Estimation of Nitrite—Nitric Oxide Derivative—In Horses with Intestinal Colic by ESR Spectroscopy

Abstract

Diseases of the gastrointestinal tract of horses are caused by many factors and have a complex pathogenesis. Developing effective methods of differential diagnostics is of high fundamental and applied importance. The pathogenesis of diseases of the digestive tract of horses accompanied by the development of inflammation and oxidative stress, can be associated with a lack of the nitrogen monoxide which controls many signaling pathways in the body. The level of the nitric oxide (NO) is involved in the regulation of the immune and nervous systems, the tone of all the blood vessels, and the courses of many pathological processes. The nitric oxide activates guanylate cyclase (sGC) and leads to vascular relaxation. The aim of this investigation was to study the metabolites of nitric oxide in horses suffered from intestinal diseases. The levels of nitric oxide in the blood serum of horses depending on their age and health state was studied. The concentration of nitrites in the blood serum of horses aged 6–25 years was 3.4 ± 4.2 μM, and in the young horses (1–5 years) the level of this indicator was 8.2 ± 5.4 μM. A sharp decrease in nitrite was observed in all the horses with intestinal diseases of 2 ± 0.9 μM, especially with tympanitic caecun of 0.6 ± 0.4 μM and with spasmodic colic of 1.8 ± 0.5 μM. The level of nitrosylhemoglobin HbNO in the blood of the diseased animals was higher than that in clinically healthy horses, regardless of age.

Association of the severity of colic in horses with oxidative stress biomarkers, acute-phase proteins, and certain trace elements

“…Moreover, mononuclear phagocytes release NO following inflammatory conditions. NO has anti-inflammatory properties, but following the production of reactive compounds such as nitrite peroxide, detrimental repercussions may occur [ 2 ]. MDA might be an indicator of intestinal ischemia and rebleeding, which is an oxidative stress factor produced as a byproduct of fat cell peroxidation.…”