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本实验观察外源性 ATP 对正常和缺氧状态下豚鼠心室乳头肌跨膜电位和收缩功能的影响。在正常供氧组,ATP 对动作电位的0期去极化幅度、时程(APD_(10)、APD_(50)、APD_(80))、复极2期与3期斜率均无明显变化(P>0.05)、而收缩幅度在加入10~(-4)M ATP 后1～2分钟内有短暂减弱(P<0.01).缺氧使心室肌细胞动作电位时程(APD_(10)、APD_(50)、APD_(80))缩短和复极2期斜率增大,加入10~(-4)M ATP 能阻止上述变化进一步发展.10~(-4)M ATP 也能减慢缺氧心室肌收缩减弱的进展速度。上述结果提示,外源性 ATP 对缺氧心肌的膜电位与收缩机能具有一定的保护作用。
This experiment observed exogenous ATP on normal and hypoxia guinea pig ventricular papillary muscle transmembrane potential and contractile function. In the normal oxygen supply group, there was no significant change in the 0 phase depolarization amplitude, duration (APD_ (10), APD_ (50), APD_ (80) (P <0.05), and the amplitude of contraction shorted within 1 ~ 2 minutes after the addition of 10 ~ (-4) M ATP (P <0.01) (50), APD 80) and the slope of repolarization phase 2 increased, and the addition of 10 -4 M ATP could prevent further development of the above changes.10 ~ (-4) M ATP also slowed down the hypoxic ventricular Muscle contraction slowed down the pace of progress. The above results suggest that exogenous ATP has a protective effect on the membrane potential and contractile function of hypoxic myocardium.