Abstract
Ischaemic insult in the skin flaps is a major problem in reconstructive surgery particularly in patients with diabetes mellitus. Here, we sought to investigate the effectiveness of ischaemic preconditioning (IP) on diabetic skin flaps in rat animal model. Hundred Wistar rats (90 streptozotocin treated animals and 10 nondiabetic controls) were used. Diabetes mellitus was confirmed by measuring glucose level in blood, HbA1c, and ketonuria. We used blood vessel clamping, hind limb tourniquet, and NO donors (Spermine/NO complex) to induce short-term ischaemia of tissues that will be excised for skin flaps. Animals were followed for 5 days. Flaps were photographed at day 5 and percent of necrosis was determined using planimetry. Significant decrease in percent of necrotic tissue in all groups that received preconditioning was observed. Results show that ischaemic preconditioning suppresses flap necrosis in diabetic rats irrespective of direct or remote tissue IP and irrespective of chemically or physically induced preischaemia. Spermine/NO complex treatment 10 minutes after the flap ischaemia suppressed tissue necrosis. Treatment with NO synthase inhibitor L-NAME reversed effects of IP showing importance of NO for this process. We show that IP is a promising approach for suppression of tissue necrosis in diabetic flaps and potential of NO pathway as therapeutic target in diabetic flaps.
Highlights
Skin flaps are widely used as a means of definite wound closure, in wounds with large areas of tissue loss
We aimed to investigate the effects of ischaemic preconditioning on the survival of skin flaps in diabetic rats and to compare several different methods, locations, and the timing of preconditioning/treatment
For healthy rats the HbA1c value ranges between 4% and 6% and stayed constant through entire length of the study Group A
Summary
Skin flaps are widely used as a means of definite wound closure, in wounds with large areas of tissue loss. Skin flap necrosis is major problem during the postoperative care and can result in delayed healing/nonhealing wounds and need to revisit surgical procedures. Ischaemia and inadequate blood perfusion of the flaps lead to changes in endothelial cells, excessive tissue edema, and apoptosis resulting in irreversible necrosis of flap tissue. Hyperglycaemic conditions trigger series of cellular and molecular changes that result in unresponsive endothelium, changes in protein structure due to improper glycosylation that translates to impaired blood supply in the tissues, excessive infiltration of immune cells, and increased risk for development of infections [1,2,3]. Patients with diabetes often require surgery, skin flap, or skin grafting for definite wound closure and/or limb salvation. New therapeutic approaches are needed for improving flap survival and suppression of necrosis
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