Original article: Cardiovascular
Pulmonary vasoconstriction due to impaired nitric oxide production after cardiopulmonary bypass

https://doi.org/10.1016/0003-4975(96)00146-4Get rights and content

Background

Pulmonary hypertension is a serious complication after cardiopulmonary bypass (CPB). This study tests the hypothesis that CPB provokes oxidantmediated pulmonary endothelial dysfunction, leading to reduced nitric oxide (NO) production and pulmonary vasoconstriction.

Methods

Twelve piglets underwent 2 hours of CPB. In 6 of them, CPB prime was supplemented with N-mercaptopropionylglycine and catalase, whereas the others were not treated. Left and right ventricular function were evaluated from end-systolic elastance and Starling analysis. Pulmonary vascular resistance and transpulmonary NO production (measuring NO2, NO3) were determined to assess pulmonary endothelial function.

Results

Cardiopulmonary bypass caused a significant increase in pulmonary vascular resistance (83 ± 12 to 212 ± 30 dynes · cm−5 · s kg−1, p < 0.05), associated with a reduction of NO production (8.8 ± 1.4 to 2.5 ± 0.5 μmol/min, p < 0.05) and depressed right ventricular function (56 ± 12% of control), whereas N-mercaptopropionylglycine and catalase added to the CPB allowed a substantial improvement of these deleterious effects of CPB.

Conclusions

Cardiopulmonary bypass impairs pulmonary NO production, resulting in pulmonary vasoconstriction and right ventricular dysfunction, which can be reduced by antioxidants. These findings imply the validity of NO inhalation therapy for postoperative pulmonary hypertension as a supplementation of endogenous endothelium-derived relaxing factor.

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      Perhaps more frequently, RV dysfunction develops as a manifestation of increased intraoperative PH, and PVR on the background of preoperative right ventricular dysfunction. As many aspects of cardiac surgery including the pulmonary ischemia, the deleterious effects of cardiopulmonary bypass on pulmonary vasoactivity impacts on PVR, endothelial function and NO pathways, treatment of this phenomenon by supplemental delivery of NO seems logical [68,69]. The first series of studies in cardiac surgery have addressed safety, compared efficacy of iNO to other vasodilators, established dose responses and attempted to define conditions when iNO could be especially helpful.

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    This research was supported by National Heart, Lung, and Blood Institute grants HL-40675 and HL-40922 and by the University of California Tobacco-Related Disease Research program.

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