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
Summary
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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