The pulmonary veins of albino Wistar rats were studied by means of light and electron microscopy. The media of larger veins consists of cardiac muscle fibers which extend until the vessels attain about 100 mu in diameter. This coat consists of external longitudinal fibers and internal circular fibers. The vasa vasorum are well developed and the capillaries show pseudofenestrations. The numerous adrenergic and cholinergic nerve endings do not form typical motor end-plates as seen in skeletal muscles. The ultrastructure of these media muscle fibers is similar to that of the rat hearts. The smooth muscle layer of larger pulmonary veins is not continuous as it is in smaller veins where it forms cushions. Comparison of albino rats and other rodents reveal striking differences. Action potential shape and propagation velocity (0.5-1.2 m/s) along the myocardial coat of the pulmonary vein were similar to those observed in the left atrium and so was their sensitivity to locally applied acetylcholine. The physiological direction of propagation in rat pulmonary veins is toward the lung. This fingind lends support to the hypothesis of a rhythmic, valve-like action of the striated musculature of the pulmonary venous wall during the systole and a possible role in the capacitance of the pulmonary circulation.

Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (I?, V or phase-plane display). Acetylcholine was applied to the recording site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the relative magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (¢) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow component, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current having a positive equilibrium potential, coupled to a decrease in the resting potassium conductance. According to the hypothesis, SA and AV nodal action potentials are due entirely or almost entirely to the slow component and can therefore be expected to exhibit unique electrophysiological and pharmacological properties.Differences in the voltage-time course of transmembrane action potentials recorded from a variety of cell types in the same m a m m a l i a n heart have been described by several investigators (see Hoffman and Cranefield, 1960). T h e detailed electrophysiological studies carried out on the right atrial preparation of the rabbit heart showed that action potentials from sinoatrial (SA) and atrioventricular (AV) nodes have a remarkably slow rising phase, lasting up 607