Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.
Pulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear. Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8.8 +/- 2.1 (SD) mm Hg. Emboli increased PAP (15.1 +/- 1.6 to 36.5 +/- 3.5 mm Hg; p less than .001) and decreased CO (3.8 +/- 0.6 to 2.4 +/- 0.8 liters X min-1; p less than .001). Incremental resistance (the slope of the PAP-CO line) only increased slightly. On the other hand, the marked increase in PAP was predominantly due to an increase in effective outflow pressure (from 8.8 +/- 2.1 to 28.6 +/- 3.6; p less than .001). Hydralazine was administered in a dose sufficient to double CO. This did not affect PAP and caused an inconsistent and small decrease in incremental resistance. However, a consistently significant decrease in effective outflow pressure, averaging 23%, was observed. In this canine preparation of pulmonary hypertension the predominant effect of hydralazine appears to be a decrease in the mean vascular closing or outflow pressure.
J
J
Ducas
L
L
Girling
U
U
Schick
R M
RM
Prewitt
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004195:Disease Models, Animal; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects*; D006830:Hydralazine / Q000494:pharmacology*; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000187:drug effects*; D011655:Pulmonary Embolism / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange / Q000187:drug effects; D013318:Stroke Volume / Q000187:drug effects; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D006830:Hydralazine