Effects of apelin-13 on myocardial ischemia reperfusion injury in streptozotocine induced diabetic rats.

AIM: We want to investigate the protective effects of apelin-13 on myocardial ischemia reperfusion (I/R) injury. MATERIAL AND METHODS: 30 Wistar Albino rat were divided into 5 groups (n:6), namely control group (C), diabetes group (D), diabetes+apelin-13 group (DA), diabetes+I/R group (DIR) and diabetes I/R+apelin-13 group (DIR-A). Rats were subjected to 30­min ischemia and 90­min reperfusion. Biochemical and histopathological parameters were measured. RESULTS: Caspase-3 enzyme activity was significantly higher in the DIR group than in the C, DA, and DIR-A groups. The intensity of caspase 3 enzyme activity was significantly higher in the I/R group than in all other groups. Inflammation and vascular dilatation were found significantly higher in the DIR group than in all other groups. Congestion was significantly higher in the DIR group than in the C and D groups. TOS enzyme activity was significantly higher in the DIR group than in the C, DA and DIR-A groups. TAS enzyme activity was significantly lower in the DIR group than in the C and DIR-A groups. CONCLUSION: We believe that the protective effects of apelin-13 in ischemia-reperfusion injury and its use indications can be demonstrated in detail as long as the findings we have reached in our study are supported by other studies (Tab. 2, Fig. 10, Ref. 43).

Effect of apelin-13 on erythrocyte deformability during ischaemia-reperfusion injury of heart in diabetic rats.

OBJECTIVES: Erythrocyte deformability and plasma viscosity are of crucial importance for the perfusion of tissues and organs. The aim of this study was to evaluate the effect of apelin-13 on erythrocyte deformability during IR heart injury in diabetic rats. METHODS: Eighteen Wistar Albino rats were included in the study after streptozotocin (55 mg/kg) treatment for four weeks of observation for diabetes existence. The animals were randomly assigned to one of five experimental groups. In the Group C, DC (sham-control group) and DCA (sham-control group-apelin-13), the coronary artery was not occluded or re-perfused. In the Group DIR, a branch of the left coronary artery was occluded for 30 minutes followed by 90 minutes of re-perfusion to produce IR. In the Group DIRA, a branch of the left coronary artery was occluded for 30 minutes followed by 90 minutes of re-perfusion to produce IR, and apelin-13 was administrated via 10 µg.kg-1 IP route 30 minutes before ligating the left coronary artery.Deformability measurements were performed in erythrocyte suspensions containing Htc 5% in a PBS buffer. RESULTS: The deformability index was significantly increased in diabetic rats; however, it was similar in Group DC, DCA and DIRA. It was significantly increased in the Group DIR when compared to the Group C, DIRA, DCA and DC. The relative resistance was increased in IR models. CONCLUSION: Erythrocyte deformability was decreased in rats having diabetes and IR injury. This injury might lead to further problems in microcirculation. It was shown that apeline-13 may be useful in enhancing the adverse effects of this type of injury (Fig. 1, Ref. 35).

The effects of iloprost on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of iloprost (I) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Twenty-four Wistar Albino rats were randomized into four groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Only laparotomy was applied in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes. Group iloprost (Group I) received intravenous infusion of iloprost 0.5 ng/kg/min, without ischemia and reperfusion. Group I/R/I received intravenous infusion of iloprost 0.5 ng/kg/min immediately after 2 hours of ischemia. At the end of the study, lung tissue was obtained for determining total oxidant status (TOS) and total antioxidant status (TAS) levels, histochemical and immunohistochemical determination. RESULTS: Diffuse lymphocyte infiltration was detected in immunohistochemical examination of lung tissue in Group I/R. The connective tissue around bronchi, bronchioles and vessel walls was found to be increased. Although minimal local lymphocyte infiltration was detected in some fields in Group I/R/I, the overall tissue was found to be similar to Group S. iNOS expression was significantly higher in Group I/R, when compared with Group S and significantly lower in Group I/R/I compared to Group I/R.TOS levels were significantly higher in Group I/R, when compared with groups S and I (p = 0.028, p = 0.016, respectively) and significantly lower in group I/R/I, when compared with Group I/R (p = 0.048). TAS levels were significantly higher in Group I/R, when compared with groups S, I (p = 0.014, p = 0.027, respectively) and significantly lower in Group I/R/I, when compared with Group I/R (p = 0.032). CONCLUSION: These results indicate that administration of iloprost may have protective effects against ischemia reperfusion injury (Fig. 8, Tab. 1, Ref. 30)

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Thirty-six Wistar rats were randomized into six groups (n=6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively, without ischemia and reperfusion. Group IR+VEGF and Group IR+AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively immediately after 2 hours period of ischemia. At the end of reperfusion period. Lung tissue samples were taken for biochemical examination. Total oxidant status (TOS) and total antioxidant status (TAS) levels in lung tissue were determined by using a novel automated method. p<0.05 was considered as statistically significant. RESULTS: TOS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.004, p=0.011, p=0.017, respectively) and significantly lower in groups I/R+AM and I/R+VEGF, when compared with Group I/R (p=0.018, p=0.006, respectively). TAS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.006 p=0.016, p=0.016, respectively) and significantly lower in Group I/R+AM, when compared with Group I/R (p=0.016). CONCLUSION: These findings indicate that AM and VEGF acted effectively on the prevention of lung injury induced by skeletal muscle ischemia-reperfusion injury in a rat model (Fig. 2, Ref. 30).