实验性顿抑心肌的微循环障碍

The Microcirculatory Dysfunction in Experimental Myocardial Stunning

为了探讨顿抑心肌微循环改变及机制 ,制备左前降支冠状动脉不同阻断时间 (15min和 6 0min)后再灌注犬心肌顿抑模型 ,在不同观察时间点静脉注射含全氟丙烷声振白蛋白微泡造影剂 ,采用二次谐波成像和间歇发射技术行心肌声学造影 ,计算心肌声学造影图像上心肌视频密度峰值、心肌声学造影曲线上升斜率和曲线早期下降斜率 ,测定相应时间点冠状静脉窦血乳酸浓度。结果发现 ,心肌顿抑早期心肌视频密度峰值显著增高 ,1h后恢复至结扎前水平 ;再灌注期顿抑区与正常区视频密度峰值比值、心肌声学造影曲线上升斜率比值、心肌声学造影曲线早期下降斜率比值显著高于左前降支冠状动脉结扎前 ,随着再灌注时间的延长比值逐渐回降 ;再灌注期冠状静脉窦血乳酸浓度明显增高。以上结果提示 ,心肌顿抑早期心肌微循环处于“高动力”状态 ,血流灌注增加与排空加快并存 ;顿抑心肌缺氧代谢加强 ;

Aim To research the intramyocardial microcirculatory derangement and its mechanism during myocardial stunning. Methods Twelve dogs underwent 15 or 60 min left anterior descending coronary artery (LAD)occlusion, followed by 120 min reperfusion. Another six dogs underwent sham operation. Myocardial contrast echocardiography (MCE) was performed intravenously using C3F8 exposed sonicated dextrose albumin and blood samples were taken from coronary venous sinus at different time points. Electrocardiogram gated end systolic images in short axis were acquired in harmonic mode and digitized on line. Background subtracted peak videointensity(PVI), ascending slop(α) and early descending slop(β) of MCE curve in stunned and normal myocardium areas were measured from MCE. The ratios of PVI, α, and β between stunned and normal myocardium areas were calculated. Results A marked increase in PVI occurred in all dogs with stunned myocardium in the early period of reperfusion and the PVI restored to the pre occlusion level after 60 min of reperfusion. The ratios of PVI, α, and β in the early period of reperfusion were significantly higher than the pre occlusion levels, and gradually restored toward their pre occlusion levels. Plasma lactic acid concentrations significantly increased in the early period of reperfusion, and restored to the pre occlusion levels by 120 min after reperfusion in the 15 min LAD occlusion group, but not in the 60 min group. No changes in PVI, three rations, and plasma lactic acid levels during the experiment were observed in the sham operated group. Conclusions The microcirculation of stunned myocardium is hyperdynamic. The anaerobic metabolism of stunned myocardium enhances. The intramyocardial microcirculation 'short' is a possible mechanism of the microcirculatory dysfunction of stunned myocardium.