Dissociation of exercise-induced pulmonary hemorrhage and pulmonary artery pressure via nitric oxide synthase inhibition

Abstract

Summary During intense exercise, pulmonary capillary stress failure results in exercise-induced pulmonary hemorrhage (EIPH). To date, a principal focus has been the high pulmonary artery pressures (Ppa) manifest during high intensity exercise as one of the predominant mechanisms that elevates capillary transmural pressure resulting in rupture of the blood-gas barrier. However, it is possible that vascular pressures at other locations (e.g., venular) and extravascular pressures may also be important in the etiology of EIPH. To investigate further the relationship between EIPH and Ppa, five horses ran on an equine treadmill to volitional fatigue under control (CON) and nitric oxide synthase inhibition (L-NAME, 20 mg/kg, i.v.) conditions. Administration of L-NAME significantly increased EIPH (CON, 522.0 ± 453.8; L-NAME, 1178.7 ± 937.7 × 106 RBC/ml bronchoalveolar lavage fluid; p