title: 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.
authors.affiliation: Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. mmanohar@uiuc.edu
authors.forename: M
authors.initials: M
authors.lastname: Manohar
authors.forename: T E
authors.initials: TE
authors.lastname: Goetz
authors.forename: A S
authors.initials: AS
authors.lastname: Hassan
mesh_terms: D000818:Animals; D001831:Body Temperature; D002245:Carbon Dioxide / Q000097:blood; D004724:Endoscopy; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006454:Hemoglobins; D006734:Horse Diseases / Q000503:physiopathology; D006736:Horses / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology* / Q000662:veterinary*; D007275:Injections, Intravenous; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D010805:Physical Conditioning, Animal / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D013546:Sweating; D014132:Trachea
chemical_list: D004791:Enzyme Inhibitors; D006454:Hemoglobins; D002245:Carbon Dioxide; D019001:Nitric Oxide Synthase; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester