Bagrov A Ia, Veveris M M, Ganelina I E, Nikiforova K A, Osipov V L, Rukoiatkina N I, Shtol'ba P
Research Institute of Endocrinology, Prague, Chechoslovakia.
Biull Eksp Biol Med. 1991 Jul;112(7):20-2.
Suggesting endogenous digoxin-like factor (EDLF) to display arrhythmogenic activities in myocardial ischemia (MI), we studied the effect of anti-digoxin antiserum (ADS) on the ventricular fibrillation threshold (VFT) after the coronary ligation in cats and ventricular arrhythmias caused by MI in rats and chloroform-induced hypoxia in mice. Intravenous administration of ADS (5 mg/kg) enhanced VFT in cats with MI from 11.3 +/- 1.6 to 53.3 +/- 8.1 V (M +/- m; p less than 0.01) and significantly reduced ventricular arrhythmias in rats and mice. Our experiments on the isolated electro-stimulated rat atria demonstrated that EDLF is likely not to be an adrenergic cotransmitter in the heart. Possible mechanisms of the arrhythmogenic action of EDLF are discussed.
鉴于内源性洋地黄样因子(EDLF)在心肌缺血(MI)中显示出致心律失常活性,我们研究了抗地高辛抗血清(ADS)对猫冠状动脉结扎后心室颤动阈值(VFT)以及对大鼠MI和小鼠氯仿诱导的缺氧所引起的室性心律失常的影响。静脉注射ADS(5mg/kg)可使MI猫的VFT从11.3±1.6V提高到53.3±8.1V(均值±标准误;p<0.01),并显著减少大鼠和小鼠的室性心律失常。我们在离体电刺激大鼠心房上进行的实验表明,EDLF可能不是心脏中的肾上腺素能共递质。文中讨论了EDLF致心律失常作用的可能机制。