Chronic Exposure to Carbon Monoxide and Nicotine: Endothelin ETA Receptor Antagonism Attenuates Carbon Monoxide-Induced Myocardial Hypertrophy in Rat

Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications

“…It has also been claimed that the exposure level of CO at 100 ppm can be harmless if the exposure duration is limited to a few hours . On the other hand, exposing rats for 20 h/day to CO (200 ppm) for 14 consecutive days induced a 21% increase in right ventricular hypertrophy GASOTRANSMITTER ROLE OF CARBON MONOXIDE and a 7% increase in left ventricular hypertrophy (Loennechen et al, 2002). Similar health hazards of CO inhalation have also been reported (Penney and Formolo, 1993;Loennechen et al, 1999).…”

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

“…This occurs independently of loading conditions, since it can also be observed under lowered systolic blood pressure or during ␣1-or ␤1-adrenoreceptor blockade (Loennechen et al, 1999;Mirza et al, 2005;Penney and Formolo, 1993;Penney et al, 1988). The only information available so far regarding the mechanism of CO-induced hypertrophy concerns an increase in endothelin-1 expression after chronic CO exposure (200 ppm; 8.3 × 10 −6 mol L −1 for 2 weeks, Hb CO of 28%) in the rat (Loennechen et al, 2002). Increased endothelin-1 expression in cardiomyocytes is induced by hypoxia (Ito et al, 1996) as well as by hypertrophy (Sakai et al, 1996).…”

“…Increased endothelin-1 expression in cardiomyocytes is induced by hypoxia (Ito et al, 1996) as well as by hypertrophy (Sakai et al, 1996). The blockade of endothelin-1 receptors reduces the right ventricular hypertrophy induced by CO by 60%, with no significant effect on left ventricular hypertrophy or endothelin-1 production (Loennechen et al, 2002). Whether this pathway is involved following exposure to lower chronic CO levels has not been investigated.…”

Carbon Monoxide Urban Air Pollution: Cardiac Effects

“…This pathological hypertrophy of the heart was associated in-vivo with reduced aerobic capacity. In model simulating CO exposure at level found in cigarette smoke (200 ppm for 14 consecutive days), the use of LU135252, a selective inhibitor of type A endothelin (ET-1) receptors (ET A ), in drinking water, markedly prevents right ventricular hypertrophy but not left ventricular, suggesting then a role of ET-1 in the right ventricle and/or in the pulmonary circulation during CO exposure (Loennechen et al, 2002). In another model, closer to urban area pollution, Andre et al reported that 4 weeks of CO exposure at low levels (30-100 ppm 12 hours/day) in healthy rats, promotes heart arrhythmias, even in absence of CO in the environment.…”