The ratio of flap necrosis area tended to be lower in the groups receiving oral PDE5 inhibitors than in the control group, although not statistically significant. The role of PDE5 inhibitors needs to be evaluated in larger studies before a conclusion can be made regarding their effects on flap viability.
The factors with increasing diabetes-prevalence lead to significant global increases in chronic kidney disease. Since hyperglycemia generates more ROS and attenuates cellular antioxidant-defense mechanisms, numerous studies demonstrated that hyperglycemia-induced oxidative stress played a major role in the extracellular matrix expansion in tissues. Although no direct relation between activation of beta-adrenergic (β-AR) system and kidney disease in diabetes and since β-blockers demonstrate marked beneficial effects due to their scavenging free radicals and/or acting as an antioxidant in diabetic animal studies, the eventual objective of the present study was to determine whether timolol-treatment of streptozotocin-induced diabetic rats (5 mg/kg, daily following diabetes-induction, for 12-week) has advantage to prevent hyperglycemia-induced renal-damage via enhancing the depressed antioxidant defense in the kidney. Light microscopy data and their quantification demonstrated that timolol-treatment prevented basically glomerular hypertrophy, expansion in mesangium cell size, thickening and fibrosis in glomerular basement membrane, and accumulation of glycogen into tubular epithelial cells. Additionally, electron microscopy data demonstrated that timolol-treatment could also prevent diabetes-induced changes in the kidney tissue such as hypertrophy in podocytes, lost of filtration gaps and slit-diaphragms, and vacuolization in the distal tubular cells. Biochemical analysis basically on enzymes of antioxidant-defense system, including glutathione-S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase, further supported that diabetes-induced damage in the kidney is mostly dependent on the increased oxidative stress and timolol, having an antioxidant-like action, could protect the kidney against hyperglycemia-induced damage without normalization of high-blood glucose level. Consequently, it can be suggested that although β-blockers are widely used for the treatment of cardiovascular diseases, β-blocker therapy of diabetics seems to be a new therapeutic approach against hyperglycemia-induced kidney damage in diabetic patients.
BACKGROUND: A high-carbohydrate diet leads to the metabolic syndrome (MetS), which leads to an increased risk for cardiovascular dysfunction; however, the effect of high-carbohydrate diets on systemic metabolism has not yet been fully determined. It has been observed that abnormal fatty acid metabolism and increased oxidative stress play a role in the pathogenesis of MetS-related cardiovascular diseases. OBJECTIVE: To examine the effects of high sucrose intake on left ventricular contractility and structure of heart tissue. METHODS: MetS was induced in male rats with drinking water supplemented with 32% sucrose for 16 weeks. Oral glucose tolerance test results and parameters related to insulin resistance were used to validate MetS. RESULTS: Body weight and blood glucose levels were higher in the MetS group compared with age-matched controls. The increased serum leptin and triglyceride levels and decreased ghrelin levels further supported the existence of MetS in the MetS group. The ratio of total oxidant status to total antioxidant status measured in serum was also higher in the MetS group compared with the control group. The hemodynamic parameters of the MetS group, such as heart rate, and systolic and diastolic blood pressure levels, were markedly higher in the MetS group, while left ventricular developed pressure was significantly diminished with prolonged time course. Moreover, these functional alterations in cardiac preparations were further supported with structural changes such as significant increases in myofibril undulation and increased lipid droplets. CONCLUSIONS: These data highlight the link between high carbohydrate intake, MetS and cardiac dysfunction, in part due to increased systemic oxidative stress and lipid deposition in the heart tissue.
AIm: Bacitracin is one of the most frequently used agents for the topical irrigation of the cerebral cortex. The aim of this study is to investigate whether bacitracin has histopathological and ultrastructural effects when applied topically to the cerebral cortex. mATErIAl and mEThOds: Twenty-eight rats were randomly assigned to four groups. Except the control group, each rat underwent left frontoparietal craniectomy with dural removal. Then, in the sham group a piece of dry absorbable gelatin sponge was placed over the left hemisphere; in the saline group a gelatin sponge soaked in normal saline; and in the bacitracin group a gelatin sponge soaked in 500 units bacitracin was used. After 48 hours, brain tissues were extracted for histopathological and electron microscopic analyses.rEsulTs: Among the four groups dark stained neurons were found to be statistically higher in number in the bacitracin group compared with the control, sham and saline groups. Electron microscopic evaluation revealed that, in the bacitracin group, almost all cytoplasmic organelles were poorly preserved.CONClusION: Topical application of the bacitracin on to the cerebral cortex caused histopathological and ultrastructural changes in the neural tissue. These changes may be an evidence for the neurotoxic effects of bacitracin.
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