Ventricular interaction in a canine model of acute pulmonary hypertension and its modulation by vasoactive drugs

Abstract To determine the effect of a pulmonary glass bead embolism (GBE) upon left ventricular filling, we studied 13 dogs (seven with pericardium open, six with pericardium closed) before and after embolizing the pulmonary artery with sufficient glass beads to triple the pulmonary artery pressure. Furthermore, we examined the nature of the ventricular interaction and the effect upon hemodynamics created by intravenous nitroglycerin, dobutamine and hydralazine. Each dog was implanted with segment length crystals directed in the septal free wall plane of both ventricles, Millar catheters (Millar, Houston) placed in the right ventricle, left ventricle, and pulmonary artery (PA), and a thermodilution catheter placed in the PA. GBE reduced left ventricular end diastolic length (LVEDL) and stroke work, and shifted the left ventricular diastolic pressure-segment relationship (LVDPSR) upwards. The presence of a pericardium had little effect on the biventricular response to any of the test interventions. Nitroglycerin reduced right ventricular end diastolic length (RVEDL) and shifted the LVDPSR downwards. It did not increase LVEDL. Dobutamine increased left ventricular stroke work (LVSW) without altering LVEDL or the LVDPSR. Hydralazine did not change LVEDL, LVSW or shift LVDPSR. We conclude that GBE depresses left ventricular function by the Frank Starling mechanism and shifts the LVDPSR upwards. Because pericardiectomy die not prevent the decrease in LVEDL mediated by GBE, and nitroglycerin did not increase LVEDL despite decreasing RVEDL, a series interaction must dominate.