Abstract

Background: Anesthetic preconditioning (AP) is known to mimic ischemic preconditioning. The purpose of this study was to investigate the effects of an interrupted sevoflurane administration protocol on myocardial ischemia/reperfusion (I/R) injury. Methods: Male Wistar rats (n = 60) were ventilated for 30 min with room air (control group, CG) or with a mixture of air and sevoflurane (1 minimum alveolar concentration—MAC) in 5-min cycles, alternating with 5-min wash-out periods (preconditioned groups). Cytokines implicated in the AP response were measured. An (I/R) lesion was produced immediately after the sham intervention (CG) and preconditioning protocol (early AP group, EAPG) or 24 h after the intervention (late AP group, LAPG). The area of fibrosis, the degree of apoptosis and the number of c-kit+ cells was estimated for each group. Results: Cytokine levels were increased post AP. The area of fibrosis decreased in both EAPG and LAPG compared to the CG (p < 0.0001). When compared to the CG, the degree of apoptosis was reduced in both LAPG (p = 0.006) and EAPG (p = 0.007) and the number of c-kit+ cells was the greatest for the LAPG (p < 0.0001). Conclusions: Sevoflurane preconditioning, using an interrupted anesthesia protocol, is efficient in myocardial protection and could be beneficial to reduce perioperative or periprocedural ischemia in patients with increased cardiovascular risk.

Highlights

  • Preconditioning protocols can protect the myocardium against ischemia/reperfusion injury (I/R) by preconditioning protocols

  • Ischemic preconditioning (IP) increases the number of c-kit+ and flk-1+ progenitor cells in the myocardium subjected to ischemia and reperfusion [6]

  • We found that the mean vascular endothelial growth factor (VEGF) level was elevated 3 h post-exposure at 137.78 pg/mL vs. 61.15 pg/mL

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Summary

Introduction

Preconditioning protocols can protect the myocardium against ischemia/reperfusion injury (I/R) by preconditioning protocols. Ischemic preconditioning (IP) by short, repetitive bouts of ischemia represents the most powerful endogenous cardioprotective mechanism [1,2]. Pharmacological preconditioning protocols using volatile anesthetics termed anesthetic preconditioning (AP) represent low-risk procedures with a cardioprotective potency that is similar to IP [3]. Both IP and AP occur in a biphasic pattern, consisting of an early preconditioning phase, within the first 2–3 h, and a late preconditioning phase after 12–24 h [4]. IP increases the number of c-kit+ (receptor for stem cell factor) and flk-1+ progenitor cells in the myocardium subjected to ischemia and reperfusion [6]. When compared to the CG, the degree of apoptosis was reduced in both

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