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.
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.
Entities:
Keywords:
Carbon monoxide; Electrophysiology; Ion channels; Smoking; Sudden (infant) death
Authors: P J Schwartz; M Stramba-Badiale; A Segantini; P Austoni; G Bosi; R Giorgetti; F Grancini; E D Marni; F Perticone; D Rosti; P Salice Journal: N Engl J Med Date: 1998-06-11 Impact factor: 91.245