[Disorders of supporting mechanisms of resting membrane potentials of the cardiomyocytes during stress and their prevention]. / Narushenie mekhanizmov podderzhaniia potentsiala pokoia membran kardiomiotsitov pri stresse i ikh preduprezhdenie.

Incubation of the rats' hearts in low temperature (4 degrees C) in the course of 1.5 h reduced the rest membrane potential (RP) of the cardiomyocytes from 86 +/- 2 to 60 +/- 2 mv. Rapid rewarming to 36 degrees C resulted in hyperpolarization of the membrane potential to 103 +/- 3 mv with maximal speed of restitution of RP about 0.35 mv/sec. These results were determined by electrogenic Na-pump. In the heart of rats, exposed to 6-hour immobilization stress, the speed of restitution of RP decreased to 0.15 +/- 0.01 mv/sec and the hyperpolarization effect was eliminated. This was indicated on the disturbance of Na-pump of the cardiomyocytes membranes. Preliminary treatment with gamma-hydroxybutyric acid or antioxidants alpha-tocopherol and ionol prevented stress-induced disturbances of the cardiomyocytes.

[Effect of stress on the cardiomyocyte transmembrane potential of the working heart and its recovery after hypothermia]. / Vliianie stressa na transmembrannyi potentsial kardiomiotsitov rabotaiushchego serdtsa i ego vosstanovlenie posle gipotermii.

Emotional-painful stress in rats was shown to decrease insignificantly transmembrane cardiomyocyte potential (TCP) measured in isolated hearts. The recovery of TCP following its depression due to the preparation cooling was twice slower in stress-exposed than in control animals. This is in keeping with the data on stress-induced disturbances of Na, K-ATPase activity (an enzyme playing a leading role in TCP maintenance). It is suggested that the disturbance in cation pump function activity plays a certain role in the onset of arrhythmias and cardiac fibrillation during stress.