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 hypertensi on (PAH) were compared. PAH was induced by submitting one group (HP) t o hypoxia (FiO2 range: 6-10%) and the other group (ME) to microemboli through glass microbead injection into the pulmonary circulation. Hypo xia-induced PAH was moderate (PAP: +65%; PVR: +152%) contrasting with marked PAH after microbead injection (PAP: +190%; PVR: +389%). For sim ilar effects on left ventricular contractility (LV dP/dt max and segme ntal myocardial shortening), heart rate and systemic vascular resistan ce, left ventricular end-diastolic pressure showed significant differe nces between the two groups (HP group: +75%, ME group: -9%), and so di d left ventricular end-diastolic length (HP: +9%, ME: -11%). Thus, con trary 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 si gnificantly different. Hypoxia, and not microbead injection, was respo nsible for systemic hypertension (MAP: +34% and -4%, respectively). Th e microbead model resulted in a significantly higher PVR/SVR ratio com pared to the hypoxic model (HP: 0.14, ME: 0.41). Hypoxia increased lef t and right myocardial blood flows whereas microbead injection affecte d only right ventricular blood flow, leading to significantly differen t RV/LV endocardial perfusion ratios (HP: +10%, ME: +98%). We conclude that microbead-induced PAH is more appropriate than hypoxia-induced P AH for hemodynamic and pharmacological studies.