Pulmonary Arterial Hypertension Induces Compensatory Increase of Left Ventricular Contractility Indexes in Rats in Response to Its Filling Insufficiency.

Pulmonary arterial hypertension (PAH) is accompanied by changes in the pulmonary and systemic circulation. We studied the effect of PAH on the function of the left ventricle (LV). Left ventricular pressure and volume were simultaneously recorded in vivo in rats with monocrotaline-induced PAH (60 mg/kg). LV contractility and mechanical indexes were calculated. In addition, the relationships between LV maximum rate of contraction (dP/dt) or relaxation (dP/dt) and left ventricular end-diastolic volume (EDV) were assessed. PAH leads to a significant decrease in cardiac output at a constant HR as well as to a decrease in stroke volume at unchanged LV ejection fraction. In rats with PAH, the slopes of the dP/dt-EDV and dP/dt-EDV curves were greater than in control animals by 1.93 and 2.5 times, respectively. Thus, PAH leads to a compensatory increase in the dependence of LV contractility and "intensity" of LV relaxation on EDV.