arteries, but in patients with normal coronary arteriograms, it caused dilatation in seven patients (smooth dilators) and constriction in nine patients (smooth constrictors). In the smooth dilators, however, serotonin evoked no significant changes (+1.4 +/- 4.1%), whereas in the smooth constrictors and in patients with diseased coronary arteries, serotonin caused dose-dependent constriction. The vasoconstrictor responses to serotonin were similar in patients with minimal (-26.5 +/- 4.7%) and more advanced atherosclerosis (-30.9 +/- 5.3%). In one patient with coronary artery disease, serotonin caused a temporary coronary occlusion. All other patients dilated in response to isosorbide dinitrate. The vasomotor responses to acetylcholine and to serotonin were thus shown to be completely in parallel.
impairment of endothelium-dependent vasodilation unmasks potent vasoconstrictor responses to serotonin both in early and advanced coronary atherosclerosis. These changes may play an important role in the pathogenesis of a dynamic coronary artery stenosis.
在实验性动脉粥样硬化中，内皮依赖性血管舒张功能受损会导致对血清素（一种由聚集血小板释放的物质）的强力血管收缩反应暴露出来。为了确定在患病的人类冠状动脉中是否会发生类似变化，通过定量冠状动脉造影术评估了16例冠状动脉造影正常的患者、10例轻度（狭窄小于30%）和5例重度（狭窄大于50%）冠状动脉粥样硬化患者对选择性冠状动脉内注入乙酰胆碱和血清素（两者均为内皮依赖性血管舒张剂）以及对硝酸异山梨酯（一种直接作用于平滑肌的舒张剂）的反应。乙酰胆碱在患病冠状动脉中引起收缩，但在冠状动脉造影正常的患者中，它在7例患者中引起扩张（平滑肌扩张者），在9例患者中引起收缩（平滑肌收缩者）。然而，在平滑肌扩张者中，血清素未引起显著变化（+1.4±4.1%），而在平滑肌收缩者和患病冠状动脉患者中，血清素引起剂量依赖性收缩。轻度（-26.5±4.7%）和重度动脉粥样硬化（-30.9±5.3%）患者对血清素的血管收缩反应相似。在1例冠状动脉疾病患者中，血清素导致暂时性冠状动脉闭塞。所有其他患者对硝酸异山梨酯均有扩张反应。因此，对乙酰胆碱和血清素的血管舒缩反应显示完全平行。
内皮依赖性血管舒张功能受损在早期和晚期冠状动脉粥样硬化中均会暴露对血清素的强力血管收缩反应。这些变化可能在动态冠状动脉狭窄的发病机制中起重要作用。
