Sun L
Zhonghua Yi Xue Za Zhi. 1990 Nov;70(11):621-3, 44.
The present study was carried out on intact heart of rat to determine the myocardial toxicity of moniliformin (MLFN) in vitro and in vivo Perfusion of MLFN 0.1 mumol/L in isolated heart decreased myocardial contractile force by 52 +/- 17%, and the effect was not reversible after the infusion of MLFN had stopped. The intravenous LD50 of MLFN in mice was found to be 17.51 +/- 1.64 mg/kg. Intravenous injection of MLFN at 1/4 LD50 markedly inhibited cardiac hemodynamic variables relative to myocardial contractile function. Particularly, it decreased left ventricular pressure development (dP/dt max) by 52 +/- 6%, and induced ventricular arrhythmia. The results showed that MLFN severely damaged the heart function of healthy rats.
本研究在大鼠完整心脏上进行,以确定串珠镰刀菌素(MLFN)在体外和体内的心肌毒性。在离体心脏中灌注0.1μmol/L的MLFN可使心肌收缩力降低52±17%,且在停止灌注MLFN后该作用不可逆转。发现MLFN在小鼠中的静脉注射半数致死量(LD50)为17.51±1.64mg/kg。静脉注射1/4 LD50的MLFN相对于心肌收缩功能显著抑制心脏血流动力学变量。特别是,它使左心室压力上升速率(dP/dt max)降低52±6%,并诱发室性心律失常。结果表明,MLFN严重损害了健康大鼠的心脏功能。