ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01931.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01932.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Passive and Active Electrical Responses.Introduction: The purpose of this investigation was to study the electrical activity of the crayfish myocardium.Methods and Results: In isolated crayfish hearts, intracellularly injected hyperpolarizing pulses propagate electrotonically to distances up to 1 mm, and the myocardium behaves as an irregular functional syncytium.Conclusion: The existence of low‐resistance intercellular connections provides a basis for the analysis and interpretation of many of the results obtained in this article, and makes it possible to propose the following tentative conclusions: (1) in the crayfish myocardium, not all muscle cells are innervated, yet many sites in the crayfish myocardium receive the same polyneural innervation; (2) in many records, the burst of junction potentials that follow each action potential are electrotonic in nature; (3) the cardiac muscle fibers of the crayfish heart are electrically excitable, and the generated action potentials do propagate actively at least for short distances; (4) the gaps between the innervated sites are filled with noninnervated but connected muscle cells that are passively and actively engaged; and (5) an exaggerated richness of innervation is not needed since the crayfish heart can provide effective and quasisynchronous mechanical systoles because of its efficiently combined characteristic

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01933.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

AV Nodal Conduction During Atrial Fibrillation and Flutter.Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths.Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (>120 msec) between the ventricular pacing cycle length that achieved>95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing>95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve>95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing>95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e.,>120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values>120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation.Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal condu

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01934.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Atrial Flutter Rate and Atrial Pressure.Introduction: During atrial flutter the effects of 1:1 atrioventricular (AV) conduction on the rate of atrial flutter was studied in 12 patients and 14 dogs.Methods and Results: (A) In all patients, the development of 1:1 AV conduction was associated with a significant increase in flutter cycle length (261.7 ± 9.9 to 281.8 ± 12.1 msec, mean increase 20.3 ± 3.2 msec, P<0.001). The flutter cycle length returned to control values when 1:1 AV conduction ceased. In four patients in whom atrial pressure was monitored, the prolongation of the atrial flutter cycle interval during 1:1 AV conduction was associated with an immediate rise in atrial pressure (4.0 ± 0.4 to 6.5 ±0.7 mmHg, P<0.003). (B) In order to examine the mechanism of this phenomenon, similar studies were carried out in dogs with experimentally induced atrial flutter. 1:1 AV conduction consistently lengthened the flutter cycle length during control conditions or following vagotomy and during the administration of isoproterenol. This was always associated with a rise in atrial filling pressure. Inferior vena cava occlusion consistently shortened the flutter cycle length and this was also independent of vagotomy and isoproterenol administration. The atrial filling pressure fell during inferior vena cava occlusion. During 1:1 AV conduction, the prolonged flutter cycle length was shortened by inferior vena cava occlusion to values prior to 1:1 AV conduction.Conclusion: The rate of atrial flutter is accelerated by reductions in atrial pressure, and slowed by increased atrial pressure. These effects are independent of the vagus nerve or an adrenergic agonist. Changes in atrial pressure and volume affect characteristics of the atrial flutter circuit, and thus can modulate the rate of atrial flu

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01935.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

A Mechanism for Anisotropic Reentry.Introduction: Numerical simulations of wavefront propagation were performed using a two‐dimensional sheet of tissue with different anisotropy ratios in the intracellular and extracellular spaces.Methods and Results: The tissue was represented by the bidomain model, and the active properties of the membrane were described by the Hodgkin‐Huxley equations. Two successive stimuli, delivered through a single point electrode, resulted in the formation of a reentrant wavefront when the second stimulus was delivered during the vulnerable period of the first wavefront.Conclusion: The mechanism for the development of reentry was that the bidomain tissue responded to point cathodal stimulation by depolarizing the tissue under the electrode in the direction perpendicular to the fiber axis, and hyperpolarizing the tissue in the direction parallel to the fiber axis. Such a distribution of depolarization and hyperpolarization modifies the refractory period of the action potential differently in each direction, resulting in block in the direction perpendicular to the fiber axis and leading to reentry and the formation of stable, rotating wavefro

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01936.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Regulation of Cardiac Ca Channels. The L‐type, voltage‐gated calcium (Ca) current plays a key role in excitation and initiation of contraction in cardiac muscle cells and is partly responsible for the plateau of the action potential. The ionic channels underlying this current are targets for modulation by the autonomic nervous system. This article reviews recent developments in understanding how these channels are regulated by phosphorylation and G proteins and attempts to relate these findings to recent studies on the molecular structure of the Ca chan

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01937.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Myocardial Anisotropy in Ischemia and Infarction. Anisotropy is defined as any property of a system that differs depending on the direction in which it is measured. In the heart, the structure of the cardiac myocytes and their electrical coupling via gap junctions confer an anisotropy in the intracellular resistance to current flow in myocardial tissue. This in turn is responsible for anisotropy in conduction in which the velocity and uniformity of impulse conduction is dependent on its direction relative to the normal myocardial fiber orientation and any underlying pathological nonuniformities in cell orientation and coupling. How cells are coupled also influences refractoriness and excitability. Recent experimental evidence has implicated uniform and nonuniform myocardial anisotropy as important substrates that play a role in the initiation and maintenance of arrhythmias in the setting of ischemia and infarction. These studies may provide a focus for the development of new antiarrhythmic modalities that depend on the modulation of cell electrical coupling.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01938.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Voltage‐Gated Potassium Channels. Many different types of potassium (K+) channels exist and they play a central role in the fine tuning of excitability properties. Of the distinct subpopulations of K+channels expressed in different cells, voltage‐gated K+channels have been studied most thoroughly at a molecular level. Over the last few years, the joint application of recombinant DNA technology together with electrophysiology, such as the voltage clamp and the patch clamp techniques, has produced a wealth of information. We have begun to unravel the genetic basis of ion channel diversity. In particular, theXenopusoocyte expression system has turned out to be of enormous experimental value. Oocytes microinjected with “cloned” mRNA have been used to gain insight into biophysical and pharmacologic properties of voltage‐gated K+, Na+, and Ca2+channels. Here, we will review our understanding of K+channel diversity based upon the fact that ion channels are encoded as a large multigene family. We have caught a first glimpse at possible molecular mechanisms underlying several biophysical properties characteristic for voltage‐gated ion channels: voltage dependence of activation and inactivation, and ion permeation and selectivity. We will discuss molecular mechanisms of K+channel activation and inactivation. We will also describe experiments that led to the identification of the “pore region,” and we will present a model of a potassium selective i

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01939.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01940.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY