Nicardipine dose-dependently reduces the effect of equinatoxin II on coronary flow in isolated porcine heart.

Death after i.v. administration of equinatoxin II (EqT II) has been attributed to the circulatory failure resulting from cardiotoxic effects. The mechanism of action is unknown. The aim of the present work was to study the effects of the toxin on vascular tone in the isolated porcine coronary artery and on coronary flow in the isolated pig heart. EqT II caused concentration-dependent contractions of rings of the isolated epicardial porcine coronary artery with an EC value of 89±5 nM (n=5-6) and maximal effect of about 140% of the contraction induced by 20 nM KCl. On Langendorff's porcine heart preparation EqT II caused a dose-dependent decrease of coronary flow. At EqT II doses lower than 0.05 μmol/100 g of heart weight there were no measurable effects of the toxin. At dose 0.5 μmol/100 g the toxin decreased coronary flow to less than 9.8±2.5 % of the control value. The constrictory effect of the toxin on isolated porcine coronary arteries was diminished by the L-type calcium channel antagonist nicardipine (NC). NC in 1 μM concentration almost completely abolished the effect of EqT II on coronary flow. Our results confirmed involvement of L-type calcium channels in the vasoconstrictory effects of EqT II on epicardial coronary arteries.