Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.
Abstract: To investigate the role of nitric oxide, NO, in facilitating cardiorespiratory function during exercise, five horses ran on a treadmill at speeds that yielded 50, 80 and 100% of peak pulmonary oxygen uptake (V(O(2)) peak) as determined on a maximal incremental test. Each horse underwent one control (C) and one (NO-synthase inhibitor; N(G)-L-nitro-arginine methyl ester (L-NAME), 20 mg/kg) trial in randomized order. Pulmonary gas exchange (open flow system), arterial and mixed-venous blood gases, cardiac output (Fick Principle), and pulmonary and systemic conductances were determined. L-NAME reduced exercise tolerance, as well as cardiac output (C, 291+/-34; L-NAME, 246+/-38 L/min), body O(2) delivery (C, 74.4+/-5. 5; L-NAME, 62.1+/-5.6 L/min), and both pulmonary (C, 3.07+/-0.26; L-NAME, 2.84+/-0.35 L/min per mmHg) and systemic (C, 1.55+/-0.24; L-NAME, 1.17+/-0.16 L/min per mmHg) effective vascular conductances at peak running speeds (all P<0.05). On the 50 and 80% trials, L-NAME increased O(2) extraction, which compensated for the reduced body O(2) delivery and prevented a fall in V(O(2)). However, at peak running speed in the L-NAME trial, an elevated O(2) extraction (P<0. 05) was not sufficient to prevent V(O(2)) from falling consequent to the reduced O(2) delivery. At the 50 and 80% running speeds (as for peak), L-NAME reduced pulmonary and systemic effective conductances. These data demonstrate that the NO synthase inhibitor, L-NAME, induces a profound hemodynamic impairment at submaximal and peak running speeds in the horse thereby unveiling a potentially crucial role for NO in mediating endothelial function during exercise.
Publication Date: 2000-04-25 PubMed ID: 10773245DOI: 10.1016/s0034-5687(00)00096-7Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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This research investigates how the inhibition of nitric oxide, a molecule associated with regulating bodily functions, affects the cardiovascular and respiratory functionality of a horse during exercise. The investigation found that suppressing nitric oxide production led to a decrease in exercise tolerance, cardiac output, oxygen distribution, and vascular conductance; implying it plays a crucial role in managing bodily systems during activity.
Introduction of the Study
- This study aimed to understand the role of nitric oxide (NO) in facilitating cardiorespiratory function during exercise by using horses as the experimental model.
- Nitric oxide is a vital molecule involved in many physiological and pathological processes. It is known to mediate diverse functions in the cardiovascular, nervous, and immune systems.
- The researchers used the nitric oxide synthase inhibitor N(G)-L-nitro-arginine methyl ester (L-NAME) to suppress nitric oxide production in the horses and observed changes in vital exercise parameters.
Methodology
- Five horses were made to run on a treadmill at speeds that drew out 50%, 80%, and 100% of their peak pulmonary oxygen uptake.
- Each horse underwent two tests – one control run and one after being administered L-NAME, in a randomized fashion.
- During these exercises, various cardiorespiratory parameters such as pulmonary gas exchange, arterial and mixed-venous blood gases, cardiac output and pulmonary and systemic conductances were monitored.
Key Findings
- L-NAME reduced exercise tolerance in horses and effectively decreased their cardiac output and body’s oxygen delivery mechanism.
- Additionally, L-NAME also lowered pulmonary and systemic effective vascular conductances in horses.
- At 50% and 80% exercise levels, the horses’ bodies compensated for the reduced oxygen delivery by increasing oxygen extraction, thereby preventing a fall in oxygen uptake.
- However, during peak exercise, this compensatory mechanism failed to prevent the fall in oxygen uptake due to diminished oxygen delivery.
Conclusion
- The research concluded that inhibiting NO synthase using L-NAME provokes substantial impairment in circulatory and respiratory dynamics in horses during exercise.
- This information unraveled the potentially crucial role nitric oxide plays in managing endothelial function (cells lining the blood vessels) during exercise.
Cite This Article
APA
Kindig CA, Gallatin LL, Erickson HH, Fedde MR, Poole DC.
(2000).
Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.
Respir Physiol, 120(2), 151-166.
https://doi.org/10.1016/s0034-5687(00)00096-7 Publication
Researcher Affiliations
- Departments of Anatomy and Physiology and Kinesiology, Veterinary Medical Sciences, 1600 Denison Avenue, Kansas State University, Manhattan, KS 66506-5602, USA.
MeSH Terms
- Acid-Base Equilibrium / drug effects
- Animals
- Blood Physiological Phenomena
- Body Temperature / drug effects
- Enzyme Inhibitors / pharmacology
- Gases / blood
- Heart / drug effects
- Heart / physiology
- Heart Rate / drug effects
- Hematocrit
- Male
- Motor Activity / physiology
- NG-Nitroarginine Methyl Ester / pharmacology
- Nitric Oxide Synthase / antagonists & inhibitors
- Oxygen Consumption / drug effects
- Respiration / drug effects
- Stroke Volume / drug effects
Grant Funding
- HL17731 / NHLBI NIH HHS
- HL50306 / NHLBI NIH HHS
Citations
This article has been cited 11 times.- Poole DC, Copp SW, Colburn TD, Craig JC, Allen DL, Sturek M, O'Leary DS, Zucker IH, Musch TI. Guidelines for animal exercise and training protocols for cardiovascular studies. Am J Physiol Heart Circ Physiol 2020 May 1;318(5):H1100-H1138.
- Poole DC, Erickson HH. Exercise-induced pulmonary hemorrhage: where are we now?. Vet Med (Auckl) 2016;7:133-148.
- Hon YY, Lin EE, Tian X, Yang Y, Sun H, Swenson ER, Taveira-Dasilva AM, Gladwin MT, Machado RF. Increased consumption and vasodilatory effect of nitrite during exercise. Am J Physiol Lung Cell Mol Physiol 2016 Feb 15;310(4):L354-64.
- Kenjale AA, Ham KL, Stabler T, Robbins JL, Johnson JL, Vanbruggen M, Privette G, Yim E, Kraus WE, Allen JD. Dietary nitrate supplementation enhances exercise performance in peripheral arterial disease. J Appl Physiol (1985) 2011 Jun;110(6):1582-91.
- Grassi B, Hogan MC, Kelley KM, Howlett RA, Gladden LB. Effects of nitric oxide synthase inhibition by L-NAME on oxygen uptake kinetics in isolated canine muscle in situ. J Physiol 2005 Nov 1;568(Pt 3):1021-33.
- Wilkerson DP, Campbell IT, Jones AM. Influence of nitric oxide synthase inhibition on pulmonary O2 uptake kinetics during supra-maximal exercise in humans. J Physiol 2004 Dec 1;561(Pt 2):623-35.
- Jones AM, Wilkerson DP, Campbell IT. Nitric oxide synthase inhibition with L-NAME reduces maximal oxygen uptake but not gas exchange threshold during incremental cycle exercise in man. J Physiol 2004 Oct 1;560(Pt 1):329-38.
- Jones AM, Wilkerson DP, Koppo K, Wilmshurst S, Campbell IT. Inhibition of nitric oxide synthase by L-NAME speeds phase II pulmonary .VO2 kinetics in the transition to moderate-intensity exercise in man. J Physiol 2003 Oct 1;552(Pt 1):265-72.
- Morgan DR, Silke B, Dixon LJ, Allen PB, Hanratty CG, McVeigh GE. Central and peripheral haemodynamic effects of L-NAME infusion in healthy volunteers. Eur J Clin Pharmacol 2003 Jul;59(3):195-9.
- Njoku CJ, Saville WJ, Reed SM, Oglesbee MJ, Rajala-Schultz PJ, Stich RW. Reduced levels of nitric oxide metabolites in cerebrospinal fluid are associated with equine protozoal myeloencephalitis. Clin Diagn Lab Immunol 2002 May;9(3):605-10.
- Manohar M, Goetz TE, Hassan AS, Rothenbaum P, Humphrey S. Inhibition of nitric oxide synthase with L-NAME does not increase lactate production at rest or during short-term high-intensity exercise in Thoroughbred horses. Vet Res Commun 2001 Aug;25(6):483-94.
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