Kindig C A, Ramsel C, McDonough P, Poole D C, Erickson H H
Kansas State University, Department of Anatomy & Physiology, 228 Coles Hall, Manhattan, Kansas 66506-5802, USA.
Equine Vet J. 2003 Sep;35(6):581-5. doi: 10.2746/042516403775467199.
Capillary stress failure-induced (exercise-induced) pulmonary haemorrhage (EIPH) during intense running in horses is thought to involve both intravascular (i.e. mean pulmonary arterial pressure [Ppa] > 100 mmHg) and extravascular (e.g. negative inspiratory pressure swings) mechanisms.
That inclined running would reduce breathing frequency (coupled to stride frequency) and increase tidal volume thus increasing lung volume changes and intrapleural pressure swings resulting in more pronounced EIPH.
Six Thoroughbred horses were run to volitional fatigue (incremental step test) on a level (L) and inclined (I; 10%) treadmill in random order. Pulmonary minute ventilation, arterial blood gases and mean Ppa were obtained during each run while EIPH severity was quantified via bronchoalveolar lavage (BAL) 30 mins post run.
Time to fatigue did not differ between trials (P > 0.05). At end-exercise, breathing frequency was reduced (L, 127.8 +/- 3.0; I, 122.6 +/- 2.1 breaths/min; P < 0.05) and tidal volume increased (L, 11.5 +/- 0.6; I, 13.1 +/- 0.5 L; P < 0.05) during inclined running. No differences existed in end-exercise plasma [lactate] between trials (L, 24.5 +/- 2.9; I, 26.2 +/- 3.4 mmol/l, P > 0.05); however, the mean peak Ppa was reduced during the inclined run (L, 105+5; I, 96 +/- 4 mmHg, P < 0.05). In the face of reduced Ppa, EIPH severity was increased significantly (P < 0.05) during the inclined vs. level run (L, 37.0 +/- 11.7; I, 49.6 +/- 17.0 x 10(6) red blood cells/ml BAL fluid).
Although inclined running lowered peak Ppa, EIPH severity was increased. It is likely that this effect resulted, in part, from an altered ventilatory pattern (i.e. increased tidal volumes and associated intrapleural pressure changes).
This conclusion supports an important role for extravascular factors in the aetiology of EIPH.
马匹在剧烈奔跑时,毛细血管应力衰竭诱发(运动诱发)的肺出血(EIPH)被认为涉及血管内(即平均肺动脉压[Ppa]>100mmHg)和血管外(如吸气负压波动)机制。
倾斜跑步会降低呼吸频率(与步频相关)并增加潮气量,从而增加肺容积变化和胸膜腔内压波动,导致更明显的EIPH。
6匹纯种马在水平(L)和倾斜(I;10%)跑步机上以随机顺序进行递增式阶梯试验,直至自愿疲劳。每次跑步期间记录肺分钟通气量、动脉血气和平均Ppa,跑步结束30分钟后通过支气管肺泡灌洗(BAL)对EIPH严重程度进行量化。
各试验间疲劳时间无差异(P>0.05)。运动结束时,倾斜跑步期间呼吸频率降低(L组,127.8±3.0;I组,122.6±2.1次/分钟;P<0.05),潮气量增加(L组,11.5±0.6;I组,13.1±0.5升;P<0.05)。各试验间运动结束时血浆[乳酸]无差异(L组,24.5±2.9;I组,26.2±3.4mmol/L,P>0.05);然而,倾斜跑步期间平均峰值Ppa降低(L组,105±5;I组,96±4mmHg,P<0.05)。尽管Ppa降低,但倾斜跑步与水平跑步相比,EIPH严重程度显著增加(P<0.05)(L组,37.0±11.7;I组,49.6±17.0×10⁶红细胞/ml BAL液)。
尽管倾斜跑步降低了峰值Ppa,但EIPH严重程度增加。这种影响可能部分是由于通气模式改变(即潮气量增加和相关胸膜腔内压变化)所致。
该结论支持血管外因素在EIPH病因学中起重要作用。