Abstract

Multiterritory perforator flap is an important plastic surgery technique, yet its efficacy can be limited by partial necrosis at the choke Ⅱ zone. Butylphthalide (NBP) has been used for many diseases but has not been studied in the multiterritory perforator flap. With the effect of NBP, we observed increasing in capillary density, inhibition of autophagy and oxidative stress, and a reduction in apoptosis of cells, all consistent with increased flap survival. However, the protective effect of NBP on multiterritory perforator flap was lost following administration of the autophagy agonist rapamycin (Rap). Through the above results, we assumed that NBP promotes flap survival by inhibiting autophagy. Thus, this study has found a new pharmacological effect of NBP on the multiterritory perforator by inhibiting autophagy to prevent distal postoperative necrosis and exert effects on angiogenesis, oxidative stress, and apoptosis within the flap.

Highlights

  • Soft tissue reconstruction is a central component of plastic surgery (Luo et al, 2020)

  • We explore the effects of n-butyl phthalate (NBP) on autophagy within perforator flaps and study autophagy-mediated effects on angiogenesis, oxidative stress, and apoptosis within a multiterritory perforator flap

  • H&E results showed that the NBP-treated group had a significant increase in the number of microvessels, and the average vascular density was higher compared with the control group (Figures 1E,G), suggesting improved angiogenesis

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Summary

Introduction

Soft tissue reconstruction is a central component of plastic surgery (Luo et al, 2020). Necrosis of the distal flap is a common postoperative complication (Chen et al, 2018) as angiogenesis is insufficient to support the growth and metabolism of distal tissues, leading to tissue level ischemic necrosis (Chen et al, 2017). This can occur after the perforating branch is established and blood vessels begin to grow distally through pedicle blood vessels (Wang et al, 2017). Prior studies have shown that inhibition of oxidative stress and apoptosis can reduce the risk of developing ischemia-reperfusion injury and distal necrosis of the flap (Lin et al, 2018)

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