|
|
||||||||
Departments of 1 Veterinary Biosciences and 2 Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801
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
-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
O2 content (CaO2) 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
CaO2 may limit performance at higher workloads.
arterial blood-gas tensions in exercise; N
-nitro-L-arginine methyl ester; exertion
This article has been cited by other articles:
![]() |
M. Manohar and T. E. Goetz Intrapulmonary arteriovenous shunts of >15 {micro}m in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses J Appl Physiol, July 1, 2005; 99(1): 224 - 229. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds J Appl Physiol, April 1, 2004; 96(4): 1349 - 1356. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise J Appl Physiol, June 1, 2003; 94(6): 2135 - 2144. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, A. S. Hassan, T. Depuy, and S. Humphrey Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds J Appl Physiol, July 1, 2002; 93(1): 99 - 106. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, S. Humphrey, and T. Depuy H1-receptor antagonist, tripelennamine, does not affect arterial hypoxemia in exercising Thoroughbreds J Appl Physiol, April 1, 2002; 92(4): 1515 - 1523. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |