Introduction: Chronic enlargement of atrium is common in atrial fibrillation, and the effects of stretch on atrial action potentials seem inconsistent. As atrial muscle is heterogeneous, we suggest that atrial stretch induces a variable electrophysiologic response and that the effects of stretch are only partially mediated by stretch-activated channels.
Methods and results: Sixteen guinea pig hearts were perfused by the Langendorff method using Kreb's solution with and without 80 microM streptomycin, which is a stretch-activated channel blocker. Suction electrodes were used to record monophasic action potentials (MAPs) of the left atrium. Left auricular pressure was monitored by a balloon. We determined the MAP duration at 50% and 90% repolarization (MAPD50 and MAPD90) in basal conditions and after a slow onset but sustained stretch of the atrium in the absence and presence of streptomycin. Stretch induced no overall consistent or significant change in mean MAPD50 and MAPD90. The individual responses were markedly variable. The most frequent response (about 50%) was a decrease in MAPD50 and MAPD90. In 25% of cases, there was no change, and in 25% we observed increases in MAPD50 and MAPD90. Streptomycin did not affect MAPD50 and MAPD90, but it dramatically modified the distribution of MAPD changes induced by stretch. In particular, streptomycin removed stretch-induced shortening of MAPD50 and MAPD90, whereas it did not affect stretch-induced lengthening.
Conclusion: Sustained stretch of atrium induces variable modifications of MAPD that are only partially inhibited by streptomycin. This suggests the participation of ionic channels other than specific stretch-activated channels in the response of atrial myocardium to sustained stretch.