Shymans'ka T V, Hoshovs'ka Iu V, Sahach V F
Fiziol Zh (1994). 2010;56(5):3-12.
Intensive constitutive production of nitric oxide (NO) during physical training improves vasodilatation and heart function. However, it remains unclear how NO takes part in myocardial adaptation to workload, which is accompanied by an increased heart inflow and intracellular calcium content. Using isolated rat heart by Langendorf preparation, we studied myocardial response to gradually increased left ventricular volume (Frank-Starling low) and increasing concentration of Ca2+ in the perfusion solution (from 1.7 mM to 12.5 mM) in trained and untrained rats. It was shown that 4 weeks swimming course improved heart function: heart rate was decreased; contractile activity (dP/dt max) and coronary flow were increased by 20% and 33%, respectively. Equal volume stretching of balloon in left ventricle provoked greater contraction in trained comparing to untrained hearts, demonstrating extended functional reserves after swimming course. Mitochondrial membrane potential was significantly increased in hearts of trained rats. Furthermore, training prevented fast increase of the end diastolic pressure during calcium upload. Mitochondrial factor release due to opening of mitochondrial permeability transition pore (MPTP) in trained hearts was detected at higher concentrations of calcium that reveals extended calcium capacity of mitochondria and lesser sensitivity of MPTP to its inductor-calcium. Blockade of NO synthesis with L-NAME application of (10(-4) M for 15 min) abolished reaction of trained heart during Frank-Starling and calcium upload. Thus, heart adaptation to physical training and extension of functional reserves in heart are provided by endogenous NO production. Key words: nitric oxide, Frank-Starling low, physical training, calcium upload, mitochondrial permeability transition, membrane potential.
体育锻炼期间一氧化氮（NO）的持续性大量生成可改善血管舒张和心脏功能。然而，NO如何参与心肌对负荷的适应性变化仍不清楚，这种适应性变化伴随着心脏流入量增加和细胞内钙含量升高。我们采用Langendorf灌流法制备离体大鼠心脏，研究了训练和未训练大鼠心肌对逐渐增加的左心室容量（Frank-Starling定律）以及灌流液中Ca2+浓度升高（从1.7 mM至12.5 mM）的反应。结果显示，为期4周的游泳训练改善了心脏功能：心率降低；收缩活性（dP/dt max）和冠状动脉血流量分别增加了20%和33%。与未训练的心脏相比，在训练后的心脏中，左心室内等容球囊扩张引发了更强的收缩反应，表明游泳训练后心脏功能储备增加。训练大鼠心脏的线粒体膜电位显著升高。此外，训练可防止钙负荷增加期间舒张末期压力的快速升高。在较高钙浓度下检测到训练后心脏中由于线粒体通透性转换孔（MPTP）开放而导致的线粒体因子释放，这表明线粒体的钙容量增加，且MPTP对其诱导剂钙的敏感性降低。应用L-NAME（10(-4) M，15分钟）阻断NO合成可消除训练后心脏在Frank-Starling定律和钙负荷过程中的反应。因此，内源性NO生成可使心脏适应体育锻炼并增加心脏功能储备。关键词：一氧化氮；Frank-Starling定律；体育锻炼；钙负荷；线粒体通透性转换；膜电位
