Wauthy, Pierre, Alberto Pagnamenta, Fabio Vassalli, Robert Naeije, and Serge Brimioulle. Right ventricular adaptation to pulmonary hypertension: an interspecies comparison. Am J Physiol Heart Circ Physiol 286: H1441-H1447, 2004. First published December 18, 2003 10.1152/ajpheart.00640.2003 adaptation is an important prognostic factor in acute and chronic pulmonary hypertension. Pulmonary vascular basal tone and hypoxic reactivity are known to vary widely between species. We investigated how RV adaptation to acute pulmonary hypertension is preserved in species with low, intermediate, and high pulmonary vascular resistance and reactivity. Acute pulmonary hypertension was induced by hypoxia, distal embolism, and proximal constriction in anesthetized dogs (n ϭ 10), goats (n ϭ 8), and pigs (n ϭ 8). Pulmonary vessels were assessed by flow-pressure curves and by impedance to quantify distal resistance, proximal elastance, and wave reflections. RV function was assessed by pressure-volume curves to quantify afterload, contractility, and ventricular-arterial coupling efficiency. First, hypoxia was associated with a progressive increase of resistance, elastance, and wave reflection from dogs to goats and from goats to pigs. RV contractility increased proportionally to RV afterload, and optimal coupling was preserved in all species. Second, embolism increased resistance and wave reflection but not elastance. The increase in RV contractility matched the increase in RV afterload and optimal coupling was preserved. Finally, proximal pulmonary artery constriction increased resistance, increased and accelerated wave reflection, and markedly increased elastance. RV contractility increased markedly and coupling showed a nonsignificant trend to decrease. We conclude that optimal or near-optimal ventricular-arterial coupling is maintained in acute pulmonary hypertension, whether in absence or presence of chronic species-induced pulmonary hypertension. heart failure; contractility; ventricular-arterial coupling IN CLINICAL PRACTICE, the diagnosis of pulmonary arterial hypertension relies on measurements of pulmonary vascular pressures and cardiac output and calculations of pulmonary vascular resistance (31). These hemodynamic measurements are of prognostic value, with survival being related to cardiac output rather than to pulmonary artery pressure (P PA ) (8,24,33). The clinical state of patients with pulmonary arterial hypertension also appears to be more related to cardiac output than to P PA (25,34). Clinical signs of right heart failure often are not clearly related to progression of pulmonary hypertension as assessed by pulmonary arterial pressure and resistance (34). These observations may be explained by the fact that heart failure in pulmonary hypertension is the consequence of uncoupling of the right ventricle (RV) to the hypertensive pulmonary circulation, which is not actually measured by routine hemodynamic evaluations (30, 34).Sagawa and co-workers (17, 32) previously developed a concept of ventriculoarterial coupling ...
