[Intracellular oxidative-reductive processes in tissues in hyperthermia]. / Vnutrikletochnye okislitel'no-vosstanovitel'nye protsessy v tkaniiakh pri gipertermii.

Experiments were conducted on male albino rats to study some intracellular metabolites (lactate, pyruvate, malate, glutamate, alpha-ketoglutarate, ammonia) and the redox process in the tissues of the liver, kidneys, myocardium, and skeletal muscles during hyperthermia (40 degrees C for one hour and 45 degrees C for one hour). Changes of the metabolite content and shifts in the redox process in the direction of oxidation in the liver and kidneys at both levels of hyperthermia are evidence of the development of tissue hypoxia of circulatory character in these organs. The mitochondrial NAD/NADH ratio in the myocardium reduced in moderate hyperthermia and increased during a heat stroke. There were no signs of cellular hypoxia in the skeletal muscles. It is concluded on basis of the results that changes of the blood flow in the organs play the leading role in the origin of thermal hypoxia.

[The temperature dependence of the respiration and phospholipid content of the mitochondria in the organs of heat-adapted rats]. / Temperaturnaia zavisimost' dykhaniia i fosfolipidnyi sostav mitokhondrii organov u adaptirovannykh k teplu krys.

A shift of breaking point to higher temperatures was illustrated on Arrhenius plots in kidney, liver and heart mitochondria of heat-adapted rats on 4.1, 2.7, 2.4 degrees C respectively. Q10 mitochondrion respiration fall in adapted animals in a range of 26-36 degrees C was indicative of temperature compensation. It was shown the elevation of phospholipid plasmalogen form content in heart and kidney mitochondria; as well as saturated fatty acids content in liver mitochondria. Structure and function changes were suggested to be the basic point of elevation of mitochondrion functional ability at high ambient temperature.