Search

Aim : The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on the lungs as a remote organ after performing hindlimb ischemia-reperfusion (I/R) and by assessing biochemical and histopathological analysis. Methods : The animals were divided into three groups: control, I/R, and I/R with CAPE. I/R period for 8 h was performed on the right hindlimb of all the anesthesied rats in I/R and CAPE with I/R group. In the CAPE with I/R group, the animals received CAPE 10 μM by intraperitoneal injection 1 h before the reperfusion. The animals in the control and I/R groups received a similar volume of saline solution by means of intraperitoneal injection. At the end of the reperfusion period, a midsternotomy was performed. Blood, bronchoalveolar lavage (BAL) and lung tissue were obtained, and were used for biochemical and histopathological examination. Results : The tissue and serum malondyaldehyde levels were significantly lower in the control ( P =0.0001 and 0.001, respectively) and in the CAPE with I/R groups ( P =0.0001 and 0.003, respectively) compared to the I/R group. Tissue Na + -K + ATPase activity in the CAPE with I/R group was significantly higher than in the I/R group ( P =0.0001). Reduced activity was found in the I/R group compared to the control group ( P =0.0001). Myeloperoxidase activity ( P =0.001) and protein concentration ( P =0.034) in BAL were significantly reduced in CAPE-treated animals when compared with the I/R group. A decreased activity and protein concentration were found in the control group compared to the I/R group ( P =0.0001 and 0.024, respectively). The lungs of the I/R group displayed intense peribronchial and perivascular leukocytic infiltration in histopathological examination compared to the CAPE with I/R group ( P Conclusion : CAPE seems to be effective in protecting remote organ injury caused by increased oxidative stress and neutrophil accumulation that results from an I/R injury.

Tissue subjected to a period of ischemia undergoes functional and morphological damage that increases during the reperfusion phase. In this study, the protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit unilateral renal ischemia-reperfusion (I/R) model. New Zealand rabbits, weighing 1.5-2 kg, were randomized to receive either aprotinin 30.000 KIU x kg(-1) and 10.000 KIU x kg(-1) x h(-1) i.v. infusion (group I, n= 7) or equivalent volumes of 0.09% sodium chloride (SF) (group II, control, n= 7) i.v. 15 minutes before a 45 minutes interruption of left renal artery blood flow and then 45 minutes of reperfusion. Blood samples were obtained before and after the ischemia-reperfusion period for measurement of nitric oxide serum (NO) levels with the nitrite/nitrate colorimetric method. Histological changes were evaluated by quantitative measurements using a numerical score (0-4) and immunohistochemical analysis of inducible nitric oxide synthase (iNOS) expression was determined. A Wilcoxon W -test was used for statistical analysis of biochemical measurements and mean values were expressed as +/-sd. Histological examination revealed the distinctive pattern of ischemic renal tissue injury with obvious signs of epithelial necrosis. The intensity of epithelial necrosis was more extensive in the SF group. Immunohistochemical analysis showed that there was severe immunostaining in the tubular epithelium in both cortical and medullary regions and iNOS expression was more intense in SF-only cases. The staining results for aprotinin cases did not differ much from the non-ischemic kidney. Biochemical analysis revealed an increase in serum NO levels in both groups (P0.05), but this was more evident in the SF group (mean NO levels were 38.63 +/- 19.03 micromol x L(-1) in group I, 50.63 +/- 24.28 micromol x L(-1) in group II). No statistically important difference was observed between the two groups. These results suggest that aprotinin may be beneficial in the prevention of systemic inflammation after transient renal ischemia.

Background and aim of study: Cardioplegic arrest remains the method of choice for myocardial protection in cardiac surgery. Caffeic acid phenethyl ester (CAPE) prevents lipid peroxidation induced by ischemia-reperfusion injury and has a potent antioxidant property. We investigated the advantages of CAPE supplemented cardioplegic solution (St. Thomas’ Hospital cardioplegic solution No.: 2) on the antioxidant defense system of myocardium against ischemia-reperfusion injury. Material and methods: Isolated rat hearts were mounted on a nonrecirculating type of Langendorff apparatus. The hearts were arrested for 60 min with cardioplegic solution given at 20-min intervals and then reperfused for 15 min. The hearts were divided into three groups. Cold saline (0.9%, 4 °C) in group 1, St. Thomas’ Hospital solution in group 2 and CAPE added St. Thomas’ Hospital solution in group 3 were used as the cardioplegic solution. Krebs–Henseleit buffer solution was used for reperfusion. The tissues were examined biochemically for oxidative stress. Results: Significant differences among the three groups existed in tissue myeloperoxidase (MPO), catalase (CAT), Na + –K + ATPase activity and in the concentrations of malonydealdehyde (MDA) and 3-nitrotyrosine (3-NT). Group 2 showed significant changes in MPO ( P = 0.04), Na + –K + ATPase enzyme activity ( P = 0.02) and the levels of MDA ( P = 0.004) and 3-NT ( P = 0.01) in comparison with group 1. Group 3 efficiently reduced MDA levels ( P = 0.004) and also led to significant decrease in levels of MPO ( P = 0.006), 3-NT ( P = 0.01) and Na + –K + ATPase activity ( P = 0.01) and increase in the level of CAT ( P = 0.004) in comparison with group 1. Significant changes were also found in the levels of MDA ( P = 0.03), MPO ( P = 0.04) and CAT ( P = 0.009) in comparison between groups 2 and 3. Conclusions: We demonstrated that the administration of CAPE into cardioplegic solutions improves the antioxidant defense system of rat heart during the ischemia-reperfusion injury.

PubMedID: 12770509 The objective of this study was to investigate the effects of Daflon 500mg on tissue damage in kidney after ischemia/reperfusion hindlimb, by assessing blood biochemical assay and histopathological analysis. Rats were given Daflon 80mgkg-1 day-1 for 10 days. On 11th day of treatment, 4h ischemia followed by 4h reperfusion period was performed on right hind limb of the rats. Control groups were given only arabic gum and were subjected to same ischemia/reperfusion period. At the end of reperfusion period, erythrocyte superoxide dismutase, Na+-K+ ATPase and reduced glutathione levels were increased in the rats erythrocytes in Daflon group (P

WOS: 000178881300008 PubMed ID: 12361697 The objective of this study was to investigate the effects of trimetazidine (TMZ) on tissue damage in kidney after hindlimb ischemia-reperfusion (I/R), by assessing blood biochemical assay and histopathological analysis. Adult male Wistar rats were divided into two groups. TMZ 10 mg kg(-1) day(-1) was administrated twice a day for 10 days to the treatment group (group T, n = 10). Sham group was given only 5% gum arabic (group S, n = 10). On 11th day of treatment, 8 h I/R period was performed on right hindlimb of the rats. At the end of reperfusion period, a 5 ml blood withdrawn from ascending aorta for biochemical assays and their right kidneys were harvested for histopathological examination. Superoxide dismutase, Na+-K+ ATPase, and reduced glutathione levels were significantly increased in group T (P < 0.001). On the other hand, myeloperoxidase and malondialdehyde levels were significantly less in group T than group S (P < 0.001). Kidneys from the sham-operated group displayed intense leukocytic infiltration in histopathological examination. These overall results strongly suggested that TMZ contributes renal protection from hindlimb I/R injury by decreasing systemic oxidative stress. (C) 2002 Elsevier Science Ltd. All rights reserved.