Sotalol is a ,3-adrenergic blocker that also prolongs action potential duration and myocardial refractoriness over the short term (class III effect). Its short-term antiarrhythmic effects were compared with those of metoprolol, which has neither short-term class III nor membranestabilizing action, on reentrant ventricular arrhythmias produced by programmed stimulation in 17 conscious dogs 3 to 8 days after myocardial infarction. Ventricular arrhythmias were prevented or significantly slowed by sotalol in 11 of 19 studies (58%) compared with in one of 14 (7%) studies with metoprolol. Sotalol prolonged refractoriness in the infarct zone, measured from an implanted "composite" electrode, by 41 45% (mean ± SD, p < .01), which was significantly greater than the increases it produced in effective refractory period of the normal ventricle (14.0 + 5.5%) or QT interval (12.5 ± 7.8%). Metoprolol had no effect on infarct-zone refractoriness. Sotalol differentially increases refractoriness in potential reentry circuits in ischemic myocardium. Its antiarrhythmic effect in this model is not due to /8-blockade, and is presumably related to prolongation of action potential duration. Circulation 68, No. 4, 865-871, 1983. SOTALOL is unique among currently available 38-adrenergic blockers in that it produces short-term prolongation of myocardial action potential duration and effective refractory period (ERP) in vitro. According to Vaughan-Williams' classification,3 therefore, sotalol has class III as well as class II antiarrhythmic properties. It has recently been shown that sotalol prolongs monophasic action potential duration in man,4'5 and produces acute increases in the ERPs of human atria, ventricles, and atrioventricular accessory pathways.6 7The purpose of this study was to examine the shortterm effects of sotalol on reentrant ventricular arrhythmias and epicardial infarct-zone potentials in experimental canine myocardial infarction.8 9 The effects of sotalol were compared with those of metoprolol, a cardioselective /3-adrenergic blocker that is devoid of short-term class III
Pulsatile, intravenous insulin infusion designed to mimic the portal insulin concentrations that emerge physiologically after a meal, has been postulated to improve glucose tolerance in Type 1 (insulin-dependent) diabetic patients. We studied the effects of insulin pulsing (10 i.v. pulses of human insulin of 0.035 U kg-1 idealised body weight were given, each of 20 s duration, with intervals of 6 min, three times per day covered with adequate administration of glucose) on 2 successive days on glucose-tolerance in nine well-controlled Type 1 diabetic patients on continuous subcutaneous insulin infusion therapy (age 26 (7) years, mean (SD); duration of diabetes 10 (7) years; body mass index 23.4 (2.3) kg m-2; HbA1c 6.0 (0.6)%). On the days before and after the insulin pulsing, the patients were subjected to metabolic assessments by an oral glucose tolerance test (1 g glucose kg-1 body weight) 30 min after the subcutaneous injection of 0.15 U kg-1 body weight regular human insulin and a subsequent bicycle-ergometer test. During these metabolic assessments, plasma free insulin concentrations, plasma glucagon and the non-protein respiratory quotient remained unaffected by the insulin pulsing. However, glucose tolerance deteriorated significantly (maximal glucose concentration 120 min after glucose load was 10.0 mmol l-1 before and 13.9 mmol l-1 after insulin pulsing, P less than 0.01). In conclusion, the pattern of insulin pulsing used in this study did not ameliorate oral glucose homeostasis in well-controlled Type 1 (insulin dependent) diabetic patients.
The relationship between the inducibility of ventricular tachyarrhythmias and the presence of fractionated epicardial ventricular electrograms ('late potentials') was studied daily between days 3 and 8 after experimental myocardial infarction in 15 conscious dogs. Before each programmed stimulation, epicardial infarct zone electrograms were recorded from implanted 'composite' electrodes during sinus rhythm. There was considerable daily variation in the morphology and duration of delayed ventricular activation, but no significant difference in duration of infarct zone electrograms was seen between studies resulting in ventricular fibrillation (108 +/- 62 ms, mean +/- SD), sustained ventricular tachycardia (87 +/- 18 ms), nonsustained (94 +/- 41 ms) or no tachycardia (78 +/- 5 ms). Although fractionated ventricular electrograms were commonly recorded early after infarction, their presence and duration could not predict the inducibility of malignant ventricular tachyarrhythmias. Similar limitations may apply in clinical practice to the use of surface signal averaging of ventricular late potentials in the early post-myocardial infarction period.
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