Plastic Surgery Research Council
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DEFINING THE SALVAGE TIME WINDOW FOR THE USE OF ISCHEMIC POST-CONDITIONING IN SKELETAL MUSCLE ISCHEMIA REPERFUSION INJURY
Presenter: Mei Yang, MD
Co-Authors: Mendenhall SD; Taylor NW; Reichensperger J; Derby B; Neumeister MW
Southern Illinois University School of Medicine

Introduction: Ischemic postconditioning (IPOC) has been shown to ameliorate ischemia/reperfusion (I/R) injury in skeletal muscle and skin flaps. However, recent studies suggest that the benefits (and potential risks) of IPOC may be dependent on the duration of ischemia. The purpose of this study was to define the optimal ischemic salvage time window for which IPOC reduces I/R injury in a skeletal muscle flap.

Methods: Utilizing a gracilis pedicled flap model, 48 SD rats were divided into I/R only (control) and I/R with IPOC groups with 4 durations of ischemia (2,4,6,& 8 hrs). The IPOC goup received 6 cycles of 15 sec of reperfusion followed by 15 sec of re-clamping. Muscles were harvested 24 hrs after I/R injury to examine tissue viability (NBT staining), histology, and MPO activity. Protective gene expression related to mitochondrial metabolism (complex I,II,III), endothelial cell function (eNOS), and apoptosis (Bcl-2) were examined.

Results: NBT assay showed similar muscle flap viability between control and IPOC groups after 2 hrs of ischemia (p>0.05). Improved flap viability was detected in IPOC groups after 4 and 6 hrs of ischemia time compared to controls (p<0.05). After 8 hrs of ischemia, tissue from both groups showed low viability. Histological examination corroborated with NBT results. Higher expression of complex I, II, III, eNOS, and Bcl-2 were observed in the IPOC group after 6 hrs or less of ischemia time (p<0.05). MPO activity was similar in both groups at all time points except 8 hrs ischemia in which the control group had higher activity (p<0.05).

Conclusion: Protection by IPOC occurred after 4 & 6 hrs ischemia, with the most protection after 4 hrs. IPOC offered minimal protection from I/R injury following 2 hrs of ischemia and had a slightly detrimental effect after 8 hrs of ischemia. IPOC used within this salvage time window was accompanied by improved mitochondrial and vascular function. The loss of protective effect by IPOC with prolonged ischemia may be from an exhaustion of endogenous mitochondrial enzymes and NOS. IPOCmay prove clinically useful as a post-injury salvage technique.


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