Racetrack exercise vs treadmill exercise with respect to exercise-induced pulmonary haemorrhage (EIPH): implications for studies of putative treatments of EIPH

2019 ◽  
Vol 15 (5) ◽  
pp. 313-318
Author(s):  
L.M. Warlick ◽  
C.M. Lopez ◽  
R.H. Sides ◽  
W.M. Bayly

Multiple treadmill-based studies using low numbers of horses have evaluated potential prophylactic treatments for exercise-induced pulmonary haemorrhage (EIPH) and found no effect. However, the relevance of these findings to racing is unclear. Because severity of EIPH incurred on treadmills has not been compared to that following high-speed racetrack exercise in the same horses, we retrospectively performed this comparison using bronchoalveolar lavage fluid red cell numbers (BALFRBC) due to the relative insensitivity of tracheobronchoscopy. Six race-fit Thoroughbreds with recent tracheobronchoscopic EIPH scores ≥2 were exercised to fatigue on a treadmill at 115% V̇O2max (5% incline, 12.3-14.2 m/s), and maximally on a racetrack over 800 m and 1,100 m with average speeds ranging from 16.4-16.7 and 15.5-16.6 m/s, respectively. Run order varied but was not randomised. Bronchoalveolar lavage (BAL) was performed blindly using Bivona tubes 45-60 mins post-exercise. BALFRBC were determined using a haemocytometer. Data were expressed as median and interquartile range, and analysed using RM ANOVA with significance set at P<0.05. BALFRBC were greater after both racetrack runs than after treadmill exercise (P<0.05; treadmill: 10,305/μl (3,871-26,079); 800m: 25,000/μl (17,175-73,400); 1,100m: 19,500/μl (8,962-800,600). Treadmill exercise resulted in lower numbers and a narrower range in BALFRBC than racetrack exercise. Thus, when a small number of horses is used to study EIPH treatments on a treadmill, a lower BALFRBC would be anticipated following the baseline run than with a similar study using racetrack exercise, and might reduce the likelihood of demonstrating significant treatment effects. Results of this retrospective study raise concern regarding the advisability of extrapolating conclusions regarding efficacy of EIPH treatments from treadmill studies to racetrack scenarios.

1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.


Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S286
Author(s):  
Guzin Gursoy ◽  
Sibel Alpar ◽  
Nazire Ucar ◽  
Tulay Bakirci ◽  
Ahmet Aydin ◽  
...  

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