Comparison between acute hypoxia-induced and mechanically-induced pulmonary artery hypertension on the hemodynamics, myocardial contractility and regional blood flow in dogs.

Two groups of eight anesthetized dogs with pulmonary artery hypertension (PAH) were compared. PAH was induced by submitting one group (HP) to hypoxia (FiO2 range: 6-10%) and the other group (ME) to microemboli through glass microbead injection into the pulmonary circulation. Hypoxia-induced PAH was moderate (PAP: +65%; PVR: +152%) contrasting with marked PAH after microbead injection (PAP: +190%; PVR: +389%). For similar effects on left ventricular contractility (LV dP/dt max and segmental myocardial shortening), heart rate and systemic vascular resistance, left ventricular end-diastolic pressure showed significant differences between the two groups (HP group: +75%, ME group: -9%), and so did left ventricular end-diastolic length (HP: +9%, ME: -11%). Thus, contrary to the injection of microbeads, hypoxia did not give rise to any pulmonary barrier, and consequently the changes in cardiac output (HP: +19%, ME: -15%) and hepatic blood flow (HP: +383%, ME: -77%) were significantly different. Hypoxia, and not microbead injection, was responsible for systemic hypertension (MAP: +34% and -4%, respectively). The microbead model resulted in a significantly higher PVR/SVR ratio compared to the hypoxic model (HP: 0.14, ME: 0.41). Hypoxia increased left and right myocardial blood flows whereas microbead injection affected only right ventricular blood flow, leading to significantly different RV/LV endocardial perfusion ratios (HP: +10%, ME: +98%). We conclude that microbead-induced PAH is more appropriate than hypoxia-induced PAH for hemodynamic and pharmacological studies.