Metformin HCl has curative effect on rebuilding of ventricular diastolic functions in high-fat-diet fed rats

Myocardial lipid accumulation due to diabetes and/or obesity plays a role in the progression of left ventricular diastolic dysfunction. Our aims were to exhibit the correlation between histopathologic stage of the liver and cardiac functions, and to evaluate the effects of metformin HCl and rosiglitazone on myocardial functions. Thirty-two male Sprague-Dawley rats were divided into four groups to exhibit the correlation between histopathologic stage of the liver and cardiac functions and to determine whether metformin HCl and rosiglitazone have effects on cardiac functions. For 20 weeks, one group was fed standard rat basic diet, whereas the other groups were on high-fat-diet. During the last 4 weeks, metformin HCl was given to the third group, rosiglitazone to the fourth group. Histological evaluation of rat livers yielded significantly higher steatosis grade in high-fat-diet group and different fibrosis stages among groups. Also, there was significant correlation between diastolic functions and steatosis grade/fibrosis stage of rat liver. Electrophysiological study of hearts via Langendorff technique showed better coronary perfusion pressures and diastolic functions in standard-diet and metformin HCl groups compared to other groups. Metformin HCl improves LV diastolic dysfunction and coronary perfusion pressures

Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats

Renal ischemia-reperfusion (IR) causes remote liver damage. Oxytocin has anti-inflammatory and antioxidant effects. The main purpose of this study was to evaluate the protective function of oxytocin (OT) in remote liver damage triggered by renal IR in rats. Twenty four rats were randomly divided into four different groups, each containing 8 rats. The groups were as follows: (1) Sham operated group; (2) Sham operated+OT group (3) Renal IR group; (4) Renal IR+OT group. OT (500microg/kg) was administered subcutaneously 12 and 24 hours before and immediately after ischemia. At the end of experimental procedure, the rats were sacrificed, and liver specimens were taken for histological assessment or determination of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), paraoxonase (PON-1) activity and nitric oxide (NO). The results showed that renal IR injury constituted a notable elevation in MDA, TOS, Oxidative stress index (OSI) and significantly decreased TAS, PON-1 actvity and NO in liver tissue (p<0.05). Additionally renal IR provoked significant augmentation in hepatic microscopic damage scores. However, alterations in these biochemical and histopathological indices due to IR injury were attenuated by OT treatment (p<0.05). These findings show that OT ameliorates remote liver damage triggered by renal ischemia-reperfusion and this preservation involves suppression of inflammation and regulation of oxidant-antioxidant status.