Kuhn F E, Gillis R A, Virmani R, Visner M S, Schaer G L
Division of Cardiology, Georgetown University Medical Center, Washington, DC.
Chest. 1992 Aug;102(2):581-5. doi: 10.1378/chest.102.2.581.
Studies have demonstrated that cocaine causes coronary vasoconstriction, but this has been unassociated with myocardial ischemia. Therefore, cocaine seems unlikely to precipitate myocardial infarction in the absence of potentiating factors. We hypothesized that injury to coronary endothelium could potentiate cocaine-induced coronary vasoconstriction by decreasing EDRF. The effect of cocaine on LAD diameter was measured in dogs subjected to coronary endothelial denudation and compared with that in a non-denuded control group. Endothelial denudation was accomplished by abrasion with an inflated angioplasty balloon and confirmed in vivo by demonstrating a vasoconstrictive response to infused acetylcholine and by postmortem scanning electron microscopy. Cocaine produced a similar maximal reduction in LAD diameter in both groups. Thus, cocaine induces endothelium-independent coronary artery vasoconstriction. Failure of endothelial injury to potentiate the coronary vasoconstrictive effect by cocaine suggests that factors other than endothelial dysfunction may be important in pathogenesis of cocaine-associated myocardial infarction.
研究表明，可卡因会导致冠状动脉血管收缩，但这与心肌缺血并无关联。因此，在没有增强因素的情况下，可卡因似乎不太可能引发心肌梗死。我们推测，冠状动脉内皮损伤可能通过降低内皮舒张因子（EDRF）来增强可卡因诱导的冠状动脉血管收缩。在接受冠状动脉内皮剥脱的犬类中测量可卡因对左前降支（LAD）直径的影响，并与未剥脱的对照组进行比较。通过用充气的血管成形术球囊进行磨损来完成内皮剥脱，并通过证明对注入乙酰胆碱的血管收缩反应以及死后扫描电子显微镜在体内进行确认。两组中可卡因使LAD直径产生的最大缩小程度相似。因此，可卡因诱导不依赖内皮的冠状动脉血管收缩。内皮损伤未能增强可卡因的冠状动脉血管收缩作用，这表明除内皮功能障碍之外的其他因素可能在可卡因相关性心肌梗死的发病机制中起重要作用。
