Inder S Anand

Department of Cardiology, VA Medical Center and University of Minnesota, Minneapolis, USA

Abstract: The use of inhaled nitric oxide in acutely ill patients with high altitude pulmonary edema was first reported in 1998. We demonstrated that both nitric oxide and oxygen cause an acute decrease in pulmonary artery pressure, intrapulmonary shunting and improvement in oxygenation. There appears to be an additive effect on pulmonary hemodynamics and an even greater effect on gas exchange when both oxygen and nitric oxide are delivered simultaneously. While further studies are necessary to determine the potential long-term benefits or adverse sequelae associated with nitric oxide use, this report suggests that there may be significant benefits for patients who are acutely ill with high altitude pulmonary edema. This report may also provide some insight into the mechanism whereby nitric oxide and oxygen improve gas exchange in a hypoxic hypobaric atmosphere.

Keywords: Nitric oxide; hypoxic; high altitude pulmonary edema.

High altitude pulmonary edema (HAPE) is a life threatening condition [13] characterized by pulmonary hypertension, increased pulmonary c apillary permeability, and hypoxemia [9, 12, 19]. Although the mechanisms responsible for the development of HAPE are not entirely clear, measurements of pulmonary hemodynamics in patients with HAPE or incipient HAPE suggest that edema is caused by uneven severe hypoxic pulmonary vasoconstriction and an increase in pulmonary artery pressure in the lungs without elevation of left atrial pressure. This results in leakage of large-molecular-weight proteins and erythrocytes across the alveolar capillaries in areas of the lung that are not vasoconstricted [2, 6, 11, 15]. Earlier studies of broncho alveolar lavage (BAL) fluid had suggested that inflammation may play a role in the genesis of HAPE [19]. More recent studies have, however, disproved any role of inflammation in its pathogenesis [19, 20,21]. Taken together, these studies strongly suggests that high capillary hydrostatic pressure induces a high-permeability type lung edema in the absence of inflammation, a

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