Abstract
A reduction in the contractile force of heart muscle by barbiturate has been shown in vitro as well as in the heart-lung preparation of the dog. The effects of barbiturates on the excitable cell membrane have been studied in peripheral nerve as well as in skeletal and cardiac muscles. Measurements obtained by means of intracellular microelectrode in isolated frog sartorius muscle show a decrease in the amplitude and rate of rise of the action potential when the muscle is bathed in solutions of pentobarbital. The changes in the action potential have been ascribed to an inactivation of sodium carrier mechanism, with a resulting reduction in the selective sodium conductance change during the action potential [Thesleff (1)]. The exposure of cardiac muscle to pentobarbital has been shown to shorten the early phase and to slow the late phase of repolarization. Pentobarbital treatment of the ventricular strip of rabbit heart has been shown by Daniel et al. (2) to decrease both the gain of sodium and the loss of potassium. Daniel et al. (3) also have demonstrated the antagonism between pentobarbital and noradrenaline in both the intact dog and the heart-lung preparation. The introduction of beta-adrenergic blocking agents has received particular attention in regard to the adrenergic receptor mechanism of the heart. In the present experiments attempt has been made to elucidate the role of the adrenergic alpha- and beta-receptor mechanism on the transmembrane potential of the rabbit's atria by observing the interaction between barbiturates (pentobarbital and thiopental) and catecholamines (noradrenaline, adrenaline and isopropylnoradrenaline).
