Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats

IntroductionHydrogen sulfide (H2S) has been recognized as an important signaling molecule in cellular O2 sensing, wound healing and angiogenesis. Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic foot wounds. The Transdermal Arterial Gasotransmitter Sensor (TAGS) device measures real-time H2S emissions through the skin. In this work, we utilize the novel TAGS device to characterize transdermal H2S emissions during diabetic and non-diabetic wound healing for the first time. MethodsDorsal peninsular-shaped myocutaneous ischemic flap wounds were created under anesthesia. Sprague Dawley (SD) and Zucker Diabetic Fatty (ZDF) rats (n=10 each) were compared. Transdermal H2S emissions, laser speckle contrast images (LSCI) and planimetric photos were serially taken from the wound flap area over 14 days. After animal sacrifice, healed flap tissue was collected for histologic (H&E) analysis of panniculus carnosus (skin muscle) viability as a proxy for degree of ischemic insult. ResultsZDF rats were significantly hyperglycemic (mean 516 mg/dL vs. 201 mg/dL for SD, P=0.002). Similar mean baseline (preoperative) H2S emissions were observed in SD (16 ppb) and ZDF (12 ppb) rats (P=0.25). During revascularization and healing, ZDF wounds emitted significantly less H2S (10 ppb at day 14) as compared to SD (28 ppb at day 14, P