Reperfusion endotoxin eye damage in experimental study

Aim. To evaluate the level of endogenous intoxication in the blood and the status of the lipid peroxidation processes in eye tissues of experimental animals after acute circulatory arrest. Methods. Chronic (5 weeks) pathophysiological experiments were performed in 72 nonlinear mature male rats, in which acute circulatory arrest was modeled by neurovascular heart bundle compression, followed by resuscitation. Endogenous intoxication intensity was assessed using endogenous intoxication integral index based on the detection of oligopeptides and low and medium molecular weight substances. Free radical oxidation in eye tissues was assessed by determining the level of 2’-thiobarbituric acid-reactive products, as well as by chemiluminescence. The condition of antioxidant system was investigated by catalase activity features and reduced glutathione level. Results. There was a significant two-phased increase of endogenous intoxication index during the whole postoperative period. Fe2+-induced chemiluminescence with subsequent accumulation of lipid peroxidation secondary metabolites, as well as increased activity of catalase protective system both in early stages (days 1-3) and on the second week were revealed in eye tissues. A positive correlation of endogenous intoxication integral index and the level of 2’-thiobarbituric acid-reactive products on the first day after resuscitation was revealed. Conclusion. Endogenous intoxication syndrome is formed after the acute circulatory arrest with maximal levels of endogenous toxins in the systemic circulation on 1-3rd and on 10-14th day after resuscitation, as well as with significant intensification of lipid peroxidation processes in eye tissues at the same period.