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Abstract

Tanus-Santos et al 1 Tanus-Santos JE Moreno Jr, H Moreno RA et al. Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs. Intensive Care Med. 1999; 25: 983-989 Crossref PubMed Scopus (35) Google Scholar recently described an animal model of pulmonary air embolism where stable pulmonary hypertension was induced by a constant venous air infusion. Inhaled nitric oxide (NO) at 3 ppm did not reduce pulmonary artery pressure; the only effect observed was an increase in cardiac index, which was 23% to 24% higher in NO-treated dogs compared with controls. Pulmonary vascular resistance decreased as a consequence of the rise in cardiac index. An increase of the concentration of NO to 40 ppm had similar effects. These authors concluded that small doses of inhaled NO (3 ppm) would be as effective as higher doses (40 ppm) in massive pulmonary embolism. However, another animal model of pulmonary embolism by Bottiger et al, 2 Bottiger BW Motsch J Dorsam J et al. Inhaled nitric oxide selectively decreases pulmonary artery pressure and pulmonary vascular resistance following acute massive pulmonary microembolism in piglets. Chest. 1996; 110: 1041-1047 Crossref PubMed Scopus (72) Google Scholar where microspheres (300 μm) injected into the superior vena cava induced pulmonary hypertension in piglets, showed that 80 ppm NO was even more effective than 40 ppm. The change of pulmonary vascular resistance was only significant at 80 ppm. Both animal models cannot be regarded unequivocally as being comparable models for pulmonary thromboembolism because of the different pathomechanism. The present animal models show only small hemodynamic effects of inhaled NO with no or only minor reduction in pulmonary artery pressure. This could be due to a different grade of pulmonary vasoconstriction compared with massive pulmonary thromboembolism, as stated by Bottiger et al. 2 Bottiger BW Motsch J Dorsam J et al. Inhaled nitric oxide selectively decreases pulmonary artery pressure and pulmonary vascular resistance following acute massive pulmonary microembolism in piglets. Chest. 1996; 110: 1041-1047 Crossref PubMed Scopus (72) Google Scholar Thus, it would be interesting to study the effect of inhaled NO in an animal model of acute thromboembolism by using the injection of autologous blood clot. We suggested that a higher dose (50 ppm) might have even more effect compared with a low dose (5 ppm) in reducing critically increased right ventricular afterload in the state of severe pulmonary embolism, 3 Schenk P Mittermayer C Ratheiser K. Inhaled nitric oxide in a patient with severe pulmonary embolism. Ann Emerg Med. 1999; 33: 710-714 PubMed Google Scholar guided by studies in adult respiratory distress syndrome, where most experience with inhaled NO has been achieved. In patients with adult respiratory distress syndrome, Gerlach et al 4 Gerlach H Rossaint R Pappert D et al. Time-course and dose-response of nitric oxide inhalation for systemic oxygenation and pulmonary hypertension in patients with adult respiratory distress syndrome. Eur J Clin Invest. 1993; 23: 499-502 Crossref PubMed Scopus (340) Google Scholar showed a dose-response curve of inhaled NO (0.01, 0.1, 1, 10, 100 ppm), demonstrating that higher doses are more effective in lowering pulmonary artery pressure. In addition, in patients with pulmonary hypertension and scleroderma, Williamson et al 5 Williamson DJ Hayward C Rogers P et al. Acute hemodynamic responses to inhaled nitric oxide in patients with limited scleroderma and isolated pulmonary hypertension. Circulation. 1996; 94: 477-482 Crossref PubMed Scopus (41) Google Scholar observed a dose-response curve of inhaled NO.