NO inhalation reduces pulmonary arterial pressure but not hemorrhage in maximally exercising horses

In horses, the exercise-induced elevation of pulmonary arterial pressure (P pa) is thought to play a deterministic role in exercise-induced pulmonary h emorrhage (EIPH), and thus treatment designed to lower Ppa might reasonably be expected to reduce EIPH. Five Thoroughbred horses were run on a treadmi ll to volitional fatigue (incremental step test) under nitric oxide (NO; in haled 80 ppm) and control (N-2, same flow rate as per NO run) conditions (2 wk between trials; order randomized) to test the hypothesis that NO inhala tion would reduce maximal Ppa but that this reduction may not necessarily r educe EIPH. Before each investigation, a microtipped pressure transducer wa s placed in the pulmonary artery 8 cm past the pulmonic valve to monitor Pp a. EIPH severity was assessed via bronchoalveolar lavage (BAL) 30 min postr un. Exercise time did not differ between the two trials (P > 0.05). NO admi nistration resulted in a small but consistent and significant reduction in peak Ppa (N-2,102.3 +/- 4.4; NO, 98.6 +/- 4.3 mmHg, P < 0.05). In the face of lowered Ppa, EIPH severity was significantly higher in the NO trial (N-2 , 22.4 +/- 6.8; NO, 42.6 +/- 15.4 x 10(6) red blood cells/ml BAL fluid, P < 0.05). These findings support the notion that extremely high Ppa may refle ct, in part, an arteriolar vasoconstriction that serves to protect the capi llary bed from the extraordinarily high Ppa evoked during maximal exercise in the Thoroughbred horse. Furthermore, these data suggest that exogenous N O treatment during exercise in horses may not only be poor prophylaxis but may actually exacerbate the severity of EIPH.