一氧化氮在压力超负荷心肌肥大作用中的定量分析

目的：探讨一气化氮（NO）在压力超负荷心肌肥大反应过程中的作用。方法：建立腹主动脉缩窄性高血压大鼠模型，测定平均动脉压（MAP）和左心室／体重比值（LVW／BW）；测量大鼠心肌的体积密度（Vv）、表面积密度（Sv）、比表面（S／V）及平均自由程（λ）等。结果：高血压大鼠的MAP、LVW／Bw、心肌横断面积、平均直径、Vv、Sv明显增大、入显著减小；加L-Arg组的MAP、LVW／BW值大致恢复至正常水平，心肌横断面积及平均直径、Vv、Sv等明显小于高血压组，S／V及入则增大；加L-NAME组的MAP、LVW／BW、心肌横断面积及平均直径、Vv、Sv等持续加大，而S／V及入则变小。结论：NO可明显改变体视学各项参数，对压力超负荷引起的高血压和心肌肥大具有明显的抑制作用。

Quantitative analysis on role of NO in myocardial hypertrophy caused by pressure overload in rats

Objective: To study the role of nitric oxide(NO) in myocardial hypertrophy caused by pressure overload in rats.Methods: The coarctation of the abdominal aorta(COA) hypertension model was established in rats.The mean arterial pressure(MAP) and the left ventricular weight to body weight(LVW/BW) were measured in each rat;the stereological parameters including the myocardial volume density,the myocardial surface density,the myocardial specific surface and the mean free path were measured.Results: COA rats had significant increase in MAP and LVW/BW,and increase in myocardial transverse area and average diameter.There was significant difference between control group and experimental group in the volume density,the surface density,and the mean free path.The COA+L-arginine(L-Arg) rats restored their normal level of MAP and LVW/BW,which were remarkable smaller than COA group in and the myocardial transverse area, the average diameter,the volume density and the surface density in which were remarkable smaller than those of COA group,but the specific surface and the mean free path increased.In the COA+N~G-nitro-arginine methylester(L-NAME) rats,more and more increased the data in MAP,LVW/BW,the myocardial transverse area,the average diameter,the volume density,and the surface density,but decreased in the specific surface and the mean free path.Conclusion: NO can inhibit the hypertension and the myocardial hypertrophy caused by overloaded pressure.