T. S. Epp

The effect of herbal supplementation on the severity of exercise-induced pulmonary haemorrhage

Exercise-induced pulmonary haemorrhage (EIPH) is a serious condition that affects the health and possibly the performance of all racehorses. However, only two treatments, furosemide and the Flair™ equine nasal strip, both of which reduce capillary transmural pressure, have been successful in reducing EIPH. Alternatively, transient impairment of platelet function and coagulation during exercise has been considered an additional contributor to EIPH. Consequently, herbal formulations designed to enhance platelet function, and hence coagulation, are hypothesized to reduce EIPH. To investigate the validity of this hypothesis, five Thoroughbred horses completed three maximal incremental exercise tests on a 10% inclined treadmill in a randomized cross-over design experiment. Treatments included twice daily oral administration (for 3 days) of a placebo (PL; cornstarch) and two herbal formulas, Yunnan Paiyao (YP) or Single Immortal (SI). Blood samples for coagulation profiles, complete blood counts and biochemistry profiles were collected before each exercise test. During each test, pulmonary arterial pressure, oxygen uptake, arterial blood gases, plasma lactate and time-to-fatigue were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) at 30–60 min post-exercise. The herbal formulations were not effective in decreasing EIPH (×10 6 red blood cells ml −1 BAL fluid: PL, 27.1±11.6; YP, 33.2±23.4; SI, 35.3±15.4, P >0.05) or in changing any of the other variables measured with the exception of time-to-fatigue, which was slightly but significantly prolonged by Single Immortal compared with placebo and Yunnan Paiyao (PL, 670±9.6 s; YP, 665±5.5 s; SI, 685±7.9 s, P

Effects of conjugated oestrogens and aminocaproic acid upon exercise-induced pulmonary haemorrhage (EIPH)

Aminocaproic acid (ACA) and Premarin w (PRE) are used to treat exercise-induced pulmonary haemorrhage (EIPH) at the racetrack based upon their putative coagulation effects. We hypothesized that neither ACA nor PRE would reduce EIPH because the literature does not substantiate coagulation deficits being manifested in EIPH. Six Thoroughbreds were run from 4ms 21 until fatigue (1ms 21 s £ 1min increments; 68 inclined treadmill) after being treated with placebo, PRE (25mg) or ACA (5g) at 2-week intervals in a randomized crossover design. Coagulation and exercise-related variables were measured at rest and maximal effort. EIPH and inflammation were quantified via bronchoalveolar lavage fluid (BALF) 30‐60min post-exercise. EIPH was not altered by either treatment (3.8 ^ 1.7 (placebo), 4.6 ^ 3.2 (ACA) and 2.4 ^ 1.2 (PRE) £ 10 6 RBCml 21 BALF; p ¼ 0.12), nor was coagulation. However, inflammation was decreased (5.9 ^ 0.9 (placebo), 4.4 ^ 0.9 (ACA) and 4.2 ^ 0.4 (PRE) £ 10 5 WBCml 21 BALF; both p , 0.05). There was a trend for decreased time-to-fatigue (720 ^ 27 (placebo), 709 ^ 24 (ACA) and 726 ^ 28 (PRE) s; p ¼ 0.09 for placebo vs. ACA) and a reduction in plasma lactate (19.5 ^ 3.0 (placebo), 14.7 ^ 1.0 (ACA) and 17.6 ^ 2.5 (PRE) mmoll 21 ; p , 0.05 for placebo vs. ACA) following ACA administration. ACA and PRE were not effective in reducing EIPH, and ACA may be detrimental to performance. However, both may mitigate exercise-induced pulmonary inflammation.

Evidence supporting exercise-induced pulmonary haemorrhage in racing greyhounds

Exercise-induced pulmonary haemorrhage (EIPH) is a major health concern in performance horses, but the presence and severity of this condition in racing greyhounds has received little attention. While equids and greyhounds share many physiological attributes, there are important structural and functional differences that may help protect greyhounds from EIPH. We tested the hypothesis that greyhounds performing a simulated 503m race would experience EIPH and that the time course of recovery would be similar to the horse, even though the severity or relative extent as indexed by the concentration of red blood cells [RBCs] in bronchoalveolar lavage (BAL) fluid would be lower in comparison with that demonstrated previously in horses. Greyhound dogs (n 1⁄4 6) raced on two occasions (separated by 7 weeks) and BAL was performed 1 week before, 2 h after and each week for 4 weeks following each race to examine the [RBC], concentration of white blood cells [WBCs], WBC differentials and haemosiderophages in the lungs. Racing increased 10min post-exercise venous blood [lactate] to 18.6 ^ 0.4mmol l. No epistaxis or pink froth was observed at the nose or mouth of any of the dogs. The [RBC] in the BAL fluid was increased significantly 2 h post-race (baseline 1⁄4 109.6 ^ 11.7 £ 10; post-race 1⁄4 292.3 ^ 69.9 £ 10 RBCml BAL fluid, P , 0.05) and returned to baseline 1 week post-race (149.2 ^ 46.2 £ 10 RBCml BAL fluid, P . 0.05 versus baseline). The number of haemosiderophages was not different for any of the measurement periods. The [WBC] in the BAL fluid decreased from baseline and race values at 2, 3 and 4 weeks post-exercise (all P , 0.05). Alveolar neutrophil concentrations were also decreased from baseline and immediate post-race values for 4 weeks post-race. The increased [RBC] in the BAL fluid post-exercise is consistent with the presence of EIPH in these greyhounds. However, the relative extent of EIPH in greyhounds (as indexed by [RBC] in the BAL fluid), as compared with that in the horse, was mild, and the lack of elevation of WBC suggests that, unlike their equine counterparts, inflammatory airway disease was absent.