Prenatal exposure to carbon monoxide temporarily impairs maturation of rat cardiomyocytes: Electrophysiological evidence

Background: Maternal smoking is an independent risk factor for sudden infant death syndrome. Carbon monoxide (CO) is a major component of cigarette smoke. No information is available concerning the effect of CO and/or smoking on postnatal maturation of the heart. Objectives: To investigate the effect of prenatal exposure to CO on cellular electrophysiological maturation in male Wistar rats. Methods: The patch-clamp technique was used to measure the action potential and ionic currents (transient outward current and long-lasting type Ca²⁺ current) from rat ventricular myocytes. Results: During growth, action potential duration (APD) measurements at -20 mV and -50 mV (APD_-20 and APD_-50) progressively decreased in both groups. APD was significantly delayed in rats prenatally exposed to 150 parts per million CO: at four weeks APD_-20 and APD_-50 were 90 ms and 148 ms, respectively, in CO-exposed rats (n= 13), and 36 ms and 78 ms, respectively, in control rats (n= 14; P<0.01 and P<0.05, respectively); this normalized at eight weeks. After four weeks, the density of long-lasting type Ca²⁺ current increased by 34% and the density of transient outward current decreased by 37% in CO-exposed versus control rats; this normalized at eight weeks. Conclusions: Prenatal CO exposure affects the physiological shortening of APD in neonatal rats. It is speculated that prolonged myocyte repolarization induced by prenatal exposure to smoke may establish a period of vulnerability for life-threatening arrhythmias during infancy.