Stahl L D, Aversano T, Ambrosio G, Becker L C
J Am Coll Cardiol. 1987 Jun;9(6):1339-47. doi: 10.1016/s0735-1097(87)80475-8.
Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
顿抑心肌可由反复短暂的缺血发作产生。在缺血发作后不久,心肌中便已观察到组织化学和超微结构异常,如肌节延长和肌纤维变细,这些异常被认为是心室收缩期发生的机械性拉伸所致。为了测试单纯的机械力是否能产生顿抑心肌中所见的残余功能障碍,通过向开胸犬冠状动脉内重复六次输注氯化钾(0.2 mEq/分钟,持续2.5分钟)或利多卡因(10 mg推注,随后1至3 mg/分钟,持续5分钟)来诱导局部运动障碍。这些犬与分别经历六次持续2.5分钟和5分钟的冠状动脉反复闭塞的犬进行匹配。使用收缩期缩短分数和与负荷无关的收缩末期压力-长度关系来分析局部功能。氯化钾和利多卡因均产生了与冠状动脉闭塞所产生的运动障碍相似的局部运动障碍。尽管冠状动脉反复闭塞后的局部心室功能仍显著降低,但在最后一次药物诱导的运动障碍后5分钟内,功能完全恢复正常。总之,氯化钾和利多卡因所产生的局部功能障碍不会产生残余功能障碍,尽管收缩期的机械力与冠状动脉闭塞时所见的相似。