Original Research
Higher Lipid Peroxidation Indices in Horses Eliminated from Endurance Race Because of Synchronous Diaphragmatic Flutter (Thumps)

https://doi.org/10.1016/j.jevs.2008.08.007Get rights and content

Abstract

Eighteen racing horses from a total of 85 horses that participated in a long-distance (120-km) race were used for this study. The 18 horses that were used comprised nine horses that were eliminated from the race at the 90-km checkpoint because of synchronous diaphragmatic flutter (SDF). Another nine horses that passed the 90-km checkpoint were randomly selected and served as a control group (CT). Horses were sampled at three different times (t0, tend, t2weeks). Plasma sodium (Na+), potassium (K+), and chloride (Cl) concentrations were decreased at the end of the race to insignificant levels. A significant reduction (P ≤ .05) was observed in the ionized calcium (Ca++). Lipid peroxide (LPO) and malondialdehyde (MDA) concentrations in plasma were higher compared with values obtained before the start of the race. In SDF-eliminated horses, these parameters were higher than in the control horses. Glutathione peroxidase (GSH-Px) activity was significantly lower at the end of the race, whereas creatine phosphokinase (CPK) was similarly increased fourfold in both groups. A significant increase in lactate concentration was seen in both groups; however, this parameter was significantly higher in the SDF-eliminated horses than in the control group. Statistical significance (P < .01) was observed between LPO and MDA levels and the Ca++ concentration in the SDF group at the three sampling points. This study established elevated lipid peroxidation product level as one component of the biochemical characteristics of SDF. The low level of Ca++ in plasma of horses was associated with high levels of lipid peroxidation indexes.

Introduction

Synchronous diaphragmatic flutter (SDF) is a disease of horses characterized by increased neuromuscular irritability, causing hypersensitivity of the phrenic nerve. Electrical activity occurring when the heart beats stimulates the phrenic nerve, which passes over the heart, resulting in a contraction of the diaphragm with each beat of the heart.1 This condition is manifested clinically as sudden bilateral or unilateral movement of the flanks of the horse at the same frequency as the heart rate. Sometimes the rhythmic movement also occurs in hind legs.1 A loss of calcium ions (Ca++) in the blood serum is the cause of SDF.1, 2

High work intensity can increase heat production 40-fold to 60-fold over basal metabolism.3 The major pathway for heat loss in the horse is sweating. The volume of heat loss and sweating depends on the work expended, which is increased by distance. A horse may lose 20 to 40 L fluid in long distance races.4 This fluid loss is accompanied by an obligatory loss of minerals and electrolytes. Loss of Na+, K+, and Cl ions because of excessive sweating reduces the thirst response and leads to further dehydration. Sweating also results in excessive Ca++ loss; the dehydrated horse begins to show clinical signs of Ca++ deficiency, such as muscle twitching and spasms.5 It is reported that, in normal healthy horses, excessive dehydration or excessive work may result in a lack of energy, causing loss of function of the Ca++ pump.1

A number of studies have reported that exhaustive endurance races induce accelerated generation of reactive oxygen species (ROS). ROS result in lipid peroxidation, which induces adverse effects on the health status and performance of horses.6, 7, 8

Studies suggest that both lipid peroxidation and Ca++ are important contributors to cell damage caused by physical injury or ischemia. This may act synergistically to damage biologic membranes.9, 10 The possible interaction between those two factors has not, until recently, been addressed. It is known that, shortly after the onset of ischemia or physical injury, the extracelluler Ca++ concentration falls dramatically, resulting in intracellular Ca++ accumulation.11, 12 Intracellular Ca++ mobilization increases free Ca++ concentration in the cytoplasm, causing activation of some Ca++-dependent membrane phospholipases. Phospholipase A2 breaks down phosphatidylinositols at the site of membrane cyclooxygenase localization, resulting in release of arachidonic acid that enables cyclooxygenase activation. Hence, cyclooxygenase itself is not Ca++ dependent, but any increase of intracellular free Ca++ is critical for its activation.13, 14

Cells can tolerate mild oxidative stress and often respond by raising their levels of antioxidant defenses. However, severe oxidative stress and free radicals produce serious disturbances in cellular structure and metabolism.15 The intracellular levels of calcium ions are very low; they transiently increase in response to several factors producing important metabolic changes.16 Oxidative stress can damage the protein that keeps intracellular Ca++ low, causing an increase in the level of Ca++. If the Ca++ level rises too high, it can activate enzymes that may damage the DNA and cleave structural proteins within the cell.17

The aim of this study was to assess the possible relationship between low plasma calcium level and elevation in lipid peroxidation products (lipid peroxide [LPO] and malondialdehyde [MDA]) and the intrinsic antioxidant enzyme glutathione peroxidase (GSH-Px) in horses suffering from SDF during a long distance endurance ride.

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Description of Endurance Race

The Wadi-Rum endurance race is held yearly in early October, with an ambient temperature ranging from 15°C to 25°C and relative humidity ranging from 30% to 32% (Jordanian Department of Meteorology). Participating horses were fed a diet consisting of barley, oat, corn, and hay. Water was provided ad libitum. Owners were allowed to provide supplemental feed and salts to their horses. Information on supplementation of horse diets with antioxidant compounds, such as vitamin E or selenium, was not

Results

Erythrocyte counts, leukocyte counts, and hematocrit and hemoglobin values of horses at the end of the race were significantly increased (P < 0.05) when compared with pre-race values. These values returned to their normal physiologic levels within 23 weeks after the end of the race (Table 1).

There were no significant differences detected among the two groups at any sampling time for sodium, potassium, and chloride concentration (Table 1). These parameters decreased in both control and

Discussion

During a prolonged endurance ride, a horse can lose 25 to 50 liters of fluid. This causes hemoconcentration and severe reduction in muscular capacity. It also results in losing ions such as Na+, K+, Ca++, and Cl, causing some degree of neuromuscular irritability.1, 2 Evidence of hemoconcentration, including the changes in hemoglobin, packed-cell volume, and red blood cells observed in this study were obviously attributable to significant changes in plasma volume as a result of dehydration and

References (38)

  • Coffman J. Normal and abnormal clinical pathology. Proceedings 7th Annual Meeting Association of Equine Sports...
  • N. McMeniman et al.

    Effect of vitamin E status on lipid peroxidation in exercised horses

    Equine Vet J

    (1992)
  • L. Avellini et al.

    Training-induced modification in some biochemical defenses against free radicals in equine erythrocytes

    Vet Res Comm

    (1995)
  • J. Braughler

    Calcium and lipid peroxidation

    Proc Oxygen Radical/Upjohn Symposium

    (1987)
  • K. Al-Qudah et al.

    Status of biochemical and antioxidant variables in horses before and after long distance race

    Rev Médecine Vét

    (2006)
  • J. Farber

    Biology of disease: membrane injury and calcium homeostasis in the pathogeneses of coagulative necrosis

    Lab Invest

    (1982)
  • A. Anosov et al.

    Calcium-induced stimulation of cyclooxygenase in rabbit leukocytes and its modulation by ultraviolet radiation

    Russ J Immunol

    (1997)
  • A. Au et al.

    Stimulation of phospholipase A2 activity by oxygen-derived free radicals in isolated brain capillaries

    J Cell Biochem

    (1985)
  • P. Nicotera et al.

    Calcium-mediated mechanisms in chemically induced cell death

    Ann Rev Pharmacol Tocicol

    (1992)
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