Manohar M, Hutchens E, Coney E
Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign 61801.
Br Vet J. 1993 Sep-Oct;149(5):419-28. doi: 10.1016/S0007-1935(05)80108-3.
Exercise-induced pulmonary haemorrhage (EIPH) is a common occurrence in race horses. Although blood in cases of EIPH has been suspected to originate from the bronchial circulation, which receives approximately 1% of the left ventricular output, physiological evidence has recently emerged to indicate that the pulmonary circulation, which receives the entire output of the right ventricle, is a more likely source. High transmural pulmonary capillary pressures have been shown to cause breaks in the capillary endothelium, basement membrane as well as in the alveolar epithelium. Blood constituents escape into the interstitium and alveoli through such breaks in the blood-gas barrier--a phenomenon referred to as stress failure of pulmonary capillaries. Concomitant measurement of pulmonary arterial and venous pressures in strenuously exercising horses have revealed that both of these variables increased dramatically such that the intravascular pulmonary capillary pressure during exertion at 14 m/s (heart rate of 214 beats/min) approached 105 cm H2O (79 mmHg). Alveolar pressure during peak inhalation is likely to be negative; therefore, it is probable that transmural (intravascular minus perivascular) pulmonary capillary pressure of maximally exercising horses may be greater than 105 cm of water. Thus, the pulmonary blood-gas barrier, which has to be thin to provide for adequate diffusion of O2, is exposed to very high transmural forces associated with high cardiac output during exercise. Recent evidence suggests that the alveolar-capillary membrane may not be able to withstand the high transmural forces during maximal exertion, and that stress failure of pulmonary capillaries occurs, leading to EIPH. Intravenous furosemide premedication 4 h before exercise attenuates the exercise-induced rise in pulmonary arterial, capillary and venous pressures and, therefore, may be efficacious in reducing or limiting the extent of EIPH in race horses.
运动性肺出血（EIPH）在赛马中很常见。尽管EIPH病例中的血液一直被怀疑源自支气管循环（其接受约1%的左心室输出量），但最近出现的生理学证据表明，接受右心室全部输出量的肺循环更有可能是出血来源。已表明高跨壁肺毛细血管压力会导致毛细血管内皮、基底膜以及肺泡上皮的破裂。血液成分通过血气屏障的此类破裂处逸入间质和肺泡——这一现象被称为肺毛细血管应激性衰竭。对剧烈运动马匹的肺动脉和静脉压力进行同步测量发现，这两个变量均显著增加，以至于在以14米/秒速度运动（心率为214次/分钟）时，血管内肺毛细血管压力接近105厘米水柱（79毫米汞柱）。吸气峰值时的肺泡压力可能为负值；因此，最大运动量马匹的跨壁（血管内减去血管周围）肺毛细血管压力可能大于105厘米水柱。因此，为保证氧气充分扩散而必须很薄的肺血气屏障，在运动期间会暴露于与高心输出量相关的非常高的跨壁力之下。最近的证据表明，在最大运动量时，肺泡 - 毛细血管膜可能无法承受高跨壁力，从而发生肺毛细血管应激性衰竭，导致EIPH。运动前4小时静脉注射速尿可减轻运动引起的肺动脉、毛细血管和静脉压力升高，因此可能有效减少或限制赛马中EIPH的程度。
