Microelectrode Study of Delayed Conduction in the Canine Right Bundle Branch

Wennemark, James R.; Ruesta, Victor J.; Brody, Daniel A.

doi:10.1161/01.res.23.6.753

Cited by 39 publications

(14 citation statements)

References 16 publications

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“…The increase in A Vnodal transmission time with shortening of cycle length was due to "stagnation" between N and NH zone. This stagnation was likened to the mechanism of electrotonic transmission described for other cardiac tissues, where an inexcitable segment, interposed between two excitable regions, functions as a purely passive resistance-capacitance circuit (12,37,67,200). The stagnation is caused by cessation of active transmission at the inexcitable element, which can be crossed by electrotonic current bringing distal excitable ceUs to threshold.…”

Section: A Decremental Conduction Versus Electrotonic Transmissionmentioning

confidence: 72%

Morphology and electrophysiology of the mammalian atrioventricular node

Meijler

Janse

1988

Physiological Reviews

203

146

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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)

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Section: A Decremental Conduction Versus Electrotonic Transmissionmentioning

confidence: 72%

Morphology and electrophysiology of the mammalian atrioventricular node

Meijler

Janse

1988

Physiological Reviews

203

146

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“…The majority of knowledge about cellular electrical events accompanying cardiac ischemia is derived from experimental models in which the tissue was uniformly exposed to ischemic components throughout its length (Downar et al, 1977;Wennemark et al, 1968;Pappano, 1970;Carmeliet and Vereecke, 1969;Trautwein and Schmidt, I960;Engstfeld et al, 1961). A series of very interesting studies by Cranefield et al reported the development of a remarkable model for the abnormal conduction which might exist in clinical arrhythmias associated with myocardial infarction Cranefield et al, 1972).…”

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confidence: 99%

Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system.

Senges¹,

Brachmann²,

Pelzer³

et al. 1979

Circulation Research

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We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.

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“…Accepted for publication November 24, 1970. been demonstrated by recording mechanical activity in strips of turtle heart depressed with high external K + (8,9); Drury (10) showed slow conduction in atrial muscle, depressed by cold or by pressure, by recording electrograms in normal and depressed tissue. Most studies of conduction in depressed cardiac fibers using single cell recording of transmembrane action potentials (11)(12)(13)(14)(15)(16) have been carried out on tissue uniformly depressed throughout its length.…”

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confidence: 99%

Conduction of the Cardiac Impulse

Cranefield

Klein

Hoffman

1971

Circulation Research

271

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Depressed excitability and responsiveness were created in excised bundles of canine Purkinje fibers. A segment 8 mm long was depressed by being encased in agar containing 47 mM K + , the ends of the bundle outside the agar remaining normal. Either normal end could be excited through extracellular electrodes. Action potentials were recorded by intracellular microelectrodes at each end and within the depressed segment. Conduction velocity within the depressed segment fell as low as 0.05 m/sec. Abnormalities of impulse transmission through the depressed segment included delay, 2:1 block, higher degrees of block, rate-dependent block, and block showing the Wenckebach phenomenon. Asymmetries of conduction seen included one-way block. Action potentials in the depressed segment were of low amplitude and showed slow upstrokes. Variations in action potential duration occurred in the depressed segment when conduction failed or was very slow and when impulses were dropped. Delay in conduction too great to result simply from a slow upstroke is attributed to summation of excitatory events across regions of block in a syncytium of cells. The results prove that conduction delays great enough to permit re-entry can occur in short segments of Purkinje fibers subjected to high K+.

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Microelectrode Study of Delayed Conduction in the Canine Right Bundle Branch

Cited by 39 publications

References 16 publications

Morphology and electrophysiology of the mammalian atrioventricular node

Morphology and electrophysiology of the mammalian atrioventricular node

Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system.

Conduction of the Cardiac Impulse

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