[Effect of stress on the cardiomyocyte transmembrane potential of the working heart and its recovery after hypothermia].
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.
D000818:Animals; D006321:Heart / Q000503:physiopathology*; D007035:Hypothermia / Q000503:physiopathology*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D013315:Stress, Psychological / Q000503:physiopathology*; D013696:Temperature; D013997:Time Factors
D007473:Ion Channels; D012964:Sodium; D011188:Potassium
Vliianie stressa na transmembrannyĭ potentsial kardiomiotsitov rabotaiushchego serdtsa i ego vosstanovlenie posle gipotermii.