Dignan R J, Dyke C M, Abd-Elfattah A S, Lutz H A, Yeh T, Lee K F, Parmar J, Wechsler A S
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
Ann Thorac Surg. 1992 Feb;53(2):311-7. doi: 10.1016/0003-4975(92)91339-b.
We hypothesized that coronary artery endothelial cell function and smooth muscle function are modified by global myocardial ischemia and used bradykinin-induced secretion of endothelium-derived relaxing factor as a marker of endothelial cell function. Bradykinin and sodium nitroprusside together determined maximum smooth muscle relaxation. Potassium chloride-induced contraction determined smooth muscle contractility. Endothelium-mediated smooth muscle relaxation expressed as a ratio of total coronary smooth muscle relaxation before and after ischemia quantified endothelial cell function. The effect of global normothermic ischemia on in situ coronary arteries from 7 swine hearts was studied. Coronary arterial rings taken from 0 to 220 minutes of ischemia at 20-minute intervals were studied in vitro. The data revealed unexpected tolerance of endothelium-mediated relaxation to ischemia. Endothelium-derived relaxing factor function was maintained to 160 minutes and smooth muscle function, to 120 minutes of ischemia. Coronary artery dysfunction seen in other studies after less ischemia may be the result of injury introduced during reperfusion, may be the consequence of myocardial injury, or may be due to events operative at the level of small arterioles.
我们推测，整体心肌缺血会改变冠状动脉内皮细胞功能和平滑肌功能，并将缓激肽诱导的内皮源性舒张因子分泌作为内皮细胞功能的标志物。缓激肽和硝普钠共同决定最大平滑肌舒张。氯化钾诱导的收缩决定平滑肌收缩性。以缺血前后总冠状动脉平滑肌舒张的比率表示的内皮介导的平滑肌舒张量化了内皮细胞功能。研究了整体常温缺血对7个猪心脏原位冠状动脉的影响。对每隔20分钟从缺血0至220分钟取出的冠状动脉环进行体外研究。数据显示内皮介导的舒张对缺血具有意外的耐受性。内皮源性舒张因子功能在缺血160分钟时仍维持，平滑肌功能在缺血120分钟时仍维持。在其他研究中，缺血时间较短后出现的冠状动脉功能障碍可能是再灌注期间引入损伤的结果，可能是心肌损伤的后果，或者可能是小动脉水平上发生的事件所致。
