NITRIC-OXIDE IMPROVES PULMONARY VASCULAR IMPEDANCE, TRANSPULMONARY EFFICIENCY, AND LEFT-VENTRICULAR FILLING IN CHRONIC PULMONARY-HYPERTENSION

Objective: Chronic pulmonary hypertension is difficult to treat and de spite the introduction of several therapeutic options, no single thera py is universally recommended, Nitric oxide has had some role clinical ly in improving pulmonary hemodynamics in this setting; however, basic investigation has not been performed in an appropriate large animal m odel of stable pulmonary hypertension, This study was designed to exam ine the effects of inhaled nitric oxide on pulmonary hemodynamics in t he setting of a canine model of monocrotaline pyrrole-induced chronic pulmonary hypertension and used Fourier analysis for assessment of pul monary vascular impedance, Methods: Sixteen mongrel dogs (22 to 25 kg) were used, Animals underwent percutaneous pulmonary artery catheteriz ation to measure right-sided hemodynamics before and 6 weeks after a r ight atrial injection of either monocrotaline pyrrole (n = 8) or place bo (n = 8), Six weeks after the injection all hearts were instrumented with an ultrasonic flow probe, sonomicrometric dimension transducers, and micromanometers, Data were collected at baseline and after nitric oxide administration, Harmonic derivation of functional data was achi eved with Fourier analysis, Results: Six weeks after the injection, si gnificant increases in pulmonary artery pressure and pulmonary vascula r resistance were observed in the monocrotaline pyrrole group, Nitric oxide led to significant decreases in pulmonary vascular impedance, Si gnificant improvements in pulmonary blood how, transpulmonary efficien cy, and left ventricular filling were also observed, Conclusions: This investigation demonstrates the well-known clinical effects of nitric oxide in improving pulmonary hypertension, which were also associated with an increase in pulmonary blood flow, transpulmonary efficiency, a nd left ventricular filling in the setting of monocrotaline pyrrole-in duced pulmonary hypertension.