摘要
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。
Objechve: To investigate the mechanism of the pressure over-loaded myocardium hypertrophy from hemo- dynamic histopathology and molecular biology, and evaluate the reversal effects of losartan, fosinpril, RAS blockade, on it. Methods: (1)The male Wistar rats, weighing 200(20g, a blunted 6 gauge needle was placed adjacent to abdominal aorta proximal to renal arterie's bifurcation, a ligature was made, then the needle was withdrawn. (2)All rats were divided into 5 groups. (3) Hemodynamic studies were carried out in each group by use of a 2 F catheter 4 weeks after operation. Rasults: Contrast to the sham-operated group, the MAP and LVEDP of the vehicle pop were elevated significantly (P<0 .05). However, contrast to the vehicle group, that of the losartan group, the fosinopril group and combined group were lower significantly (p< 0. 05 ). Conclusion: Losartan, fosinopril are effective in myocardiac hypertrophy reversal partly by limiting the increase of MAP and LVEDP in aortic-banded rats.
出处
《湖北民族学院学报（医学版）》
2000年第3期1-3,共3页
Journal of Hubei Minzu University(Medical Edition)
基金
上海第二医科大学博士点建设基金
