Document Detail


Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.
MedLine Citation:
PMID:  10773245     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
C A Kindig; L L Gallatin; H H Erickson; M R Fedde; D C Poole
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Respiration physiology     Volume:  120     ISSN:  0034-5687     ISO Abbreviation:  Respir Physiol     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-07-28     Completed Date:  2000-07-28     Revised Date:  2009-11-11    
Medline Journal Info:
Nlm Unique ID:  0047142     Medline TA:  Respir Physiol     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  151-66     Citation Subset:  IM    
Affiliation:
Departments of Anatomy and Physiology and Kinesiology, Veterinary Medical Sciences, 1600 Denison Avenue, Kansas State University, Manhattan, KS 66506-5602, USA.
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MeSH Terms
Descriptor/Qualifier:
Acid-Base Equilibrium / drug effects
Animals
Blood Physiological Phenomena
Body Temperature / drug effects
Enzyme Inhibitors / pharmacology*
Gases / blood
Heart / drug effects*,  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 Support
ID/Acronym/Agency:
HL17731/HL/NHLBI NIH HHS; HL50306/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Gases; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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