Schroter R C, Marlin D J, Denny E
Department of Biological and Medical Systems, Imperial College of Science, Technology and Medicine, London, UK.
Equine Vet J. 1998 May;30(3):186-92. doi: 10.1111/j.2042-3306.1998.tb04486.x.
Exercise-induced pulmonary haemorrhage (EIPH) in horses, although of major welfare and economic importance worldwide, is of uncertain cause. It is accepted that the dorsocaudal region of the lung is particularly prone to the condition, but present theories of causation cannot satisfactorily explain the mechanism or pattern of occurrence. We propose that EIPH results from locomotory impact induced trauma; the mechanism being similar to that producing lung tissue damage following thoracic impact injury. In impact injury, the localised impulsive load on the chest wall is transmitted by pressure waves through the lung at a slower speed than in the chest wall. The waves are subsequently reflected from the distal chest wall and other structures, producing a complex pattern of wave motion; waves travelling from regions of large cross-section to narrower ones are amplified in magnitude, consequently these regions can experience very high local stresses. Compression/dilation and shear waves are produced within the parenchyma and the latter particularly have been implicated as the cause of parenchymal damage and rupture with oedema and haemorrhage. This form of soft tissue damage has been shown to occur at remarkably low loads with an impact velocity greater than about 11 m/s and pressure exceeding approximately 14 kPa. In the horse, the lung is subjected to comparable levels of locomotory derived impulsive force during moderate to high speed exercise and this is the basis of the mechanism causing EIPH. During locomotion, the force following ground-strike of the front legs is transmitted, with some attenuation, through the forelimbs to the scapulae. The anatomical arrangement of the scapula, coupled with the direction of the force at the shoulder (scapulo humeral joint) produces an impulsive force on the rib cage, approximately just below mid height of the frontal aspect of the chest approximately over the fourth rib. As a result, pressure waves are transmitted through the lung parenchyma towards the dorsal and caudal regions; these waves are subsequently reflected at the distal chest wall, spine and diaphragm causing a complex pattern of wave interaction. The observed locations of EIPH are at the sites where wave intensity is expected to be greatest due to changes in cross section and reflection. Based on available information, it is estimated that impulsive forces of more than 100 kPa, lasting approximately 10 ms, would be applied to the chest wall by each scapula in a 500 kg horse when galloping; this level of force would be sufficient to cause oedema and haemorrhage as observed in impact induced injury.
马匹运动性肺出血（EIPH）在全球范围内虽对福利和经济具有重大影响，但其病因尚不明确。人们公认肺的背尾区域特别容易出现这种情况，但目前的病因理论无法令人满意地解释其发生机制或模式。我们提出，EIPH是由运动冲击导致的创伤引起的；其机制类似于胸部冲击伤后导致肺组织损伤的机制。在冲击伤中，胸壁上的局部脉冲载荷通过压力波以比胸壁中更慢的速度在肺中传播。这些波随后从胸壁远端和其他结构反射回来，产生复杂的波动模式；从大横截面区域传播到较窄区域的波在幅度上会放大，因此这些区域可能会承受非常高的局部应力。在实质组织内会产生压缩/扩张波和剪切波，尤其是后者被认为是实质组织损伤、破裂以及水肿和出血的原因。这种软组织损伤已被证明在冲击速度大于约11米/秒且压力超过约14千帕的情况下，在极低的载荷下就会发生。在马身上，在中高速运动期间，肺会受到相当水平的由运动产生的脉冲力，这就是导致EIPH的机制基础。在运动过程中，前腿着地后的力会经过一定程度的衰减，通过前肢传递到肩胛骨。肩胛骨的解剖结构，再加上肩部（肩胛肱关节）处力的方向，会在胸廓上产生一个脉冲力，大约就在胸部正面高度略低于中部、大约在第四肋骨上方的位置。结果，压力波通过肺实质向背侧和尾侧区域传播；这些波随后在胸壁远端、脊柱和膈肌处反射，导致复杂的波相互作用模式。观察到的EIPH发生位置正是由于横截面变化和反射而预计波强度最大的部位。根据现有信息估计，一匹500公斤重的马在奔跑时，每个肩胛骨会对胸壁施加超过100千帕、持续约10毫秒的脉冲力；这种力的水平足以导致如冲击伤中所观察到的水肿和出血。
