Con: Intraoperative use of nitric oxide for treatment of pulmonary hypertension in patients with congenital heart disease is not effective

Abstract

PATIENTS with pulmonary hypertension (PHTN) have had no effective treatment available because of the lack of a selective pulmonary vasodilator. In 1980, a labile humoral factor produced by endothelial cells (endothelium-derived relaxing factor) was shown to mediate vascular dilation. 1 Palmer RM Ferrige AG Moncada S Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature. 1987; 327: 524-526 Crossref PubMed Scopus (9259) Google Scholar Nitric oxide (NO) has been shown to be biologically identical to endothelium-derived relaxing factor. Once released, NO diffuses into vascular smooth muscle cells; activates soluble guanylate cyclase, which increases the concentration of cyclic guanosine monophosphate and initiates a cascade of events that results in smooth muscle relaxation. 2 Fiscus RR Molecular mechanisms of endothelium-mediated vasodilation. Semin Thromb Hemost. 1988; 14: 12-22 PubMed Google Scholar In vitro and in vivo evidence indicate that NO may be an important mediator of pulmonary vascular tone. 2 Fiscus RR Molecular mechanisms of endothelium-mediated vasodilation. Semin Thromb Hemost. 1988; 14: 12-22 PubMed Google Scholar , 3 Furchgott RF Vanhoutte PM Endothelium-derived relaxing and contracting factors. FASEB J. 1989; 3: 2007-2018 Crossref PubMed Scopus (1669) Google Scholar Many reports have appeared evaluating the effect of NO as a selective pulmonary vasodilator in the treatment of PHTN. It has not been clearly established, however, whether NO is effective for patients with congenital heart disease during cardiac surgery and whether outcome is improved when NO is used.