Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses.
Abstract: Because sensitivity of equine pulmonary vasculature to endogenous as well as exogenous nitric oxide (NO) has been demonstrated, we examined whether endogenous NO production plays a role in exercise-induced arterial hypoxemia. We hypothesized that inhibition of NO synthase may alter the distribution of ventilation-perfusion mismatching, which may affect the exercise-induced arterial hypoxemia. Arterial blood-gas variables were examined in seven healthy, sound Thoroughbred horses at rest and during incremental exercise protocol leading to galloping at maximal heart rate without (control; placebo = saline) and with N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (20 mg/kg iv). The experiments were carried out in random order, 7 days apart. At rest, L-NAME administration caused systemic hypertension, pulmonary hypertension, and bradycardia. During 120 s of galloping at maximal heart rate, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, hyperthermia, and acidosis occurred in the control as well as in NO synthase inhibition experiments. However, statistically significant differences between the treatments were not found. In both treatments, exercise caused a significant rise in hemoglobin concentration, but the increment was significantly attenuated in the NO synthase inhibition experiments, and, therefore, arterial O(2) content (Ca(O(2))) increased to significantly lower values. These data suggest that, whereas L-NAME administration does not affect pulmonary gas exchange in exercising horses, it may affect splenic contraction, which via an attenuation of the rise in hemoglobin concentration and Ca(O(2)) may limit performance at higher workloads.
Publication Date: 2001-08-18 PubMed ID: 11509505DOI: 10.1152/jappl.2001.91.3.1105Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- Non-P.H.S.
Summary
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The research article focuses on determining the role of endogenous nitric oxide (NO) production in arterial hypoxemia experienced by Thoroughbred horses during exercise. The study found no significant alterations in the exercise-induced arterial hypoxemia, despite the inhibition of NO synthase.
Research Methodology
- The research involved studying arterial blood-gas variables in seven healthy Thoroughbred horses.
- The horses were monitored while at rest and also during increasing exercise intensity leading to galloping at their maximum heart rate.
- The tests were performed under control conditions and with the administration of L-NAME which inhibits the production of nitric oxide.
- Two sets of experiments were conducted, one week apart, on a random order basis.
Findings and Interpretations
- Administration of L-NAME, at rest, resulted in systemic hypertension, pulmonary hypertension, and slower heart rate.
- During a 120 second period of galloping at maximum heart rate, significant arterial hypoxemia, hemoglobin desaturation, hypercapnia, increased body temperature, and acidosis were observed. These symptoms occurred irrespective of whether nitric oxide synthase was inhibited or not.
- There was no statistically significant difference found between the control and NO synthase inhibited treatments. However, the increase in hemoglobin concentration caused by exercise was significantly tempered in the NO synthase inhibition experiments, leading to a noticeable decrease in the increment of arterial oxygen content.
Implications of Findings
- The results indicate that, while L-NAME administration does not affect pulmonary gas exchange in exercising horses, it could affect the contraction of the spleen.
- This effect on the spleen could in turn reduce the rise in hemoglobin concentration and arterial oxygen content, potentially limiting the performance of the horses at higher workloads.
Cite This Article
APA
Manohar M, Goetz TE, Hassan AS.
(2001).
Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses.
J Appl Physiol (1985), 91(3), 1105-1112.
https://doi.org/10.1152/jappl.2001.91.3.1105 Publication
Researcher Affiliations
- Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. mmanohar@uiuc.edu
MeSH Terms
- Animals
- Body Temperature
- Carbon Dioxide / blood
- Endoscopy
- Enzyme Inhibitors / pharmacology
- Female
- Hemoglobins
- Horse Diseases / physiopathology
- Horses / physiology
- Hydrogen-Ion Concentration
- Hypoxia / physiopathology
- Hypoxia / veterinary
- Injections, Intravenous
- Male
- NG-Nitroarginine Methyl Ester / pharmacology
- Nitric Oxide Synthase / antagonists & inhibitors
- Oxygen / blood
- Partial Pressure
- Physical Conditioning, Animal / physiology
- Physical Exertion / physiology
- Sweating
- Trachea
Citations
This article has been cited 2 times.- Tennent-Brown BS, Goetz TE, Manohar M, Hassan AS, Freeman DE, Bundy JS, Evans MR. Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses. Eur J Appl Physiol 2006 Jul;97(4):462-70.
- Manohar M, Goetz TE, Hassan AS. Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses. Eur J Appl Physiol 2005 Jan;93(4):480-8.
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