顿抑心肌的微循环障碍机制研究

目的 :探讨顿抑心肌微循环改变及机制。方法 :制备左前降支冠脉(LAD)阻断不同时间 ( 15和 60min)后再灌注 2h犬心肌顿抑模型 ,在不同观察时间点行静脉心肌声学造影 (MCE) ,计算心肌视频密度峰值(PVI)、MCE曲线上升斜率 (α)和曲线早期下降斜率 ( β) ,分别代表心肌血流灌注量、灌注速度和排空速度。测定相应时间点冠状静脉窦血乳酸浓度。结果 :⑴心肌顿抑早期PVI显著增高 ,1h后恢复至结扎前水平 ;⑵再灌注期顿抑区与正常区PVI比值、α比值、β比值显著高于LAD结扎前 ,随着再灌注时间的延长比值逐渐回降 ;⑶再灌注期冠状静脉窦血乳酸浓度明显增高。结论 :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 ;心肌内微循环短路可能是心肌顿抑微循环障碍的机制。

A Study on the Mechanism of Microcirculatory Dysfunction in Myocardial Stunning

Objective: To research the intramyocardial microcirculatory derangement and its mechanism during myocardial stunning.Method: 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 are 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 are observed in the sham-operated group.Conclusion: The microcirculation of stunned myocardium is hyperdynamic. The anaerobic metabolism of stunned myocardium is enhanced. The intramyocardial microcirculation "short" is a possible mechanism of the microcirculatory dysfunction of stunned myocardium.