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为进一步探讨运动性心肌肥大形成的自分泌和旁分泌机制 ,本实验采用放射免疫方法比较了运动性和高血压性肥大心脏心肌局部和血浆多种心源性活性肽变化。与正常对照大鼠相比 ,游泳运动 10周大鼠 ,左心重 /体重(心系数 )提高 2 5 % (P <0 0 1) ,心肌局部血管紧张素Ⅱ (AngiotensinⅡ ,AngⅡ )、内皮素 (endothelin,ET)和心钠素 (atrialna triureticfactor,ANF)含量分别提高 197%、4 4%和 2 3 % (P <0 0 5 ) ,血浆AngⅡ、ET和ANF含量分别提高 4 1%、67%和19% (P <0 0 5 )。与自发性高血压大鼠 (Spontaneouslyhypertensiverat,SHR)相比 ,运动大鼠心肌AngⅡ、ET和ANF分别降低 64 %、84 %和 10 5 % (P <0 0 5 ) ,血浆AngⅡ、ET和ANF分别降低 2 6%、4 5 %和 4 5 % (P <0 0 5 )。结果表明运动肥大心脏心源性活性肽变化特征与高血压肥大心脏不同。这些不同变化是否对运动性心肌肥大调节具有意义值得进一步研究。
In order to further explore the mechanism of autocrine and paracrine formation of exercise-induced cardiac hypertrophy, we used radioimmunoassay to compare the changes of various cardiac-derived active peptides in both local and plasma of exercise- and hypertensive hypertrophic myocardium. Compared with the normal control rats, left ventricular mass index increased by 25% (P <0.01), myocardial angiotensin Ⅱ (AngⅡ) and endothelin endothelin, ET and ANF were increased by 197%, 44% and 23%, respectively (P <0 05), and plasma levels of AngⅡ, ET and ANF were increased by 41% and 67% And 19% (P <0 05) respectively. Compared with spontaneously hypertensive rats (SHR), the levels of AngⅡ, ET and ANF decreased by 64%, 84% and 105% (P <0 05), respectively Decreased by 26%, 45% and 45% (P <0.05). The results show that the characteristics of cardiac hypertrophy in exercise hypertrophy heart are different from hypertensive heart. Whether these different changes have significance for exercise-induced cardiac hypertrophy deserves further study.