Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses

2010 ◽  
Vol 32 (6) ◽  
pp. 546-550 ◽  
Author(s):  
M. MANOHAR ◽  
T. E. GOETZ ◽  
P. ROTHENBAUM ◽  
S. HUMPHREY
1996 ◽  
Vol 81 (4) ◽  
pp. 1589-1593 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz

Manohar, Murli, and Thomas E. Goetz. Pulmonary vascular pressures of exercising Thoroughbred horses with and without endoscopic evidence of EIPH. J. Appl. Physiol.81(4): 1589–1593, 1996.—Exercise-induced pulmonary hemorrhage (EIPH) is a common occurrence in racehorses. The objective of this study was to compare pulmonary vascular pressures of healthy Thoroughbred horses with and without postexertion endoscopically detectable fresh blood in the trachea. The nasopharynx, larynx, and trachea (down to the carina) of horses were examined weekly with an endoscope 55–60 min postexertion, and the diagnosis of EIPH was confirmed by the presence of fresh blood in the trachea. Measurements of heart rate and right atrial, pulmonary arterial, and pulmonary arterial wedge pressures were made during quiet rest and during treadmill exercise performed at 14.5 m/s on a 5% uphill grade. This workload elicited maximal heart rate of the horses. Mean pulmonary capillary pressure was estimated to be halfway between the mean pulmonary arterial pressure and the mean pulmonary arterial wedge pressure. These data from 7 healthy sound exercise-trained horses that were positive on 12 consecutive occasions (at 1-wk intervals) for the postexercise presence of fresh blood in the trachea were compared with those in 8 healthy horses that were consistently negative for the evidence of fresh blood in the trachea on postexercise endoscopic examination over 12–16 wk. The heart rate and the right heart and/or pulmonary vascular pressures in the two groups of horses were similar at rest. Exercise was attended by a large significant ( P < 0.05) increase in these pressures and heart rate in both groups. However, statistically significant differences between endoscopically EIPH-positive and endoscopically EIPH-negative horses for heart rate and right atrial and pulmonary vascular pressures were not found during exercise. Thus these data revealed that the magnitude of exercise-induced right atrial as well as pulmonary arterial, capillary, and venous hypertension in endoscopically EIPH-positive horses that are otherwise healthy is quite similar to that in endoscopically EIPH-negative horses during comparable exertion.


2005 ◽  
Vol 2 (1) ◽  
pp. 17-25 ◽  
Author(s):  
TS Epp ◽  
P McDonough ◽  
DJ Padilla ◽  
JH Cox ◽  
DC Poole ◽  
...  

AbstractExercise-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 (×106 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<0.05). Thus, these results do not support the use of these herbal formulations in the prevention of EIPH.


1998 ◽  
Vol 84 (6) ◽  
pp. 1902-1908 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz

The present study was carried out to examine the effects of nitric oxide synthase inhibition with N ω-nitro-l-arginine methyl ester (l-NAME) on the right atrial as well as on the pulmonary arterial, capillary, and venous blood pressures of horses during rest and exercise performed at maximal heart rate (HRmax). Experiments were carried out on seven healthy, sound, exercise-trained Thoroughbred horses. Using catheter-tip manometers, with signals referenced at the point of the shoulder, we determined phasic and mean right atrial and pulmonary vascular pressures in two sets of experiments [control (no medications) and l-NAME (20 mg/kg iv given 10 min before exercise studies)]. The studies were carried out in random order 7 days apart. Measurements were made at rest and during treadmill exercise performed on a 5% uphill grade at 6, 8, and 14.2 m/s. Exercise on a 5% uphill grade at 14.2 m/s elicited HRmax and could not be sustained for >90 s. In quietly standing horses,l-NAME administration caused a significant rise in right atrial, as well as pulmonary arterial, capillary, and venous pressures. This indicates that nitric oxide synthase inhibition modifies the basal pulmonary vasomotor tone. In both treatments, exercise caused progressive significant increments in right atrial and pulmonary vascular pressures, but the values recorded in the l-NAME study were not different from those in the control study. The extent of exercise-induced tachycardia was significantly decreased in thel-NAME study at 6 and 8 m/s but not at 14.2 m/s. Thus, l-NAME administration may not modify the equine pulmonary vascular tone during exercise at HRmax. However, as indicated by a significant reduction in heart rate,l-NAME seems to modify the sympathoneurohumoral response to submaximal exercise.


2001 ◽  
Vol 91 (6) ◽  
pp. 2674-2678 ◽  
Author(s):  
Casey A. Kindig ◽  
Paul McDonough ◽  
Melissa R. Finley ◽  
Brad J. Behnke ◽  
Troy E. Richardson ◽  
...  

In horses, the exercise-induced elevation of pulmonary arterial pressure (Ppa) is thought to play a deterministic role in exercise-induced pulmonary hemorrhage (EIPH), and thus treatment designed to lower Ppa might reasonably be expected to reduce EIPH. Five Thoroughbred horses were run on a treadmill to volitional fatigue (incremental step test) under nitric oxide (NO; inhaled 80 ppm) and control (N2, same flow rate as per NO run) conditions (2 wk between trials; order randomized) to test the hypothesis that NO inhalation would reduce maximal Ppa but that this reduction may not necessarily reduce EIPH. Before each investigation, a microtipped pressure transducer was placed in the pulmonary artery 8 cm past the pulmonic valve to monitor Ppa. EIPH severity was assessed via bronchoalveolar lavage (BAL) 30 min postrun. Exercise time did not differ between the two trials ( P > 0.05). NO administration resulted in a small but consistent and significant reduction in peak Ppa (N2, 102.3 ± 4.4; NO, 98.6 ± 4.3 mmHg, P < 0.05). In the face of lowered Ppa, EIPH severity was significantly higher in the NO trial (N2, 22.4 ± 6.8; NO, 42.6 ± 15.4 × 106 red blood cells/ml BAL fluid, P < 0.05). These findings support the notion that extremely high Ppa may reflect, in part, an arteriolar vasoconstriction that serves to protect the capillary bed from the extraordinarily high Ppa evoked during maximal exercise in the Thoroughbred horse. Furthermore, these data suggest that exogenous NO treatment during exercise in horses may not only be poor prophylaxis but may actually exacerbate the severity of EIPH.


2001 ◽  
Vol 91 (3) ◽  
pp. 1396-1400 ◽  
Author(s):  
Casey A. Kindig ◽  
Paul McDonough ◽  
Gus Fenton ◽  
David C. Poole ◽  
Howard H. Erickson

The purpose of this investigation was to study the effects of an equine nasal strip (NS), furosemide (Fur), and a combination of both (NS + Fur) on exercise-induced pulmonary hemorrhage (EIPH) at speeds corresponding to near-maximal effort. Five Thoroughbreds (526 ± 25 kg) were run on a flat treadmill from 7 to 14 m/s in 1 m · s−1 · min−1 increments every 2 wk (treatment order randomized) under control (Con), Fur (1 mg/kg iv 4 h prior), NS, or NS + Fur conditions. During each run, pulmonary arterial (Ppa) and esophageal (Pes) pressures were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) 30 min postrun. Furosemide (Fur and NS + Fur trials) reduced peak Ppa ∼7 mmHg compared with Con ( P < 0.05) whereas NS had no effect ( P > 0.05). Maximal Pes swings were not different among groups ( P > 0.05). NS significantly diminished EIPH compared with the Con trial [Con, 55.0 ± 36.2; NS, 30.8 ± 21.8 × 106 red blood cells (RBC)/ml BAL fluid; P < 0.05]. Fur reduced EIPH to a greater extent than NS (5.2 ± 3.0 × 106 RBC/ml BAL; P < 0.05 vs. Con and NS) with no additional benefit from NS + Fur (8.5 ± 4.2 × 106 RBC/ml BAL; P > 0.05 vs. Fur, P < 0.05 vs. Con and NS). In conclusion, although both modalities (NS and Fur) were successful in mitigating EIPH, neither abolished EIPH fully as evaluated via BAL. Fur was more effective than NS in constraining the severity of EIPH. The simultaneous use of both interventions appears to offer no further gain with respect to reducing EIPH.


1963 ◽  
Vol 204 (6) ◽  
pp. 987-990 ◽  
Author(s):  
J. Albrecht Koehler ◽  
Theofilos J. Tsagaris ◽  
Hiroshi Kuida ◽  
Hans H. Hecht

The demonstration in a previous study of the effectiveness of an antihistaminic drug in blocking some of the systemic but not the pulmonary vascular effects of endotoxin led to the study of the effect of an inhibitor of serotonin synthesis, alpha-methyl 3,4-dihydroxyphenylalanine (α-m dopa). One group of seven dogs was pretreated with a single dose of 250 mg, and a second group of six animals with three doses of 250 mg, each given at 10-min intervals. Results in these two groups were compared with those in six control animals. Purified E. coli endotoxin, 1 mg/kg, was administered intravenously in all 19 experiments. Intravenous administration of α-m dopa alone had no effect on measured physiologic parameters. Compared with the endotoxin response in control animals, pretreatment with either dose level appeared to have no effect on the magnitude or duration of systemic arterial hypotension, portal venous hypertension, or drop in cardiac output. However, pretreatment with 250-mg and 750-mg doses was associated with significant reduction and abolition, respectively, of pulmonary arterial hypertension. The results are consistent with the interpretation that the pulmonary vasoconstrictive response to endotoxin is mediated through the release of serotonin and that α-m dopa blocks this response by interfering with the synthesis of this intermediary.


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