Rapid drug infusion for termination of atrial fibrillation in an experimental model.

Episodes of paroxysmal atrial fibrillation (PAF) in the ambulatory patient might be terminated promptly by intravenous infusion from an implanted drug delivery system. We have explored this concept in a series of experiments using rapid intra-atrial infusions in dogs. In the acute studies, rapid intra-atrial infusions of procainamide were delivered during continual measurements of epicardial monophasic action potentials (MAP), atrial effective refractory periods (ERP), and right to left atrial conduction times (CT) in 9 dogs. In the chronic studies, 20 episodes of sustained PAF were induced in 4 dogs after six weeks of rapid or burst atrial pacing from a specially programmed implanted pacemaker. Rapid infusions of procainamide were then delivered to the right atrium through a previously implanted catheter connected to a subcutaneous access port. Procainamide significantly increased the duration of the atrial MAP, ERP and CT in the acute experiments. It also terminated induced PAF within five minutes of the end of infusion in all twenty of the chronic experiments. We conclude that rapid intra-atrial infusion of procainamide is very effective in this animal model of PAF, and that such infusion prolongs atrial MAP, ERP and CT.

Characteristics of motor unit discharge in subjects with hemiparesis.

We studied the discharge rates and recruitment characteristics of single motor units in paretic and contralateral arm muscles of 6 hemiparetic subjects. Motor unit activity in biceps brachii was recorded at different elbow torques, and the activity related both to the mean level of surface electromyographic activity, and to the degree of weakness. In 3 of the 6 subjects, there were significant reductions in mean discharge rate of motor units in the paretic muscle. All 6 subjects showed compression of the range of motoneuron recruitment forces, and a failure to increase motor unit discharge rate during voluntary force increases in paretic muscles. These rate reductions could potentially alter the precise match of motoneuron properties to the mechanical properties of the innervated muscle fibers, and reduce the efficiency of muscle contraction. This reduction could lead, in turn to increased effort, to fatigue, and ultimately to a sense of weakness for voluntary force generation.