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• W3150794407 abstract "We read with interest the elegant article by De Wet and associates,1De Wet C.J. Affleck D.G. Jacobsohn E. Avidan M.S. Tymkew H. Hill L.L. Inhaled prostacyclin is safe effective and affordable in patients with pulmonary hypertension right heart dysfunction and refractory hypoxemia after cardiothoracic surgery.J Thorac Cardiovasc Surg. 2004; 127: 1058-1067Abstract Full Text Full Text PDF PubMed Scopus (119) Google Scholar who demonstrated that inhaled prostacyclin (PGI2) prevents pulmonary hypertension, right-heart dysfunction, and refractory hypoxemia after cardiothoracic surgery. We would like to add some observations regarding the mechanisms of action that might be of interest and of possible value in the further clinical implementation of inhalational PGI2. First, pulmonary hypertension is associated with increased superoxide (O2·-) formation that is largely mediated by an upregulation of intravascular reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.2Muzaffar S. Jeremy J.Y. Angelini G.D. Stuart-Smith K. Shukla N. The role of the endothelium and nitric oxide synthases in modulating superoxide formation induced by endotoxin and cytokines in porcine pulmonary arteries.Thorax. 2003; 58: 598-604Crossref PubMed Scopus (75) Google Scholar, 3Muzaffar S. Shukla N. Lobo C. Angelini G.D. Jeremy J.Y. Iloprost inhibits superoxide formation and NADPH oxidase expression induced by the thromboxane A2 analogue, U46619, and isoprostane F2α in cultured porcine pulmonary artery vascular smooth muscle cells.Br J Pharmacol. 2004; 141: 488-496Crossref PubMed Scopus (81) Google Scholar, 4Muzaffar S, Shukla N, Angelini GD, Jeremy JY. Nitroaspirins and morpholinosydnonimine but not aspirin inhibit the formation of superoxide and the expression of gp91phox induced by endotoxin and cytokines in pig pulmonary artery vascular smooth muscle cells and endothelial cells. Circulation. 2004;110:1140-7.Google Scholar, 5Muzaffar S, Shukla N, Angelini GD, Jeremy JY. Hypoxia and the expression of gp91phox and endothelial nitric oxide synthase in the pulmonary artery. Biochem Soc Trans. In press.Google Scholar O2·- reacts with endogenous nitric oxide (NO) to form reactive nitrogen species, which effectively reduces NO bioavailability.2Muzaffar S. Jeremy J.Y. Angelini G.D. Stuart-Smith K. Shukla N. The role of the endothelium and nitric oxide synthases in modulating superoxide formation induced by endotoxin and cytokines in porcine pulmonary arteries.Thorax. 2003; 58: 598-604Crossref PubMed Scopus (75) Google Scholar Because NO is a vasodilator and an inhibitor of inflammation, the reduction of NO formation is considered axiomatic in pulmonary hypertension.2Muzaffar S. Jeremy J.Y. Angelini G.D. Stuart-Smith K. Shukla N. The role of the endothelium and nitric oxide synthases in modulating superoxide formation induced by endotoxin and cytokines in porcine pulmonary arteries.Thorax. 2003; 58: 598-604Crossref PubMed Scopus (75) Google Scholar O2·- also reduces endogenous vascular PGI2 formation.3Muzaffar S. Shukla N. Lobo C. Angelini G.D. Jeremy J.Y. Iloprost inhibits superoxide formation and NADPH oxidase expression induced by the thromboxane A2 analogue, U46619, and isoprostane F2α in cultured porcine pulmonary artery vascular smooth muscle cells.Br J Pharmacol. 2004; 141: 488-496Crossref PubMed Scopus (81) Google Scholar We recently demonstrated that the PGI2 analogue iloprost is a potent inhibitor of NADPH oxidase expression and activity in porcine pulmonary arteries and therefore of O2·- formation.3Muzaffar S. Shukla N. Lobo C. Angelini G.D. Jeremy J.Y. Iloprost inhibits superoxide formation and NADPH oxidase expression induced by the thromboxane A2 analogue, U46619, and isoprostane F2α in cultured porcine pulmonary artery vascular smooth muscle cells.Br J Pharmacol. 2004; 141: 488-496Crossref PubMed Scopus (81) Google Scholar Therefore by reducing O2·- formation, PGI2 protects and enhances NO formation, which itself inhibits NADPH oxidase.4Muzaffar S, Shukla N, Angelini GD, Jeremy JY. Nitroaspirins and morpholinosydnonimine but not aspirin inhibit the formation of superoxide and the expression of gp91phox induced by endotoxin and cytokines in pig pulmonary artery vascular smooth muscle cells and endothelial cells. Circulation. 2004;110:1140-7.Google Scholar The reduction of O2·- also prevents the formation of isoprostanes, which are vaconstrictors and promoters of NADPH oxidase expression.3Muzaffar S. Shukla N. Lobo C. Angelini G.D. Jeremy J.Y. Iloprost inhibits superoxide formation and NADPH oxidase expression induced by the thromboxane A2 analogue, U46619, and isoprostane F2α in cultured porcine pulmonary artery vascular smooth muscle cells.Br J Pharmacol. 2004; 141: 488-496Crossref PubMed Scopus (81) Google Scholar One interesting facet of the effect of inhalational PGI2 reported by De Wet and associates1 was that it prevented refractory hypoxemia. We found that hypoxia promotes the expression of NADPH oxidase in porcine pulmonary arteries.5Muzaffar S, Shukla N, Angelini GD, Jeremy JY. Hypoxia and the expression of gp91phox and endothelial nitric oxide synthase in the pulmonary artery. Biochem Soc Trans. In press.Google Scholar Hypoxemia, by promoting O2·- formation, would create a self-perpetuating cascade that would worsen hypertension and further augment hypoxemia. PGI2, by blocking the expression of NAPDH oxidase, might break this cycle and protect the pulmonary vasculature during surgical intervention through this antioxidant mechanism. Inhalational PGI2 might also prevent perioperative and postoperative intrapulmonary inflammation because PGI2 prevents the adhesion of leukocytes and platelets to vascular walls.6Jeremy J.Y. Jackson C.L. Bryan A.J. Angelini G.D. Eicosanoids, fatty acids and restenosis following coronary artery bypass graft surgery and balloon angioplasty.Prostaglandins Leukot Essent Fatty Acids. 1996; 54: 385-402Abstract Full Text PDF PubMed Scopus (33) Google Scholar Similarly, the preservation of intrapulmonary NO-forming capacity would also afford protection against inflammation because NO has similar anti-inflammatory properties to PGI2.7Jeremy J.Y. Dashwood M.R. Mehta D. Izzat M.B. Shukla N. Angelini G.D. Nitric oxide, prostacyclin and cyclic nucleotide formation in externally stented porcine vein grafts.Atherosclerosis. 1998; 141: 297-305Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar This is of importance because leukocytes and platelets release vasoconstrictors and inflammogens, including thromboxane A2 and cytokines, all of which upregulate the expression of NADPH oxidase and the formation of O2·-.2Muzaffar S. Jeremy J.Y. Angelini G.D. Stuart-Smith K. Shukla N. The role of the endothelium and nitric oxide synthases in modulating superoxide formation induced by endotoxin and cytokines in porcine pulmonary arteries.Thorax. 2003; 58: 598-604Crossref PubMed Scopus (75) Google Scholar, 3Muzaffar S. Shukla N. Lobo C. Angelini G.D. Jeremy J.Y. Iloprost inhibits superoxide formation and NADPH oxidase expression induced by the thromboxane A2 analogue, U46619, and isoprostane F2α in cultured porcine pulmonary artery vascular smooth muscle cells.Br J Pharmacol. 2004; 141: 488-496Crossref PubMed Scopus (81) Google Scholar, 4Muzaffar S, Shukla N, Angelini GD, Jeremy JY. Nitroaspirins and morpholinosydnonimine but not aspirin inhibit the formation of superoxide and the expression of gp91phox induced by endotoxin and cytokines in pig pulmonary artery vascular smooth muscle cells and endothelial cells. Circulation. 2004;110:1140-7.Google Scholar The beneficial effect of inhalational PGI2 on left ventricular function reported by De Wet and associates1 could be related to its antioxidative effect on the lungs. There is substantial evidence that reactive oxygen species, including O2· and peroxynitrite, impair left ventricular function.8Lefer D.J. Granger D.N. Oxidative stress and cardiac disease.Am J Med. 2000; 109: 315-323Abstract Full Text Full Text PDF PubMed Scopus (391) Google Scholar Thus it is reasonable to suggest that the suppression of intrapulmonary oxygen free radical formation by PGI2 might contribute to the beneficial downstream protective effect of the prostanoid on the left ventricle. Finally, in a broader context the administration of the stable analogue iloprost in cardiac surgery might be indicated for other more long-term conditions. In particular, PGI2 has been shown to inhibit vascular smooth muscle cell proliferation and migration, platelet and leukocyte adhesion, and metalloproteinase expression,6Jeremy J.Y. Jackson C.L. Bryan A.J. Angelini G.D. Eicosanoids, fatty acids and restenosis following coronary artery bypass graft surgery and balloon angioplasty.Prostaglandins Leukot Essent Fatty Acids. 1996; 54: 385-402Abstract Full Text PDF PubMed Scopus (33) Google Scholar all key components of vein graft disease. As such, iloprost might be useful in preventing vein graft failure." @default.
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