Abstract
To investigate the effect of remote ischemic post-conditioning (RIPoC) against ischemia-reperfusion (I/R) injury on flaps of rats. Sprague-Dawley rats were randomized into the Sham, Control, RIPoC1 and RIPoC2 groups. All the animals were submitted to a 5×4 cm superficial inferior epigastric artery flap. Eight hours of flap ischemia was induced and two protocols of limb RIPoC were applied. Tissue MDA level and SOD activity in 24-h reperfusion were assessed. Flap survival was assessed 7 days postoperatively. Compared to the Control group, the RIPoC1 group showed statistically decreased MDA level at 6-, 12-, and 24-h reperfusion (P = 0.01, P < 0.01 and P < 0.01, respectively), and statistically increased SOD activity at 12- and 24-h reperfusion (P < 0.05 and P < 0.01, respectively). Flap survival rate on the 7th day was significantly higher in the RIPoC1 group than the control group (47.9 ± 6.4 vs . 29.4 ± 7.1 %, P < 0.01). Three cycles of 5-min Limb remote ischemic post-conditioning rather than a single cycle of 15-min limb RIPoC has protective effect on flaps against ischemia-reperfusion injury by attenuating oxidative stress.
Highlights
Free flap transplantation is frequently used in plastic and reconstructive surgery
We aimed to evaluate the antiischemic properties of two protocols of limb Remote ischemic post-conditioning (RIPoC) in a rat model of epigastric island flaps subjected to ischemia reperfusion (I/R) injury, and the possible effect of RIPoC on reduction of I/R-induced oxidative stress
RIPoC1 significantly attenuated the decrease in superoxide dismutase (SOD) activity at 12- and 24-h reperfusion timepoints (P < 0.05 and P < 0.01, respectively) while RIPoC2 only attenuated the decrease in SOD activity at 24-h reperfusion timepoints (P < 0.05)
Summary
Excessive production of free radicals and/or reactive oxygen species during reperfusion triggers lipid peroxidation and initiates ischemia reperfusion (I/R) damage[1]. Numerous labs have demonstrated that ischemic post-conditioning (IPostC), defined as brief intermittent episodes of ischemia at the onset of reperfusion, is an endogenous protective strategy against I/R injury for multiple organs[4,5,6]. The underling mechanism of IPostC involves limiting the oxidative stress by reducing reactive oxygen metabolites and increasing antioxidant enzymes’ activity in tissues after prolonged ischemic insult[7]. Recent preclinical papers show that RIPoC performed in the limbs can generate effective cardioprotection and neuroprotection against I/R injury similar to IPostC9,10, yet its protective effect on skin flap has not yet been well investigated
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