Effect of Clostridium perfringens alpha toxin on the cardiovascular system of rats.
Clostridium perfringens alpha toxin decreased heart rate, then elevated blood pressure, and finally caused some changes of electrocardiogram readings. The toxin decreased peripheral blood flow before blood pressure started to increase and the blood flow continued to decrease, without any affect on electrocardiogram readings, until the maximal pressure rise caused by the toxin. The toxin caused a rise in blood pressure in a dose-dependent manner. On the other hand, anti-alpha toxin antiserum inhibited both phospholipase C activity and pressor activity. When the toxin was pretreated with cysteine, calcium disodium ethylenediamine tetraacetate and calcium trisodium ethylenetriamine pentaacetate, pressor activity decreased, as well as phospholipase C activity. The results indicate that alpha toxin possesses pressor activity as well as phospholipase C activity.
D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity*; D001794:Blood Pressure / Q000187:drug effects; D002135:Calcium-Binding Proteins; D004562:Electrocardiography; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D051381:Rats; D012039:Regional Blood Flow / Q000187:drug effects; D012867:Skin / Q000098:blood supply; D010738:Type C Phospholipases / Q000032:analysis
D001427:Bacterial Toxins; D002135:Calcium-Binding Proteins; D010738:Type C Phospholipases; C040649:alpha toxin, Clostridium perfringens