Luo G W, Li X G
Zhongguo Yao Li Xue Bao. 1989 Nov;10(6):523-5.
FeSO4 0.1-0.7 mmol/L shortened the action potential duration, decreased the action potential amplitude (APA) and maximal upstroke velocity of 0 phase (Vmax), and reduced the contractile force of myocardium in a concentration-dependent manner. FeSO4 0.2 mmol/L depressed the APA and Vmax of papillary muscles in Tyrode's solution containing MnCl2 3 mmol/L, and reduced the APA, Vmax and duration of slow action potentials in potassium-depolarized papillary muscles. These results suggest that Fe2+ may inhibit the transmembrane movement of Ca2+ and Na+ in myocardial cells. This may be one of the mechanisms of heart failure and circulatory collapse in acute iron poisoning.
0.1 - 0.7毫摩尔/升的硫酸亚铁(FeSO4)以浓度依赖的方式缩短动作电位时程,降低动作电位幅度(APA)和0期最大除极速度(Vmax),并减弱心肌收缩力。0.2毫摩尔/升的硫酸亚铁使含3毫摩尔/升氯化锰(MnCl2)的台氏液中的乳头肌的APA和Vmax降低,并使钾去极化乳头肌的慢动作电位的APA、Vmax和时程缩短。这些结果提示,Fe2+可能抑制心肌细胞中Ca2+和Na+的跨膜运动。这可能是急性铁中毒时心力衰竭和循环衰竭的机制之一。