Effects of potassium on automaticity and conduction of canine hearts

Vassalle, Mario; Greenspan, Kalman; Jomain, Serge L.; Hoffman, Brian F.

doi:10.1152/ajplegacy.1964.207.2.334

Cited by 67 publications

(11 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Their release may contribute to 1oth the a-and 8-adrenergic effects implicated in ventricular ectopic activity and VF early after coronary occlusion. The lack of an increase in idioventricular rate during coronary occlusion alone may also be caused in part by suppression of idioventricular rate by increased extracellular K+ (24), known to accumulate in the extracellular space early after coronary occlusion (25).…”

Section: Resultsmentioning

confidence: 99%

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Sheridan¹,

Penkoske²,

Sobel³

et al. 1980

J. Clin. Invest.

373

106

View full text Add to dashboard Cite

A B S T R A C T Alpha compared to beta adrenergic contributions to dysrhythmias induced by left anterior descending coronary occlusion and by reperfusion were assessed in chloralose-anesthetized cats (n = 96). Alpha receptor blockade with either phentolamine or prazosin significantly reduced the number of premature ventricular complexes during coronary reperfusion (321±62-14±10 premature ventricular complexes, P <0.001), abolished early ventricular fibrillation (from 25% in controls to 0%), and prevented the increase in idioventricular rate seen with coronary reperfusion. However, ,8-receptor blockade was without effect. Ventricular dysrhythmias induced by coronary occlusion alone (without reperfusion) were attenuated markedly by a-receptor blockade under conditions in which perfusion (measured with radiolabeled microspheres) within ischemic zones was not affected. Alternative sympatholytic interventions including pretreatment with 6-hydroxydopamine to deplete myocardial norepinephrine from 8.8±+1.4 to 0.83+0.2 ng/mg protein and render the heart unresponsive to tyramine (120 gg/kg) attenuated dysrhythmias induced by both coronary occlusion and reperfusion in a fashion identical to that seen with a-receptor blockade. Although efferent sympathetic activation induced by left stellate nerve stimulation increased idioventricular rate from 66+6 to 144±7 beats/min (P < 0.01) before coronary occlusion, this response was blocked by propranolol but not by phentolamine. In contrast, during reperfusion the increase in idioventricular rate induced by left stellate nerve stimulation (to 203±14) was not inhibited by propranolol but was abolished by phentolamine (79 ± 10). Intracoronary methoxamine (0.1 uM) in animals depleted of myocardial catecholamines by 6-hydroxy-

show abstract

Section: Resultsmentioning

confidence: 99%

Alpha adrenergic contributions to dysrhythmia during myocardial ischemia and reperfusion in cats.

Sheridan¹,

Penkoske²,

Sobel³

et al. 1980

J. Clin. Invest.

373

106

View full text Add to dashboard Cite

show abstract

“…It is known that following elevation of extracellular potassium concentration areas of the right atrium remain excitable at a time when the P wave has disappeared from the electrocardiogram (22). Atrial fibers which show a resistance to elevated potassium concentration have been classified as specialized fibers (20,23).…”

Section: Response To Acetylcholinementioning

confidence: 99%

“…Several investigators have shown that specialized atrial fibers exist which are resistant to levels of hyperkalemia that render regular atrial fibers inexcitable. Indirect evidence was offered by Vassalle et al (22) who observed that sinoventricular rhythms were maintained at potassium levels which caused quiescence of regular atrial tissue and disappearance of the P wave from the electrocardiogram. Electograms with double complexes have been observed in dog atria along the interatrial band (18) and have been interpreted to result from the difference in conduction velocities of regular and specialized atrial fibers beneath the recording electrode.…”

mentioning

confidence: 99%

Evidence for Specialized Fibers in the Canine Right Atrium

Hogan

Davis

1968

Circulation Research

View full text Add to dashboard Cite

Right atria from excised beating dog hearts were immersed in Tyrode solution with the endocardial surface of the anterior wall exposed. Glass microelectrodes were used to impale fibers in different anatomical areas of this preparation. Fibers with action potentials similar in contour to those of ventricular Purkinje fibers were found along the caval border of the crista terminalis in the area of the posterior internodal tract. The action potential of these fibers (plateau fibers) had a resting potential of -85 to -95 mv, a sharp spiked overshoot, a long plateau phase, and inherent diastolic depolarization. The maximum velocity of the action potential upstroke of plateau fibers was consistently greater than that of simultaneously recorded fibers which lacked a plateau phase (regular fibers). Epinephrine or isoproterenol produced an increase in both rate and magnitude of diastolic depolarization of plateau fibers and on occasion converted them to true pacemakers. Acetylcholine accelerated repolarization of plateau fibers with disappearance of the plateau. Increases in extracellular concentration of potassium ions from 2.7 to 10.8 mM rendered regular atrial fibers inexcitable, but plateau fibers continued to show action potentials. Plateau atrial fibers possess several characteristics exhibited by specialized conducting and impulse generating fibers. The possibility that these fibers constitute the posterior internodal tract and function in preferential conduction of excitation to the A-V node was discussed. ADDITIONAL KEY WORDShigh extracellular potassium concentration posterior internodal tract epinephrine diastolic depolarization acetylcholine latent pacemaker activity isoproterenol• While it is generally accepted that fibers of the sJnoatrial (S-A) node serve as the pacemakers in the normal mammalian heart, the manner in which excitation spreads from this node through the atria and to the atrioventricular (A-V) node is not completely settled. Lewis et al. (1) concluded from studies using surface electrodes that excitation spreads radially from the S-A node through a syncytium composed of homogeneous tissue. The concept of radial spread of the impulse was challenged by Eyster and Meek (2-5) who presented evidence for spread of excitation from the S-A node to the From the Department of Physiology, University of Wisconsin Medical School, Madison, Wisconsin 53706.This investigation was supported in part by grants from the Wisconsin Heart Association and U. S. Public Health Service Grants 5-T1-HE53705-08 and 2-T1-HE5540-06.Accepted for publication June 27, 1968.CiratlM 'on esearch, Vol. XXIII, September 1968 A-V node along a preferential pathway. Also evidence for rapid spread of the impulse from the right to the left atrium was given by Bachmann (6) who described a special bundle of tissue linking the atria ventrally. Both anatomical and electrophysiological evidence has accumulated to support the contentions of Eyster and Meek for a preferential internodal pathway. In a recent review, Robb and Petri (7...

show abstract

“…The myocardium is much more sensitive to the effects of hyperkalemia than are the specialized conduction tissues such as the sinoatrial node and the Hisbundle. It has been shown in experimental models that atrial tissue is more sensitive to the effects of hyperkalemia than the ventricular tissue [4,5]. Hyperkalemia-induced failure of atrial pacemaker capture has been reported [1].…”

mentioning

confidence: 99%