Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/reperfusion injury. Heat shock protein 72 (HSP-72) protects against κDa ischemia/reperfusion damage in vivo. The effect of diabetes on HSP-72 expression in vivo is unknown. The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. Rats were assigned to four groups: control (C), streptozotocin-induced diabetic (D), acute hyperglycemia (A), and L-Nω-nitro-l-arginine treated (L). Rats were subjected to hyperthermia and allowed to recover for 4 hours. Intestine and liver samples from heated (H) and nonheated (NH) rats were analyzed for HSP-72 by Western blot. HSP-72 levels were increased significantly in CH compared to CNH rats. No deaths occurred in CH rats; however, death rates were significant in AH, DH, and LH rats. DH rats died earlier than LH and AH rats. HSP-72 in liver and intestine was reduced significantly in LH rats. When compared with CH rats the surviving AH and DH rats exhibited similar HSP-72 levels in the liver. Diabetes, acute hyperglycemia, and L-Nω-nitro-l-arginine treatment lower heat stress tolerance. NOS is required for HSP-72 expression, but not survival. Diabetics who survive heat stress moderately express HSP-72. Characterization of altered thermotolerance and HSP-72 may provide mechanisms for the deranged diabetic stress response.
