Key result
In a porcine model of acute pulmonary regurgitation, lowering pulmonary vascular resistance via nitric oxide inhalation reduced the pulmonary regurgitant fraction to 24% ± 4% and improved right ventricular function.
Why the study?
Does manipulation of pulmonary vascular resistance affect pulmonary regurgitant fraction and right ventricular function in a porcine model of acute pulmonary regurgitation?
Does manipulation of pulmonary vascular resistance affect pulmonary regurgitant fraction and right ventricular function in a porcine model of acute pulmonary regurgitation?
Lowering pulmonary vascular resistance via ventilation strategies or nitric oxide significantly reduces pulmonary regurgitant fraction and improves right ventricular function in a porcine model of acute pulmonary regurgitation.
Hypothesis-generating for pulmonary vascular resistance modulation in acute pulmonary regurgitation; human studies required before clinical consideration.
INTRODUCTION: Pulmonary regurgitation (PR) is a major concern after right ventricular (RV) outflow tract surgery. We assessed the impact of physiological changes in pulmonary vasculature on hemodynamic severity of PR and RV function and their potential clinical implications for postoperative management using a porcine model with severe PR. MATERIALS AND METHODS: Eight porcine models of acute PR were established by means of resection of pulmonary valve on cardiopulmonary bypass. After separation from bypass and stabilization, blood flow in the main pulmonary artery was measured by a pulsed Doppler flowmeter, and RV systolic function was assessed on the basis of RV segment shortening (RVSS), which was analyzed by sonomicrometry. In the acute PR model, we verified the impact of pulmonary vascular resistance (Rp) on pulmonary regurgitant fraction (PRF) and RV function. Pulmonary vascular resistance was changed by manipulating the level of PaCo 2 and by inhalation of nitric oxide (NO). RESULTS: After bypass, the mean PRF was 40% ± 5%, and there was a deterioration of RV function. Under each ventilation condition (high CO2, low CO2, and NO 20 ppm), Rp was 836 ± 207 dyne × s × cm(-5), 499 ± 125 dyne × s × cm(-5), and 340 ± 102 dyne × s × cm(-5), respectively, and PRF was 60% ± 10%, 37% ± 5%, and 24% ± 4%, respectively, under each condition. They also showed a positive correlation in all animals. Cardiac output and RVSS were decreased by hypercapnia, while they were significantly improved after NO inhalation. CONCLUSIONS: This study indicates that low Rp after right ventricular outflow tract reconstruction (RVOTR) resulting in acute PR is advantageous in reducing the severity of PR and RV volume load. These findings may have clinical implications for early and long-term postoperative management of patients subjected to RVOTR with resulting pulmonary valve incompetence.
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Ko et al. (2015) studied Acute pulmonary regurgitation (n=8). Manipulation of pulmonary vascular resistance (high CO2, low CO2, and nitric oxide inhalation) vs. Different ventilation conditions was evaluated on Pulmonary regurgitant fraction (PRF) and right ventricular function. In a porcine model of acute pulmonary regurgitation, lowering pulmonary vascular resistance via nitric oxide inhalation reduced the pulmonary regurgitant fraction to 24% ± 4% and improved right ventricular function.
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