Myocardial eNOS expression and NO changes in diabetic rats with ischemia-reperfusion injury in rats.doc

 PAGE \* MERGEFORMAT 25 Myocardial eNOS expression and NO changes in diabetic rats with ischemia-reperfusion injury in rats Abstract measured in different cycles of streptozotocin (STZ)-induced diabetic rat cardiac eNOS expression, NO change and its implications for ischemia / reperfusion (I / R) injury. 【Methods】 block and open the establishment of the left anterior descending coronary artery in rats with acute myocardial I / R model, with TTC staining to measure myocardial I / R after the infarct area; Western blot analysis to measure myocardial eNOS expression; morphometry (Morphometric ) Determination of nitro-tyrosine (Nitrotyrosine, NT) levels; Determination of NO by nitrate reductase levels. 【Results】 2 weeks after treatment in the STZ diabetic group (2WD) than the corresponding period of myocardial infarct size in control group (2WC) significantly reduced, STZ treatment for 16 weeks (16WD), infarct size than the corresponding control group (16WC) increased; endothelial of nitric oxide synthase (eNOS) expression in 2WD in the cardiomyocytes was increased by 34% compared with 2WC However, in 16WD significantly reduced compared 16WC; superoxide nitrite ions (Peroxynitrite, ONOO-) generated a product of nitro-tyrosine ammonia landmark acid (nitrotyrosine, NT) in the 2WD group were lower than 2WC about 49%, but in 16WD group was significantly increased compared 16WC; blood nitric oxide (Nitric oxide, NO) level compared with 2WC group 2WD groups increased, but the 16WD group than 16WC group significantly reduced. 【Conclusion】 STZ-induced diabetes, early, late on myocardial I / R injury showed the opposite effect. This may be due to early and late reverse diabetes, myocardial eNOS expression and NO changes caused. Keywords: Diabetic myocardial ischemia reperfusion endothelial nitric oxide synthase nitric oxide nitrotyrosine Abstract: 【Objective】 To determine the effects of different-term STZ-induced diabetes on ischemia / reperfusion (I