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 Ca(2+) 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 Ca(2+) 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.