急性压力超负荷致心肌肥大过程中心肌内分泌因子活化及相互作用

Activation and interaction of myocardial endocrine factors during pressure over-load-induced cardiac hypertrophy

目的 探讨急性压力超负荷致大鼠心肌肥大过程中心肌内分泌活化及相互间的作用。方法 放免法、比色法及免疫组织化学检测腹主动脉缩窄高血压大鼠心肌组织中血管紧张素Ⅱ、碱性成纤维细胞生长因子 (bFGF)蛋白表达及一氧化氮含量的变化 ,并观察卡托普利对它们的作用。结果 腹主动脉缩窄大鼠动脉血压逐渐升高 ,术后 4h即显著升高 ;术后 30min心肌组织中血管紧张素Ⅱ含量显著升高 ,此后并保持在高水平 ;心肌bFGF蛋白表达于术后 4h开始升高并于第 10天达高峰后逐渐恢复至正常水平 ;心肌中一氧化氮含量却于术后 10min迅速显著降低并持续受抑。小剂量卡托普利对大鼠血压无明显影响 ,但可完全抑制心肌中血管紧张素Ⅱ的升高 ,而且使bFGF活化滞后、一氧化氮含量降低减轻。结论 压力超负荷可诱导心肌血管紧张素Ⅱ、bFGF含量升高及一氧化氮含量降低 ,而血管紧张素Ⅱ可加速bFGF活化、加速一氧化氮含量的降低。

Objective To determine whether the endocrine would be activated by pressure overload in rat induced by abdominal aorta constriction and the interaction between endocrine factors. Methods By radioimmunoassay and colorimetry we determined the changes of the content of myocardial angiotensin Ⅱ,bFGF protein expression and nitric oxide in rats after pressure overload and those after treated with captopril,then analyzed the relationship between the changes and pressure over load.Results The concentration of myocardial angiotensin Ⅱ increased significantly at 30 min after pressure overload,and then was kept in high level. The myocardial bFGF protein expression elevated markedly at 4h after operation,reached the peak during 5d to 10d,and then felt to control levels.Whereas,the concentration of myocardial nitric oxide decreased rapidly at 30 minutes after operation,and was kept in low level.the blood pressure was not reduced and the effects of pressure overload,such as elevation of angiotensin Ⅱ was inhibited completely,rise of bFGF protein expression was alleviated by pretreatment with low dose of captopril.Conclusion The elevation of myocardial angiotensin Ⅱ and bFGF protein expression and the decrease of myocardial nitric oxide could be induced by pressure overload,moreover the elevation of bFGF protein expression and decrease of nitric oxide could be accelerated and aggravated by angiotensin Ⅱ.