Reversal of ventricular contracture during hypothermic cardioplegic arrest.

Ventricular contracture was produced in isolated perfused rat hearts by a novel method using repeated administration of an anoxic cold hyperkalemic cardioplegia solution. Contracture could be reversed by reperfusion with the same solution, without calcium (Group 1), oxygenated (Group 2), or oxygenated and calcium free (Group 3). Group 1 hearts underwent partial reversal of contracture; in Group 2, contracture was reversed more completely, but the effect was transient. Hearts in Group 3 had contracture reversed completely to a level lower than prearrest end diastolic pressure. Hearts in contracture were profoundly depleted of high-energy phosphates (ATP, 9% of control; creatine phosphate, 27%) and the success of contracture reversal was paralleled by the extent to which each solution repleted ATP and PCr. Ventricular contracture produced by energy depletion is rapidly reversed by restoration of oxygen to the myocardium. Reducing extracellular calcium by acalcemic perfusion is ineffective as an isolated measure but is synergistic with reoxygenation and enhances contracture reversal.

Effects of antiarrhythmic drugs on the chronic pacing threshold and the endocardial R wave amplitude in the conscious dog.

To determine the effects of antiarrhythmic drugs on the chronic pacing threshold and the endocardial R wave amplitude, we tested seven drugs (representative of Vaughn Williams' antiarrhythmic class-I-IV) on four to six dogs after the implanted ventricular endocardial bipolar leads had reached chronic stable thresholds. The seven antiarrhythmic drugs tested were procainamide (oral [p.o.] and intravenous [IV], class IA), lidocaine (IV, class IB), tocainide (p.o., class IB), flecainide (p.o. and IV, class IC), propranolol (p.o. and IV, class II), amiodarone (p.o. and IV, class III), and verapamil (p.o. and IV, class IC), propranolol (p.o. and IV, class II), amiodarone (p.o. and IV, class III), and verapamil (p.o. and IV, class IV). The drugs were administered in sufficient doses to achieve plasma levels associated with antiarrhythmic efficacy in humans. All oral drugs were given for sufficient time to achieve expected steady state levels. The pacing thresholds, both voltage and current, and the endocardial R wave amplitude were measured in the conscious dog with a Medtronic pacing system analyzer at a pulse width of 0.1, 0.5, 1.0, and 2.0 ms at intervals following IV or p.o. administration of each antiarrhythmic drug. We found that there were no significant effects of the tested seven antiarrhythmic drugs on the chronic pacing threshold and the endocardial R wave amplitude at any of the pulse widths. We conclude that in the healthy dog antiarrhythmic drugs do not alter the pacing threshold and the endocardial R wave amplitude.