急性兔肺动脉栓塞时心肌标志物和心肌损伤的变化及意义

Significance of myocardium marker and myocardial damage in a rabbit model with embolization of pulmonary lobar artery

目的:制备高危、低危兔急性肺血栓栓塞症(APTE)模型,探讨高危、低危肺栓塞兔的血流动力学、心肌标志物和心肌损伤的变化及意义。方法:24只新西兰大耳白兔随机分为对照组、肺血栓栓塞低危组、高危组3组,每组8只。采用自体血栓回输法建立动物模型。常规取造模前、造模后1、2、4、8h行动脉血气分析、肌钙蛋白I(cTnI)及N端前脑钠肽(NT-proBNP)的测定和血流动力学监测,12h时处死家兔,取肺组织和右室心肌行病理切片。结果:①血流动力学:高危组栓塞即刻有平均动脉压(MAP)下降及右室收缩压(RSVP)升高,4h后MAP和RSVP值开始恢复,高危组栓塞后与对照组有显著性差异(P<0.01);②ELISA监测结果:高危组2h后NT-proBNP开始升高,4h后cTnI开始升高,8h时各值继续升高,且4、8h与对照组有显著性差异(P<0.01);③病理检查显示:高危栓塞组兔肺组织和右室心肌病理损伤明显,可见炎性细胞的浸润,同时可见心肌细胞的空泡样变性坏死。结论:急性肺栓塞cTnI、NT-proBNP的变化及血流动力学改变与右室心肌的受累程度有关,临床上可通过监测cTnI、NT-proBNP来对肺动脉栓塞患者进行危险分层,同时在治疗时,应加强对高危肺栓塞患者心肌的保护。

Objective：To study effects of different durations of thromboembolism on hemodynamics,pulmonary arteriography and fight ventricle myocardial pathology in a rabbit model with embolization of pulmonary lobar artery. Methods：Twenty four rabbits were randomly divided into control group, mild pulmonary thromboembolism （PE） model group and severe PE model group,with 8 rabbits each. PE was induced by infusing autoiogous blood clots （fight jugular vein）. Arterial blood gas were analyzed and the plasma＇s concentrations of cTnl and NT-proBNP were examined by ELISA before and 1 h,2 h,4 h,8 h after injection,and the hemodynamic monitoring was used by homemade catheter with multi-channel physiological recorder. The pathological changes of the lung and right ventricle myocardium were examined with light microscope at 12 h after injection. Resuits：（1） hemodynamic monitoring showed that RV systolic pressures （RVSP）increased and MAP declined significantly in the severe PE model group,then gradually return to normal after 4 h. There were obviously differences between the severe PE model group and control group （P 〈 0.01） and no differences between the mild PE model group and control group（P 〉 0.05） ;（2）ELISA showed that NT-proBNP in the severe PE model group increased at 2 h,peaked at 8 h compared to those in the control group and the mild PE model group（P 〈 0.01）. cTnI in severe PE model increased at 4 h,peaked at 8 h,but no obuious changes in control group and mild PE group; （3） Histopathological study showed that injury of right ventricle myocardium and lung were obvious in severe PE model group with inflammatory cell infilitration, and also show there was vacuolar degeneration of right ventricle myocardiu in severe PE model group,but was less in mild PE model group. Conclusion：The change of cTnI,NT-proBNP and hemodynamic prove that severe PE results right ventricle dysfunction. We can use cTnI,NT-proBNP as facilitate triage of PE, and should pay attention to injury of right ventricle myocardium and RV dysfunction in clinic.