Equine exercise-induced pulmonary hemorrhage: the role of high left-heart pressures secondary to exercise-induced hypervolemia, and high inspiratory pressures

• Published in: Journal of applied physiology (1985) 2024-11, Vol.137 (5), p.1359-1373
• Main Authors: Bayly, Warwick M, Leguillette, Renaud, Sides, Raymond H, Massie, Shannon, Guigand, Charline, Jones, K Blythe, Warlick, Linnea M, Thueson, Emily L, Troudt, Tristan A, Slocombe, Ronald F, Jones, James H
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure - physiology; Blood Volume - physiology; Female; Hemorrhage - physiopathology; Horse Diseases - physiopathology; Horses; Inhalation - physiology; Lung - physiopathology; Lung Diseases - etiology; Lung Diseases - physiopathology; Male; Physical Conditioning, Animal - physiology; Pulmonary Wedge Pressure - physiology; Ventricular Function, Left - physiology
• ISSN: 8750-7587; 1522-1601; 1522-1601
• DOI: 10.1152/japplphysiol.00575.2023

Exercise-induced pulmonary hemorrhage (EIPH) is common in racehorses. Stress failure of the blood-gas barrier causes EIPH when the transmural pulmonary capillary (Pcap)-alveolar pressure difference (Ptm) exceeds the barrier's stress failure threshold. Why Pcap increases is incompletely understood. We hypothesized that alterations in blood volume (BV) could affect left ventricular (LV) and pulmonary arterial wedge (PAW) pressures and Pcap, and correspondingly affect EIPH severity. Six thoroughbreds with EIPH exercised at the same treadmill speed (≈11.9 m/s [11.1, 12.2]; median [IQR]) before (≈119% V̇o ; B), 2 h after 14 L depletion of blood (≈132% V̇o ; D), and 2 h after reinfusing the blood (≈111% V̇o ; R). LV, pulmonary arterial (PAP), PAW, and intrapleural (Ppl) pressures were measured throughout exercise. Pcap = (PAP + PAW)/2 and Ptm = (Pcap - Ppl). EIPH severity was assessed 60 min postexercise by tracheoendoscopy (EIPHgrade) and bronchoalveolar lavage erythrocyte number (BALRBC). A mixed-effect model and Tukey post hoc test analyzed the effects of BV changes on LV, PAW, Pcap, Ppl, Ptm, and EIPH. ≤ 0.05 was significant. Peak intrapleural inspiratory pressure (Ppl ) was high (-41 mmHg), unaffected by changes in BV ( = 0.44), and did not contribute to fluctuations in Ptm and EIPH severity, whereas changes in BV did (EIPHgrade: = 0.01, BALRBC: = 0.003). EIPH prevalence was 100% with B and R but 50% with D. MaxPtm was not different between B (146 mmHg [140, 151]) and R (151 mmHg [137, 160]) but was lower for D (128 mmHg [127, 130]; B: = 0.005, R: = 0.02). Vascular pressures and Ppl fluctuated constantly during exercise and independently influenced Ptm. Left ventricular end diastolic (LVED) pressure was correlated with Ptm ( = 0.90, = 0.03) and EIPH = 0.82, = 0.004). Exercise BV was strongly correlated with EIPH severity in racehorses ( = 0.86, = 0.009). Hypervolemia induced by the infusion of erythrocyte-rich blood stored in the spleen is normal in high-speed thoroughbred exercise and increases capillary-alveolar transmural pressure (Ptm), leading to exercise-induced pulmonary hemorrhage (EIPH). In this study, decreasing blood volume reduced Ptm and EIPH. Large negative inspiratory pressures also contribute to high Ptm and the occurrence of EIPH. Ptm is dynamic and oscillates constantly during exercise. A significant relationship existed between circulating blood volume and EIPH severity in racehorses.