Ischemia‐Reperfusion Injury of Adipofascial Tissue: An Experimental Study Evaluating Early Histologic and Biochemical Alterations in Rats

Abstract

Fat necrosis remains a serious complication in reconstructive flaps. In clinical setting, it is well known that fat tissue is more susceptible to ischemic events. We aimed to evaluate early histological and biochemical changes of adipofascial tissue in an experimantal model. An epigastric flap model in rats was used to evaluate the effect of ischemia-reperfusion (I-R) injury on adipofascial tissue. Two groups of animals (one with ischemia alone and other ischemia-reperfusion group) were used to evaluate the degree of histological edema, congestion and extravascular bleeding, and early biochemical alterations within the adipofascial flaps. The biochemical parameters included glutathione (GSH) and malondialdehyde (MDA). In each group, contralateral groin subcutaneous adipose tissue served as control. These evaluations were compared to normal unmanipulated, contralateral abdominal subcutaneous adipose tissue. The ischemia-reperfused flap group showed histologically significantly much edema congestion and bleeding than the control groups (P < .0001). The control group showed less edema in fat tissue than the ischemia-alone group (P < .05). All of the flaps in the ischemia-only group showed significantly less bleeding and edema than I-R group (P < .001). The ratio of MDA/GSH was 33 in control, 37 in ischemia alone, and 82 in ischemia-reperfusion groups, respectively. This study confirms that significant histologic and biochemical alteration occurs after ischemia and ischemia-reperfusion events in adipose tissue. Marked drop in adipose tissue antioxidant levels after I-R suggested that preemptive measures to this decrease should be undertaken in clinical settings.

Cryolipolysis for Noninvasive Fat Cell Destruction

“…14,15 Reperfusion of adipose tissue rendered ischemic by cold exposure may result in oxidative stress, including elevation of lipid peroxidation and reduced glutathione levels, ultimately resulting in cell death. 25,26 These results suggest that adipocyte apoptosis provided the stimulus for the observed inflammatory response, although it is likely that this response also contributes to the total number of adipocytes killed. The inflammatory response observed appeared similar to that reported previously in subcutaneous fat after exposure to intense cold.…”

Thioredoxin Protects Skin Flaps from Ischemia-Reperfusion Injury

“…Moreover, the repeated occlusion and release of the pedicle can promote thrombus formation and vasospasm, which may jeopardize flap survival. Plenty of evidence shows that the concentration of various antioxidants, such as glutathione and uric acid, decrease in response to the reactive oxygen species burst during skin flap ischemia-reperfusion, 29,30 and supplementation of the antioxidants may help neutralize the oxidative stress and enhance the tissue tolerance to reactive oxygen species. 31 In our study, prophylactic administration of recombinant human thioredoxin-1 significantly improves the flap tissue tolerance through its antioxidant and antiapoptotic activity, and avoids extra invasive procedures.…”

Emerging role of adipose tissue hypoxia in obesity and insulin resistance

“…It may also explain the impact of ischemia/reperfusion in the adipose tissue (71). The hypoxia is able to induce inflammation in adipose tissue by induction of gene expression in adipocytes and macrophages.…”

“…In ischemia research, hypoxia has been well-documented in the induction of cell death in heart and brain (129). In adipose tissue, ischemia induces damages in several forms, such as edema congestion and bleeding (71). …”