Effects of procainamide on the dispersion of recovery of excitability during coronary occlusion.

Abstract

30, 1976. lengthened in the nonischemic as well as in the ischemic areas, but the changes were such that the temporal dispersion caused by the coronary ligation was reduced from 12.2% to 5.5% (P < 0.01) after 10 minutes, and to 5.0% (P < 0.02) after 20 minutes of drug infusion. It is concluded that procainamide exerts different overall effects on the nonischemic and acutely ischemic canine myocardium. It is postulated that this action may play a role in the suppression of re-entrant arrhythmias. MethodsFourteen mongrel dogs weighing 17 to 26 kg were anesthetized with intravenous sodium pentobarbital, 30 mg/kg, intubated and mechanically respirated with a Harvard respirator. The left femoral vein was catheterized for administration of drugs and to obtain blood samples for determination of procainamide levels, and the aortic pressure monitored via a catheter introduced in the left femoral artery, using a Statham P23Db transducer. After induction of complete heart block by injecting 0.2 ml of formaldehyde in the septum in the area of the bundle of His, heart rate was kept constant at a basic cycle length (SI -SI) of 500 msec by right ventricular pacing using a S-88 Grass stimulator. Four pairs of fine stainless-steel, Teflon-coated plunge electrodes (0.003 inch diameter) were inserted into the left ventricular myocardium, two pairs in an area subserved by the left anterior descending coronary artery that subsequently was made ischemic and the other two pairs in an area with intact coronary blood flow. Premature stimuli (S2) were introduced in each left ventricular zone through a pair of stimulating electrodes and a pair of sensing electrodes was placed at a distance of 5-8 mm.

Strength-interval relations in a chronic canine model of myocardial infarction. Implications for the interpretation of electrophysiologic studies.

“…',6 10,13,15,18 Basic properties of excitability and refractoriness have also been studied as a means of better defining arrhythmia and antiarrhythmic mechanisms. [35][36][37][38][39][40][41][42][43][44][45][46][47] However, most clinical data have been limited to studies using measurements of refractoriness obtained with stimuli of only one intensity, and this intensity has been twice diastolic threshold. The findings in the present study demonstrate possible problems in interpreting data obtained using stimuli of only one intensity ( figs.…”

Effect of procainamide on induced ventricular tachycardia

“…7 The effects of procainamide on refractoriness may be more important in suppressing tachycardia in the setting of acute ischemia, or in preventing fibrillation. For example, after coronary ligation in dogs, Levites, Haft, and Calderon 14 found greater prolongation of refractory period at ventricular sites that had abbreviated refractoriness due to ischemia, such that dispersion of refractory periods was less after procainamide. Other recent work,2 however, suggests that reentrant arrhythmias in the late canine myocardial infarction period are abolished mainly by slowed conduction (in that stud y, by lidocaine).…”