title: Hyperglycemia increases susceptibility to ischemic necrosis.
abstract: Diabetic patients are at risk for spontaneous foot ulcers, chronic wounds, infections, and tissue necrosis. Current theories suggest that the development and progression of diabetic foot ulcers are mainly caused by arteriosclerosis and peripheral neuropathy. Tissue necrosis plays a primordial role in the progression of diabetic foot ulcers but the underlying mechanisms are poorly understood. The aim of the present study was to investigate the effects of hyperglycemia per se on the susceptibility of ischemic tissue to necrosis, using a critical ischemic hind limb animal model. We inflicted the same degree of ischemia in both euglycemic and streptozotocin-induced hyperglycemic rats by resecting the external iliac, the femoral, and the saphenous arteries. Postoperative laser Doppler flowmetry of the ischemic feet showed the same degree of reduction in skin perfusion in both hyperglycemic and euglycemic animals. Nevertheless, we found a significantly higher rate of limb necrosis in hyperglycemic rats compared to euglycemic rats (71% versus 29%, resp.). In this study, we revealed that hyperglycemia per se increases the susceptibility to limb necrosis in ischemic conditions. Our results may help to better understand the physiopathology of progressive diabetic wounds and underline the importance of strict glycemic control in patients with critical limb ischemia.
authors.affiliation: Division of Plastic, Reconstructive and Aesthetic Surgery, University Hospitals of Geneva and Faculty of Medicine, University of Geneva, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland.
authors.forename: D
authors.initials: D
authors.lastname: Lévigne
authors.forename: M
authors.initials: M
authors.lastname: Tobalem
authors.forename: A
authors.initials: A
authors.lastname: Modarressi
authors.forename: B
authors.initials: B
authors.lastname: Pittet-Cuénod
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity; D048909:Diabetes Complications / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000473:pathology; D017719:Diabetic Foot / Q000473:pathology; D004198:Disease Susceptibility; D005121:Extremities / Q000473:pathology; D006943:Hyperglycemia / Q000150:complications* / Q000473:pathology; D007511:Ischemia / Q000150:complications* / Q000473:pathology; D017078:Laser-Doppler Flowmetry; D008297:Male; D009336:Necrosis / Q000150:complications* / Q000473:pathology; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D012867:Skin / Q000473:pathology; D013311:Streptozocin
chemical_list: D013311:Streptozocin