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目的研究中药复方潜阳合剂对腹主动脉缩窄致高血压左室肥厚的影响,并探讨其作用机制。方法使用腹主动脉缩窄致高血压左室肥厚模型,Wistar大鼠随机分成假手术组和模型组,将高血压造模成功的大鼠随机分成模型组、培哚普利组和潜阳合剂组,每组10只,并开始灌胃,各组药物干预8周。使用心脏超声评价左室肥厚水平,尾动脉仪测量大鼠左前肢血压,天狼猩红染色观察心肌胶原含量,免疫组化法测定心肌组织Ⅰ型、Ⅲ型胶原纤维的含量。结果腹主动脉缩窄后12周,与假手术组相比,模型组血压升高,左室后壁及室间隔厚度增厚(P<0.001),左室舒张末内径和收缩末内径缩小(P<0.001);与模型组相比,培哚普利组和潜阳合剂组血压降低,左室后壁和室间隔厚度降低(P<0.001),舒张末内径(P<0.001)和收缩末内径(P<0.05)改善;与模型组相比,培哚普利组、潜阳合剂组大鼠心肌组织胶原较少,Ⅰ型和Ⅲ型胶原纤维表达减少。结论潜阳合剂可以改善腹主动脉缩窄致高血压大鼠的左室肥厚,其机制与降压、抑制心肌胶原纤维增生相关。
Objective To study the effect of Chinese herb compound Qiangyang mixture on left ventricular hypertrophy induced by narrowing abdominal aorta and to explore its mechanism. Methods Hypertensive left ventricular hypertrophy model was induced by abdominal aortic constriction. Wistar rats were randomly divided into sham-operation group and model group. Rats with successful hypertension were randomly divided into model group, perindopril group, Group, 10 in each group, and began gavage, each group of drug intervention for 8 weeks. Left ventricular hypertrophy was assessed by echocardiography, left ventricular blood pressure was measured by caudal artery instrumentation, myocardial collagen content was measured by Sirius red staining, and type I and type III collagen fibers were detected by immunohistochemistry. Results After 12 weeks of abdominal aortic constriction, compared with the sham operation group, the blood pressure of the model group was increased, the thickness of the left ventricular posterior wall and interventricular septum thicker (P <0.001), and the diameter of left ventricular end-diastolic and end-systolic diameter reduced P <0.001) .Compared with the model group, the blood pressure, the thickness of the left ventricular posterior wall and the interventricular septum decreased (P <0.001), the end diastolic diameter (P <0.001) and the end-systolic diameter (P <0.05). Compared with the model group, the collagen of myocardium in perindopril group and QianYang Mixture group was less and the expression of type Ⅰ and Ⅲ collagens decreased. Conclusion Qianneng mixture can improve left ventricular hypertrophy in hypertensive rats induced by abdominal aorta constriction. Its mechanism is related to antihypertensive treatment and inhibition of myocardial collagen fibrosis.