Perinatal left ventricular performance in fetal sheep: interaction between oxygen ventilation and contractility

Left ventricular (LV) output nearly triples at birth, in association with increases in serum catecholamines. Similar increases in catecholamines in utero, however, do not increase output. We hypothesized that catecholamines increase contractility in utero, but that output cannot increase until LV loading conditions are changed by oxygen ventilation. To address this hypothesis, we studied nine fetal sheep acutely placed in a warm water bath (40 degrees C). Conductance and manometric catheters were placed in the LV to generate pressure-volume loops during caval occlusion in the nonventilated and oxygen-ventilated states, each under control, dobutamine, and propranolol conditions. Contractility was estimated by the end-systolic pressure-volume relationship, preload by end-diastolic volume, and afterload by arterial elastance. Oxygen ventilation increased LV output 1.4-fold, despite a decrease in contractility to about three-fourths of the nonventilated value. Heart rate remained constant, whereas preload increased and afterload decreased significantly. During oxygen ventilation, dobutamine increased output to 2.3 times the control, nonventilated value, associated with increases in contractility and heart rate and no change in preload and afterload. Although dobutamine increased contractility and heart rate similarly in the nonventilated and oxygen ventilated states, output increased significantly more during ventilation. Similarly, propranolol decreased contractility and heart rate equally in both states, but output decreased far more during ventilation. Thus, oxygen ventilation is associated with advantageous changes in LV load such that the positive inotropic and chronotropic effects of dobutamine are translated into greater increases in LV output.