Modulation of the Purkinje-ventricular muscle junctional conduction by elevated potassium and hypoxia.

Abstract

Action potential transmission in the canine ventricle normally occurs from the Purkinje (P) system into the ventricular muscle (VM) at specific P-VM junction sites. Transitional (T) cells are located between the Purkinje and the ventricular (V) cells at these P-VM junction sites. It has been shown that exposure to elevated [K'], in combination with hypoxia produces an increase in the P-VM conduction time. To examine this increase in P-VM conduction time, simultaneous measurements of the action potential upstrokes of T cells and the activation times of the local P and V cells at P-VM junctional sites were obtained from in vitro canine papillary muscles. The effects of elevated [K+]0 and hypoxia on conduction from P cells to T cells was then compared with the conduction from T cells to V cells to assess the relative contribution of each to the increase in the P-VM conduction time. We found that this intervention has approximately equal effects on the two sequential steps involved in P-VM conduction. We then analyzed the increased delay from T cells and V cells on the basis of three hypothetical mechanisms: 1) increased coupling resistance, 2) decreased V cell excitability, and 3) decreased cellular responsiveness of the T cells. Our results show that the effects of elevated [K+J0 and hypoxia on T-VM delay can be accounted for by a decreased responsiveness of the T cells without any significant electrical uncoupling between T and V cells or decrease in VM excitability. (Circulation 1989;79:1100-1105 T he normal activation sequence of the ventricular tissue requires that an action potential propagating through the His-Purkinje system initiate activation of the underlying subendocardial ventricular muscle (VM). Numerous in vitro studies have focused on the process of Purkinje-ventricular muscle (P-VM) transmission, generally in canine preparations.1-5 It has been clearly shown that transitional (T) cells are positioned between the Purkinje (P) and ventricular (V) cells at the P-VM junctional sites. However, the specific membrane properties of these T cells and the pattern of electrical coupling between P and T cells and between T and V cells is not known. For normal orthodromic conduction, it appears that the T cells have action potential upstrokes with two phases. The first phase reflects the local activation of the T cells due to a depolarizing current

Action potential conduction between a ventricular cell model and an isolated ventricular cell

“…The conduction between two cardiac cells (or two groups of cardiac cells) can be considered to be determined by three components: 1) the intercellular conductance for intercellular current flow; 2) the amount of depolarization required in the follower cell to initiate an action potential (the "sink" for current flow); and 3) the ability of the leader cell to maintain a high membrane potential to serve as the "source" of current for the follower cell. During discontinuous conduction with long delays there are well documented abnormalities in the early plateau of the action potentials, recorded either from the Purkinje-ventricular junction (Tan et al, 1989) or from a pair of ventricular cells (Weingart and Maurer, 1988). We recently showed (Sugiura and Joyner, 1992) that, when two isolated guinea pig ventricular cells were coupled to each other by a variable conductance, the required intercellular conductance for successful conduction was increased by low doses of nifedipine, which specifically decreases the L-type calcium current (Kohlhardt and Fleckenstein, 1977).…”

Conduction delays across the specialized conduction system of the heart: Revisiting atrioventricular node (AVN) and Purkinje-ventricular junction (PVJ) delays

“…Anatomical and microelectrode experiments have identified “transitional” cells separating PF from myocytes at PVJs. Transitional cells were described as thin, capacitor-like structures that electrically isolate PFs from direct electrical coupling with ventricular myocytes and may account for delays at PVJ ( 61 ). However, due to redundancies in PVJs, it is possible that the real conduction delay across PVJ can be longer than that measured here because ventricular activation in one PVJ can initiate AP propagation in the ventricular myocardium, which may result in seemingly shorter conduction delays in other PVJs ( 62 ).…”

In silico ischaemia-induced reentry at the Purkinje-ventricle interface

“…Under normal conditions, RPVJ was adjusted to 16 Ω•cm 2 , which resulted in a delay in conduction from Purkinje to ventricle of 2.21 ms. RPVJ value was increased up to 40 Ω•cm 2 to simulate the effects of ischemia. 32,33 Purkinje and ventricular fibers were 1.5 cm (100 cells) and 3 cm (300 cells) in length, respectively. The stimulation protocol consisted of a train of 11 pulses applied at cell #0 of the Purkinje fiber in the two models.…”