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Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO2) may have beneficial effects on the pulmonary circulation. We tested the hypothesis that exposure to CO2 would protect against chronic pulnlonary hypertension in newborn rats. Atmospheric CO2 was maintained at <0.5% (normocapnia), 5.5%, or 10% during exposure from birth for 14 days to normoxia (21% O2) or moderate hypoxia (13% O2). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries, and distal arterial muscularization. Exposure to 10% CO2 (but not to 5.5% CO2) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals (P < 0.05), whereas both concentrations of CO2 normalized right ventricular performance. Exposure to 10% CO2 attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO2 on the lung and consequent modulating effects on the endothelin pathway. [ABSTRACT FROM AUTHOR]

Summary: Most laboratory studies of cardiac arrest use models of ventricular fibrillation, but in the emergency room, operating room or intensive care unit, cardiac arrest frequently results from asphyxia. We sought to investigate the effect of different durations of asystole secondary to asphyxia on myocardial function after resuscitation. In a laboratory based experimental series, anaesthetized rats received either 4 or 8min of asphyxial cardiac arrest, and following standardized resuscitation, serial transthoracic echocardiography was performed. Severe depression of left ventricular fractional shortening occurred in both groups with partial recovery only in the 4-min arrest group, while left ventricular end-diastolic diameter was increased in the 4-min group. The pH, HCO3 − and SBE were reduced in both groups after resuscitation, but the degree of acidosis was greater in the 8-min group. In this model, transthoracic echocardiography demonstrated both systolic and diastolic impairment following asphyxial cardiac arrest, and a clear dose–effect relationship between duration of asphyxia and degree of impairment. A shorter duration of asphyxia was associated with a lesser increase in left ventricular end-diastolic dimension, compared with more protracted asphyxia; the shorter arrest was associated with better recovery of contractile function and acidosis. Increased duration of asphyxia causes increased systolic and diastolic dysfunction. These findings may have significant implications for resuscitative therapeutics. ECHO assessment may permit specific targeting of therapy directed towards systolic or diastolic function during CPR. [Copyright &y& Elsevier]