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研究由血液动力病理组织和分子生物学引起的压力超负荷性心肌肥厚的机制，并评价洛沙坦、福辛普利对它的作用。方法：对３０只雄性Ｗｉｓｔａｒ大鼠，经肾动脉分叉上方２～４ｍｍ处分离腹主动脉，平行放置６号钝针头，结扎后拔出针头造成压力超负荷性心肌肥厚模型。术后４周各组经颈总动脉２Ｆ导管直接法测量动脉平均压（ＭＡＰ）和左室舒张末期压（ＬＶＥＤＰ）。结果：（１）血液动力学；与假手术组 ＭＡＰ、ＬＶＥＤＰ比较，术后第４周模型组 ＭＡＰ、ＬＶＥＤＰ显著升高（ｐ＜０．０５）；并与心肌肥厚程度相关（Ｐ＜０．０５）。洛沙坦、福辛普利可降低压力超负荷引起的大鼠ＭＡＰ、ＬＶＥＤＰ增高和ＨＷ／ＢＷ和ＬＶ／ ＢＷ增高（Ｐ＜０．００５）；（３）两者联合未发现进一步的协同效应。结论：洛沙坦、福辛普利能明显改善由腹主动脉狭窄引起的血液动力学改变，并与其减轻压力超负荷性心肌肥厚程度密切相关，两者联合治疗未见有明显协同作用。
To investigate the mechanism of hypertensive cardiac hypertrophy caused by hemodynamic pathology and molecular biology and to evaluate the effects of losartan and fosinopril on it. Methods: Thirty male Wistar rats were divided into 2 to 4 mm above the bifurcation of the renal artery, and the obturator was placed parallel to the 6th obturator needle. After the ligation, the needle was withdrawn to cause the model of pressure overload myocardial hypertrophy. At 4 weeks after operation, mean arterial pressure (MAP) and left ventricular end-diastolic pressure (LVEDP) were measured by direct carotid artery 2F catheter. Results: (1) Hemodynamics; Compared with MAP and LVEDP, the MAP and LVEDP in the model group at 4 weeks after operation were significantly increased (p <0.05), and correlated with the degree of myocardial hypertrophy (P <0. 05). Losartan and fosinopril could reduce the increase of MAP, LVEDP and HW / BW and LV / BW of rats (P <0.005) induced by pressure overload; (3) No further synergistic effect was found . CONCLUSION: Losartan and fosinopril can significantly improve hemodynamic changes caused by abdominal aortic stenosis, which are closely related to the degree of myocardial hypertrophy induced by pressure overload. There is no obvious synergistic effect between them.