To the Editor:—

Dr. Haddad et al.  1have written an interesting and informative article regarding the beneficial effects of inhaled nitric oxide (inhaled NO) in perioperative and critical care patients. They believe that inhaled NO causes vasodilation that is proportional to the pulmonary vascular resistance in the presence of pulmonary vasoconstriction. Moreover, they have indicated that the effects of inhaled NO on cardiac function are dependent on the degree of right ventricular dysfunction. 1We would like to mention recent evidence supporting the idea of using inhaled NO in the therapy of massive pulmonary embolism. 2–4Selective pulmonary vasodilator therapy with inhaled NO can attenuate effectively the pulmonary vasoconstriction caused by active mediators, such as endothelin-1 5,6and thromboxane A2, 4,6which have been implicated in the pulmonary vasoconstriction and cardiodepression seen in pulmonary embolism. Indeed, inhaled NO blunted thromboxane A2 release, 4lowered pulmonary artery pressure, and increased cardiac output after massive air embolism in dogs 2and in four cases of pulmonary embolism. 3Although extrapolating these findings to the clinical situation is still a matter of debate, we believe that these recent findings support the use of inhaled NO during pulmonary embolism. Finally, it is possible to discontinue administration of inhaled NO if anything untoward happens.

Haddad E, Lowson SM, Johns RA, Rich GF: Use of inhaled nitric oxide perioperatively and in intensive care patients. A nesthesiology 2000; 92: 1821–5
Tanus-Santos JE, Moreno H Jr, Zappellini A, de Nucci G: Small-dose inhaled nitric oxide attenuates hemodynamic changes after pulmonary air embolism in dogs. Anesth Analg 1999; 88: 1025–9
Capellier G, Jacques T, Balvay P, Blasco G, Belle E, Barale F: Inhaled nitric oxide in patients with pulmonary embolism. Intensive Care Med 1997; 23: 1089–92
Tanus-Santos JE, Moreno H Jr, Moreno RA, Martins ML, Pereira R, de Nicci G: Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs. Intensive Care Med 1999; 25: 983–9
Dschietzig T, Laule M, Alexiou K, Schror K, Baumann G, Stangl K: Coronary constriction and consequent cardiodepression in pulmonary embolism are mediated by pulmonary big endothelin and enhanced in early endothelial dysfunction. Crit Care Med 1998; 26: 510–7
Tanus-Santos JE, Gordo WM, Udelsmann A, Cittadino MH, Moreno H Jr: Nonselective enothelin-receptor antagonism attenuates hemodynamic changes after massive pulmonary air embolism in dogs. Chest 2000; 118: 175–9