I973) distinguishes between at least three separate effects. Class i mode of action is the one exhibited by quinidine, procainamide, and lignocaine among others. It is recognized from recordings of transmembrane potentials from heart muscle cells (Ling and Gerard, I949) and appears in such recordings as a depression of the maximal rate of depolarization of the cell membrane. The class 2 mode of action consists of inhibition of adrenergic activity, either at the receptor site or by interference with the release of sympathetic transmitters. The class 3 mode of action is also demonstrated with the micro-electrode technique. This mechanism is a prolongation of the action potential, a delayed repolarization. Such a mechanism has been shown in atrial tissue during hypothyroidism (Freedberg, Papp, and Vaughan Williams, I970) and is the mode of action of amiodarone (Singh and Vaughan Williams, 1970).Recently it was shown that patients with a tendency to relapse to atrial fibrillation after DC conversion to sinus rhythm had a fast atrial muscle Received 23 May I973.
The authors have previously shown that 40% of patients whose ventricular arrhythmias respond to propranolol require plasma concentrations in excess of those producing substantial beta-receptor blockade (greater than 150 ng/ml). However, the electrophysiologic actions of propranolol have only been examined in human beings after small intravenous doses achieving concentrations of less than 100 ng/ml. In this study, the electrophysiologic effects of a wider concentration range of propranolol was examined in nine patients. Using a series of loading and maintenance infusions, measurements were made at baseline, at low mean plasma propranolol concentrations (104 +/- 17 ng/ml) and at high concentrations (472 +/- 68 ng/ml). Significant (p less than 0.05) increases in AH interval and sinus cycle length were seen at low concentrations of propranolol, with no further prolongation at the high concentrations; these effects are typical of those produced by beta-blockade. However, progressive shortening of the endocardial monophasic action potential duration and QTc interval were seen over the entire concentration range tested (p less than 0.05). At high concentrations, there was significant (p less than 0.05) further shortening of both the QTc and monophasic action potential duration beyond that seen at low propranolol concentrations, along with a progressive increase in the ratio of the ventricular effective refractory period to monophasic action potential duration. No significant changes were seen in HV interval, QRS duration or ventricular effective refractory period. In summary, the concentration-response relations for atrioventricular conductivity and sinus node automaticity were flat above concentrations of 150 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
Sustained handgrip at 30% of the maximal strength and submaximal supine bicycle exercise elicited mean blood pressure increases of similar magnitude in healthy males and in men with essential hypertension WHO Stage 1 and 2, but with different contributions of systolic and diastolic blood pressure changes. While systolic blood pressure exceeded 22.7 kPa (170 mmHg) during static exercise in every hypertensive man, this did not occur in any of the control subjects. During dynamic exercise, the arterial blood pressure increase per litre increase in cardiac output was significantly less than during static exercise, indicating different patterns of circulatory adaptation to these two forms of stress. Combination of dynamic and static exercise tests might be of value for identifying subjects with a hypertensive pattern of circulatory regulation.
Myocardial monophasic action potentials (MAP) can be recorded with the aid of suction or contact electrodes applied endocardially via a catheter. The technique necessitates high input impedance amplifiers with infinite time constant. A bipolar technique improves signal quality with regard to electrical contamination around the rapid upstroke of the MAP. Mechanical artefacts in the recordings are common and may be explained by catheter movement induced by atrial or ventricular contractions. The MAP signal can be used for a precise measurement of time of local excitation and for the study of atrial as well as ventricular repolarization. The technique has mostly been applied in the exploration of atrial and ventricular repolarization in healthy hearts and during different cardiac arrhythmias. Furthermore, several studies have documented the electrophysiological action of antiarrhythmic drugs upon the human heart. Concluding from 576 different investigations we consider the technique to have no serious side-effects.
The effective right ventricular refractory (EVRP) period was estimated in 24 patients using the extra stimulus technique. All patients were paced from the right ventricle at basic pacing intervals of 400, 500, 600 and 800 ms, respectively. In all patients the EVRP decreased when the basic pacing rate was increased. At the same basic pacing rate there was a wide variation in the EVRP between individual patients. Within an individual patient, however, providing the position of the pacing electrode remained stable, there was no significant variation in the EVRP when estimations were performed 15-30 min apart. Thus the technique can be used to assess the effect of a drug on the EVRP in an individual patient.
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