Equinatoxin, a lethal protein from Actinia equina—II. Pathophysiological action

Abstract

Effects of lethal doses of a toxic protein from Actinia equina were studied on anesthetized rats. The electrical activity of the phrenic nerves, the respiratory movements, the mechanical activity of the heart, the ECG, and the arterial blood pressure on intact, vagotomized and artificially respired animals were recorded. Shortly (15–50 sec) after beginning the i.v. injection of equinatoxin, the trains of action potentials in the phrenic nerve disappeared and respiration stopped. Bradycardia was observed, indicating elevated vagal tone. A transient fall of arterial blood pressure in vagotomized and in intact animals was registered for 10–15 sec, simultaneously with the block of respiration; thereafter an elevation of arterial blood pressure was registered for 3–7 min. The elevation of the arterial blood pressure was also observed in artificially respired animals. No spontaneous respiratory movements were registered during the period of elevated arterial blood pressure. The diaphragm remained excitable when stimulated indirectly via the phrenic nerve. Conduction disturbances, ectopic foci, myocardial ischemia, negative inotropic and negative chronotropic actions were followed on the ECG and on the in situ exposed heart.