Pearson P J, Schaff H V, Vanhoutte P M
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
Circulation. 1990 Jun;81(6):1921-7. doi: 10.1161/01.cir.81.6.1921.
Experiments were designed and performed to determine whether endothelial function remained chronically impaired after coronary artery reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia (60 minutes) followed by reperfusion (12 weeks). Rings (3-4 mm wide) of the reperfused artery and of normal left circumflex (control) coronary artery segments were suspended in organ chambers containing physiological saline solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurement. Endothelium-independent contractions to KCl or prostaglandin F2 alpha and endothelium-independent relaxations to nitric oxide or isoproterenol were comparable in control and chronically reperfused arteries. However, chronically reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to aggregating platelets. In addition, the reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to the platelet-derived compounds adenosine diphosphate, serotonin, and thrombin. However, the endothelium-dependent relaxations to acetylcholine were comparable between control and reperfused arteries. Thus, after 12 weeks of reperfusion, previously occluded coronary arteries exhibited a selective impairment of endothelium-dependent relaxation evoked by aggregating platelets. In vivo, this phenomenon could favor platelet adhesion, aggregation, and platelet-induced contraction of coronary smooth muscle and thus facilitate ischemic events such as vasospasm and coronary thrombosis.
设计并进行了实验，以确定冠状动脉再灌注后内皮功能是否长期受损。将犬左前降支冠状动脉暴露于缺血状态（60分钟），随后进行再灌注（12周）。将再灌注动脉和正常左旋（对照）冠状动脉段的环（宽3 - 4毫米）悬挂在含有生理盐溶液（37摄氏度，用95% O₂ - 5% CO₂ 通气）的器官腔室中进行等长力测量。对照动脉和长期再灌注动脉对氯化钾或前列腺素F2α的内皮非依赖性收缩以及对一氧化氮或异丙肾上腺素的内皮非依赖性舒张相当。然而，长期再灌注的冠状动脉对聚集血小板的内皮依赖性舒张受损。此外，再灌注冠状动脉对血小板衍生化合物二磷酸腺苷、5-羟色胺和凝血酶的内皮依赖性舒张也受损。然而，对照动脉和再灌注动脉对乙酰胆碱的内皮依赖性舒张相当。因此，再灌注12周后，先前闭塞的冠状动脉表现出由聚集血小板引起的内皮依赖性舒张的选择性受损。在体内，这种现象可能有利于血小板黏附、聚集以及血小板诱导的冠状动脉平滑肌收缩，从而促进诸如血管痉挛和冠状动脉血栓形成等缺血事件。
