Document Detail

Oxidant injury, nitric oxide and pulmonary vascular function: implications for the exercising horse.
MedLine Citation:
PMID:  12463399     Owner:  NLM     Status:  MEDLINE    
The athletic ability of the horse is facilitated by vital physiological adaptations to high-intensity exercise, including a thin (but strong) pulmonary blood-gas barrier, a large pulmonary functional reserve capacity and a consequent maximum oxygen uptake (VO2max) far higher than in other species. A high pulmonary artery pressure also serves to enhance pulmonary function, although stress failure of lung capillaries at high pulmonary transmural pressures, and the contribution of other factors which act in the exercising horse to increase pulmonary vascular tone, may lead to pathological or pathophysiological sequelae, such as exercise-induced pulmonary haemorrhage (EIPH). Reactive oxygen species (ROS) are an important component of the mammalian inflammatory response. They are released during tissue injury and form a necessary component of cellular defences against pathogens and disease processes. The effects of ROS are normally limited or neutralized by a multifactorial system of antioxidant defences, although excessive production and/or deficient antioxidant defences may expose healthy tissue to oxidant damage. In the lung, ROS can damage pulmonary structures both directly and by initiating the release of other inflammatory mediators, including proteases and eicosanoids. Vascular endothelial cells are particularly susceptible to ROS-induced oxidant injury in the lung, and both the destruction of the pulmonary blood-gas barrier and the action of vasoactive substances will increase pulmonary vascular resistance. Moreover, ROS can degrade endothelium-derived nitric oxide (NO), a major pulmonary vasodilator, thereby, with exercise, synergistically increasing the likelihood of stress failure of pulmonary capillaries, a contributing factor to EIPH. This review considers the implications for the exercising horse of oxidant injury, pulmonary vascular function and NO and the contribution of these factors to the pathogenesis of equine respiratory diseases.
P C Mills; A J Higgins
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Veterinary journal (London, England : 1997)     Volume:  153     ISSN:  1090-0233     ISO Abbreviation:  Vet. J.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  2002-12-04     Completed Date:  2002-12-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9706281     Medline TA:  Vet J     Country:  England    
Other Details:
Languages:  eng     Pagination:  125-48     Citation Subset:  IM    
Equine Centre, Animal Health Trust, PO Box 5, Newmarket, Suffolk, CB8 7DW, UK.
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MeSH Terms
Endothelium / physiology
Hemorrhage / physiopathology,  veterinary*
Horse Diseases / physiopathology*
Horses / physiology*
Lung / blood supply*
Lung Diseases / physiopathology,  veterinary*
Nitric Oxide / adverse effects*
Oxygen Consumption
Physical Conditioning, Animal*
Reactive Oxygen Species / adverse effects*
Respiratory Function Tests / methods,  veterinary
Reg. No./Substance:
0/Reactive Oxygen Species; 10102-43-9/Nitric Oxide
Comment In:
Vet J. 1997 Mar;153(2):119-21   [PMID:  12463397 ]

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

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