Morphology and electrophysiology of the mammalian atrioventricular node.
The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology; D001283:Atrioventricular Node / Q000033:anatomy & histology / Q000166:cytology / Q000502:physiology*; D001696:Biomechanical Phenomena; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D004594:Electrophysiology; D006327:Heart Block / Q000209:etiology / Q000503:physiopathology; D006329:Heart Conduction System / Q000502:physiology*; D006801:Humans; D008322:Mammals; D009412:Nerve Fibers / Q000033:anatomy & histology; D009431:Neural Conduction; D018377:Neurotransmitter Agents / Q000494:pharmacology / Q000502:physiology
D018377:Neurotransmitter Agents