Способ моделирования нормобарической хронической гипоксии у крыс самцов сток WISTAR

Abstract

BACKGROUND: Hypoxia is a factor of development of many diseases, and, among other things, may be the cause of male infertility. The molecular basis of pathogenesis in hypoxia can serve a basis for the development of methods of treatment and correction. AIM: development of a model of chronic normobaric hypoxia in laboratory animals. MATERIALS AND METHODS: The study involved 32 mature male rats of Wistar line of 200–280 g mass. The animals were divided to 2 experimental groups and their control groups. In the first experimental model, a model of acute normobaric hypoxia with hypercapnia was used one time according to the method of M. V. Korableva and P. I. Lukienko (1976) in modification of N. D. Avseenko, in the second — a model of chronic hypoxia according to the method of acute normobaric hypoxic hypoxia with hypercapnia in our modification: the animals were placed in a hermetically closed chamber of 1.2 liter volume connected to the gas analyzer, and stayed there until the content of oxygen in the air decreased to 10%. Animals of the control groups were placed in ventilated chambers. The experiment was performed daily for 14 days. The activity of cytochrome oxidase (CO), lactate dehydrogenase (LDH) and superoxide dismutase (SOD) in the mitochondrial fraction of seminal vesicles and epididymis was determined. RESULTS: In modeling of acute normobaric hypoxia, the activity of the studied enzymes did not show statistically significant changes. In an experiment with chronic normobaric hypoxia, the activity of SOD and CO was significantly reduced in all the studied tissues, and the activity of LDH — only in the tissues of the epididymis head. CONCLUSION: Changes in the activity of key enzymes of mitochondrial metabolism indicate the adaptation to hypoxia at the cellular and subcellular levels, which proves the effectiveness of the described model for further use in research.