The mechanism of atrioventricular delay has been studied in isolated rabbit hearts. Multiple intracellular microelectrodes have been employed to obtain simultaneous records from single fibers of atrium, A-V node and His bundle. An appreciable delay in the transmission of excitation has been found only in the atrial portion of the A-V node. Action potentials recorded from single fibers in this area show a low resting potential, slow diastolic depolarization, slow upstroke and low amplitude. These action potentials frequently show one or more notches or steps on the rising phase. Action potentials recorded from fibers of the His bundle are similar in shape and amplitude to those of peripheral Purkinje fibers. Records obtained at several sites between the atrial portion of the node and the His bundle show a gradual transition in action potential shape. The mechanism of slow transmission across the A-V node is discussed in relation to the electrical activity of fibers at the atrial end of this structure.

Intracellular microelectrodes have been used to study the site of origin and direction of spread of activity in the rabbit atrium. In this study a number of fiber groups have been found which possess specialized electrophysiological characteristics and a consistent anatomical localization. A pacemaker potentiality has been found only in tissues derived from embryologically distinct structures such as the sinus venosus, the venosus valves and the lower segment of the auricular canal. Activity normally spreads slowly from the S-A node and excites the crista terminalis along a broad front. Spread is then rapid through the crista, the pectinate muscles and the fibers of the atrial roof. The septum is normally excited from the crista terminalis. Excitation reaches the A-V node almost simultaneously from the crista terminalis and the right segment of the S-A ring bundle. This latter shows many characteristics of specialized conducting tissue. Around the A-V ring conduction velocity slows markedly in fibers which have many of the electrophysiological characteristics of A-V nodal fibers.

These results suggest that, in chondrocytes, NO is a key regulator of the signaling pathways leading from IL-I to NF-kappaB and AP-1 activation and to the expression of genes that are involved in the pathophysiology of arthritic diseases.

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.