Comparison of the Effects of Nitric Oxide, Nitroprusside, and Nifedipine on Hemodynamics and Right Ventricular Contractility in Patients With Chronic Pulmonary Hypertension*

摘要

Study objectives: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricularn(RV) contractility were compared with those of nitroprusside and nifedipine in 14 patients withnsevere chronic pulmonary hypertension.nStudy design: Micromanometer and balloon-tipped right heart catheterization were performed.nInhaled NO, IV nitroprusside, and sublingual nifedipine were administered sequentially whilenpatients breathed > 90% oxygen.nSetting: Cardiac catheterization laboratory in a tertiary care teaching hospital.nPatients: Fourteen patients with severe pulmonary hypertension unrelated to left ventricular dysfunction.nMeasurements and results:During NO inhalation, mean systemic arterial pressure (MAP) was unchanged,nbut pulmonary artery (PA) pressure ([mean 6SEM] 4962mmHgvs4462mmHg;p<0.01),npulmonary vascular resistance (PVR; 829668 vs 669664 dyne z s z cm25n;p<0.01) and RV end-diastolicnpressure (RVEDP; 1261vs1061 mm Hg; p<0.01) decreased. Stroke volume index (SVI; 3162vsn3563mL/m2n;p<0.05) increased, and the first derivative of RV pressure at 15 mm Hg developednpressure (RV 1dP/dt at DP15) was unchanged. During nitroprusside administration, MAP decreasedn(10565vs7665mmHg;p<0.01), PA was unchanged (4862vs4563mmHg;p5 not significant),nand PVR decreased (791653 vs 665653 dyne z s z cm25n;p<0.01). RV 1dP/dt at DP15 increasedn(425622 vs 465629 mm Hg/s; p < 0.05), but SVI was unchanged. Nifedipine decreased MAPn(103 6 5vs94 6 5mmHg;p < 0.01), PA and PVR were unchanged, RVEDP increased (12 6 1vsn14 6 2mmHg;p < 0.01), and RV 1dP/dt at DP15 decreased (432 6 90 vs 389 6 21 mm Hg/s;np < 0.05).nConclusions: Inhaled NO is a selective pulmonary vasodilator in patients with chronic pulmonarynhypertension that improves cardiac performance without altering RV contractility. Nitroprusside causedna similar degree of pulmonary vasodilation. In contrast to inhaled NO, nitroprusside caused systemicnhypotension associated with an increase in RV contractility. Acute administration of nifedipine did notncause pulmonary vasodilation, but RVEDP increased and RV contractility decreased..