Abstract
The mechanisms underlying remote ischemic preconditioning (r-IPC) have not been fully elucidated. In particular, it is unknown how the cardioprotective signal is transmitted from the preconditioned remote organ to the heart. We hypothesize that r-IPC activates a neural pathway, and that the cardioprotective signal reaches the heart via the vagus nerve, preconditioning the heart through the activation of muscarinic receptors. Our aim was to determine the possible role of the vagus nerve and muscarinic receptors in the mechanisms of r-IPC cardioprotection. Methods: anesthetized rabbits (n=6, r-IPC) were subjected to 3-cycle hind limb ischemia (5 min) and reperfusion (5 min). The hearts were then excised and perfused (Langendorff technique). Myocardial infarction was induced by 30 min of global ischemia followed by 2 h of reperfusion. In the non-r-IPC group (n=5), animals were subjected to a sham operation and then received the same protocol as group 1. Group 3 (r-IPC with vagal section, n=4) received the same protocol as group 2, but the left and right vagus nerves were sectioned before r-IPC. Group 4 (r-IPC with atropine, n=4) received the same protocol as group 2, but atropine was administered during the r-IPC protocol. In group 5 (vagal stimulation, n-4), the right vagus nerve was sectioned and efferently electrically stimulated. Then, the same protocol as in group 1 was performed. Results: In the non-r-IPC group, infarct size was 39.9±4.8%. r-IPC decreased infarct size to 22.7±5.7% (p<0.05). Vagal section and atropine abolished the effect of r-IPC, reaching an infarct size of 53.2±3.5% and 39.8±2.1, respectively (p<0.05). Vagal stimulation decreased infarct size to 18.1±4.7% (p<0.05). Conclusion: r-IPC activates a neural afferent pathway and the cardioprotective signal reaches the heart via the vagus nerve (efferent via). Acetylcholine acting on muscarinic receptors thus activates the IPC phenomenon.
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