Postischemic rabbit ventricular myocyte pairs had a significantly greater proportion of poorly communicating cells compared to controls (8 of 15 vs 0 of 15 and 1 of 13; p<0.02).
Does ischemia and reperfusion affect gap junctional conductance in isolated rabbit ventricular myocytes?
Postischemic rabbit ventricular myocyte pairs exhibit heterogeneous gap junctional conductance with a significant proportion of poorly communicating cells, which may contribute to reperfusion-induced arrhythmias.
Absolute Event Rate: 53.3% vs 0%
p-value: p=<0.02
Abnormalities of myocardial gap junction-mediated cell coupling have been implicated in cardiac arrhythmogenesis. The potential role of gap junctional dysfunction in the generation of reperfusion-induced arrhythmias is uncertain. The purpose of this study was to measure the effects of myocardial ischemia and reperfusion on gap junctional conductance (gj) between isolated ventricular myocytes. By using a new experimental model, myocyte pairs were isolated from Langendorff-perfused rabbit hearts 1) after 30 minutes of global normothermic ischemia followed by 30 minutes of reperfusion, 2) after 75 minutes of control perfusion, or 3) immediately after removal of the heart. Myocytes and myocyte pairs were studied using whole-cell recording techniques. Action potential characteristics of cells in all three groups were normal. Despite similar mean gj in all three groups (0.88 +/- 0.27, 1.15 +/- 0.18, and 1.24 +/- 0.25 microS, respectively; p greater than 0.05), the postischemic group was more widely distributed and had a significantly greater proportion of poorly communicating cell pairs than either control group (gj less than 25% of mean in eight of 15 myocyte pairs versus zero of 15 and one of 13, respectively; p less than 0.02). Thus, postischemic myocyte pairs represent a heterogeneous population of electrically coupled cells in which individual deficits in coupling are masked by a normal mean value. In the reperfused intact heart, local disturbances of cell coupling, similarly undetected by gross measures of conduction, could disrupt myocardial conduction and activation on a microscopic scale and thus enhance arrhythmogenicity.
Kieval et al. (Wed,) conducted a other in Myocardial ischemia and reperfusion (n=43). Global normothermic ischemia and reperfusion vs. Control perfusion or immediate removal was evaluated on Proportion of poorly communicating cell pairs (gap junctional conductance <25% of mean) (p=<0.02). Postischemic rabbit ventricular myocyte pairs had a significantly greater proportion of poorly communicating cells compared to controls (8 of 15 vs 0 of 15 and 1 of 13; p<0.02).