Oxidant injury, nitric oxide and pulmonary vascular function: implications for the exercising horse.
Abstract: 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.
Publication Date: 1997-03-01 PubMed ID: 12463399DOI: 10.1016/s1090-0233(97)80034-2Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Review
- Athletic Horses
- Athletic Performance
- Equine Diseases
- Equine Health
- Equine Research
- Equine Science
- Exercise Physiology
- Exercise-Induced Pulmonary Hemorrhage
- Hemorrhage
- Horse Training
- Horses
- Inflammation
- Lung Health
- Nitric Oxide
- Oxidative Stress
- Pathogenesis
- Pathophysiology
- Pulmonary Health
- Respiratory Disease
- Veterinary Medicine
Summary
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This study investigates how oxidant injury, changes in pulmonary vascular function, and nitric oxide could contribute to possible respiratory diseases in exercising horses, emphasizing the complex interplay of these factors and their implications on a horse’s athletic ability.
Pulmonary Adaptations and Consequences in Exercising Horses
- Horses have certain physiological adaptations like a thin, strong pulmonary blood-gas barrier, large pulmonary functional reserve and high maximum oxygen uptake. These adaptations contribute to their athletic capability.
- High pulmonary artery pressure enhances lung function in horses. But, excessive pressure can lead to stress failure of lung capillaries, a condition possibly leading to exercise-induced pulmonary haemorrhage (EIPH) – a pathology commonly found in horses that exert intense efforts.
Role of Reactive Oxygen Species (ROS)
- ROS, an essential part of the mammalian inflammatory response, is released during tissue injury. While these are necessary for cellular defences against pathogens, an overproduction or lack of proper antioxidant defenses can cause oxidant damage to healthy tissues.
- Within the lung, ROS can directly cause damage to structures and initiate the release of other inflaming mediators like proteases and eicosanoids.
Impact on Vascular Endothelial Cells and Nitric Oxide (NO)
- Vascular endothelial cells, found in the lungs, are susceptible to oxidant injury from ROS. Such injuries can potentially lead to the destruction of the pulmonary blood-gas barrier and trigger activities of vasoactive substances, which eventually raises pulmonary vascular resistance.
- ROS can degrade nitric oxide, a vasodilator within the pulmonary circulation. Consequently, the reduced nitric oxide coupled with exercise can increase the chances of stress failure of pulmonary capillaries, another factor contributing to EIPH.
Implications
- The collective influence of oxidant injury, pulmonary vascular function, and nitric oxide levels could contribute to respiratory diseases in exercising horses.
- The findings from this study can help better understand, manage, and potentially prevent the onset of these conditions in horses, particularly active ones.
Cite This Article
APA
Mills PC, Higgins AJ.
(1997).
Oxidant injury, nitric oxide and pulmonary vascular function: implications for the exercising horse.
Vet J, 153(2), 125-148.
https://doi.org/10.1016/s1090-0233(97)80034-2 Publication
Researcher Affiliations
- Equine Centre, Animal Health Trust, PO Box 5, Newmarket, Suffolk, CB8 7DW, UK.
MeSH Terms
- Animals
- Endothelium / physiology
- Hemorrhage / physiopathology
- Hemorrhage / veterinary
- Horse Diseases / physiopathology
- Horses / physiology
- Lung / blood supply
- Lung Diseases / physiopathology
- Lung Diseases / veterinary
- Nitric Oxide / adverse effects
- Oxygen Consumption
- Physical Conditioning, Animal
- Reactive Oxygen Species / adverse effects
- Respiratory Function Tests / methods
- Respiratory Function Tests / veterinary
Citations
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