title: 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.
authors.affiliation: Departments of Anatomy and Physiology and Kinesiology, Veterinary Medical Sciences, 1600 Denison Avenue, Kansas State University, Manhattan, KS 66506-5602, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Kindig
authors.forename: L L
authors.initials: LL
authors.lastname: Gallatin
authors.forename: H H
authors.initials: HH
authors.lastname: Erickson
authors.forename: M R
authors.initials: MR
authors.lastname: Fedde
authors.forename: D C
authors.initials: DC
authors.lastname: Poole
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D001790:Blood Physiological Phenomena; D001831:Body Temperature / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005740:Gases / Q000097:blood; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010101:Oxygen Consumption / Q000187:drug effects; D012119:Respiration / Q000187:drug effects*; D013318:Stroke Volume / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D005740:Gases; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester