Effects of inhaled prostacyclin as compared with inhaled nitric oxide on right ventricular performance in hypoxic pulmonary vasoconstriction.
OBJECTIVE
Recently, inhalation of prostacyclin (PGI2) has been shown to cause selective pulmonary vasodilation. However, the effects of inhaled PGI2 on right ventricular (RV) performance are still unknown and therefore were compared with those of inhaled nitric oxide (NO).


METHODS
Reported measurements design.


METHODS
Animal research laboratory.


METHODS
Six anesthetized, ventilated dogs (28 +/- 2 kg).


METHODS
Pulmonary hypertension was induced by decreasing FIO2 to 0.09-0.11 ('hypoxic pulmonary vasoconstriction', HPV). Subsequently, a single dose of either NO (50 ppm) or PGI2-aerosol (0.9 +/- 0.3 ng/kg/min) was randomly added to the inspired gas.


RESULTS
Measurements were performed before induction of HPV and 10 minutes after application and withdrawal of each drug. Central hemodynamics, global RV function, and local RV function (n = 5, sonomicrometry) were assessed. HPV resulted in an increase of pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), RV stroke work, right coronary artery flow, maximal rate of RV pressure increase (RV dP/dtmax), and maximal velocity of shortening of contractile elements (Vmax). In contrast, RV ejection fraction, RV end-diastolic volume, RV end-diastolic fiber length, and systolic fiber shortening were unchanged. Both PGI2-aerosol and NO attenuated the HPV-induced increase in PAP and PVR without affecting arterial pressure. NO, but not PGI2, resulted in an increase of RV ejection fraction from 42 to 46% (p < 0.05). Right coronary flow dropped from 29 to 21 mL/min during PGI2 (p < 0.05). RV stroke work, RV dP/dtmax, and Vmax decreased subsequent to both NO and PGI2, whereas local RV function was not affected.


CONCLUSIONS
In pulmonary hypertension induced by HPV, PGI2-aerosol and inhaled NO reduced RV afterload and, hence, RV oxygen demand, with only minor changes of stroke volume and cardiac output, indicating an improvement of overall efficiency of RV contraction. RV ejection fraction increased on NO, but not with PGI2. This might be explained by the fact that the reduction of pulmonary vascular resistance during PGI2 amounted to only 65% of the effect of NO. In summary, both inhaled NO and PGI2-aerosol showed beneficial effects on RV performance and may prove helpful in the treatment of acute pulmonary hypertension.
Zwissler
B
B
Department of Anesthesia, Ludwig-Maximilians-University Munich, Federal Republic of Germany.
Welte
M
M
Messmer
K
K
D000280:Administration, Inhalation; D000336:Aerosols; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002306:Cardiac Volume / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003971:Diastole; D004285:Dogs; D011464:Epoprostenol / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009569:Nitric Oxide / Q000008:administration & dosage / Q000627:therapeutic use*; D010101:Oxygen Consumption / Q000187:drug effects; D011651:Pulmonary Artery; D013318:Stroke Volume / Q000187:drug effects; D013599:Systole; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction; D016278:Ventricular Function, Right / Q000187:drug effects*; D017725:Ventricular Pressure / Q000187:drug effects
D000336:Aerosols; D009569:Nitric Oxide; D011464:Epoprostenol