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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 prepare a model of acute pulmonary embolism (APTE) in rabbits with high-risk and low-risk and to investigate the changes and significance of hemodynamics, myocardial markers and myocardial injury in high-risk and low-risk pulmonary embolism rabbits. Methods: Twenty-four New Zealand white rabbits were randomly divided into control group, low-risk group of pulmonary thromboembolism and high-risk group of 3, with 8 in each group. Animal models were established by autologous thrombosis. Conventional arteries were taken before modeling, arterial blood gas analysis at 1, 2, 4, and 8 h after modeling, cTnI and NT-proBNP determination and hemodynamic monitoring, 12h When rabbits were sacrificed, pathological sections of lung tissue and right ventricular myocardium were taken. Results: ① Hemodynamics: Immediate reduction of mean arterial pressure (MAP) and right ventricular systolic pressure (RSVP) immediately after thromboembolism in high-risk group began to recover after 4 h, while those in high-risk group were significantly higher than those in control group (P <0.01). ②The results of ELISA showed that NT-proBNP began to increase after 2h in high-risk group, cTnI began to increase after 4h, and continued to increase at 8h, and there was significant difference between 4h and 8h <0.01) .③Pathological examination showed that the pathological changes of lung tissue and right ventricular myocardium in high-risk embolism group were obvious, infiltration of inflammatory cells was observed, and vacuolar degeneration and necrosis of cardiomyocytes were seen at the same time. CONCLUSION: The changes of cTnI and NT-proBNP in acute pulmonary embolism and the changes of hemodynamics are related to the extent of right ventricular myocardial involvement. Clinically, cTnI and NT-proBNP can be used to risk stratify patients with pulmonary embolism. At the same time, , Should strengthen the protection of myocardium in patients with high risk of pulmonary embolism.