Approximately 30% of patients suffer supraventricular dysrhythmias after cardiac bypass. While the heart can be constructively preconditioned to maintain function against subsequent ischemic insult using a variety of stimuli across many species, preconditioning in experimental animals is associated with decreased postischemic reperfusion cardiac dysrhythmias. This mode of therapeutic preconditioning has not been previously examined in human atrial myocardium. We therefore hypothesized that preconditioning provides both antidysrhythmic and functional protection to human atria. To study this, human atrial trabeculae were suspended in organ
baths, paced at 1 Hz, while force development and ectopy were recorded before and after simulated
ischemia. The study consisted of five groups: (1) control trabeculae (n = 12), (2) trabeculae exposed to dysrhythmogenic stimuli (
phenylephrine 50 microM and
isoproterenol 25 microM (n = 8)), (3) trabeculae exposed to
ischemia-reperfusion (I/R) injury and then
drug stimulated (n = 10), (4) trabeculae preconditioned with
adenosine (
ADO 125 microM) then
drug stimulated (n = 10), and (5) trabeculae preconditioned with ischemic preconditioning (IPC) then
drug stimulated (n = 6) each at end reoxygenation. Differences between groups were assessed using X2 analysis and ANOVA (Bonferroni/Dunn). Results demonstrated that human atrial trabeculae did not exhibit dysrhythmia at baseline or when stimulated with alpha and beta agonists. After I/R, control trabeculae exhibited stimulated reperfusion dysrhythmia, while trabeculae preconditioned with either
ADO or transient
ischemia exhibited decreased stimulated dysrhythmia (each P < 0.05
vs. I/R). Functionally, I/R decreased developed force (DF) to 16 +/- 2% of baseline (%BDF) while
ADO pretreatment increased postischemic DF to 41 +/- 3% BDF (P < 0.05
vs. I/R) while IPC increased DF to 49 +/- 3% BDF (P < 0.05
vs. I/R). We conclude that (1) human atrial trabeculae can ve functionally preconditioned with either
ADO or IPC, and (2) protective preconditioning/ cardioprotection does extend to dysrhythmia control and is therapeutically accessible in human atrial myocardium.