Stopping of spontaneous beating of cultured mouse and rat myocardial cells by a toxin (thermostable direct hemolysin) from Vibrio parahaemolyticus.
Low concentrations of thermostable direct hemolysin from Vibrio parahaemolyticus stopped the spontaneous beating of cultured mouse and rat myocardial cells. These low concentrations depolarized the maximal diastolic potential and inhibited the generation of action potential of cultured myocardial cells. The toxin lost its activity when preincubated with ganglioside, GT1 or GM1. GT1 was more effective than GM1. High concentrations of the toxin caused morphological damage of cultured mouse and rat myocardial cells, but did not stop the beating, or cause morphological damage of cultured chick myocardial cells.
D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology*; D002478:Cells, Cultured; D004355:Drug Stability; D006321:Heart / Q000502:physiology; D006460:Hemolysin Proteins / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009200:Myocardial Contraction / Q000187:drug effects*; D051381:Rats; D013779:Tetrodotoxin / Q000494:pharmacology; D014736:Vibrio parahaemolyticus
D001427:Bacterial Toxins; D006460:Hemolysin Proteins; D013779:Tetrodotoxin