Ali Gül

The effects of caffeic acid phenethyl ester on tissue damage in lung after hindlimb ischemia-reperfusion

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 microM by intraperitoneal injection 1h 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<0.05). 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.

N-Acetylcysteine for Preventing Pump-Induced Oxidoinflammatory Response During Cardiopulmonary Bypass

PurposeTo investigate the effect of N-acetylcysteine on preventing pump-induced oxidoinflammatory response during cardiopulmonary bypass (CPB).MethodsForty patients undergoing coronary artery bypass grafting (CABG) were randomly divided into a study group (n = 20), given 50 mg kg−1N-acetylcysteine intravenously for 3 days, and a control group (n = 20) given saline. Serum samples were collected for measurement of myeloperoxidase (MPO), malondialdehyde (MDA), interleukin-6, Α1-acid glycoprotein (AAGP), and C-reactive protein (CRP) during surgery and postoperatively.ResultsThe MPO and MDA values showed a similar pattern during and after CPB in the study group, with significantly less variance than in the control group. Interleukin-6 showed similar patterns in the two groups, but the data from 30 min after the start of CPB and from 6 h post-CPB were significantly different. The AAGP and CRP values were both elevated during CPB in the two groups without a significant difference, but 6 and 24 h post-CPB, the values were significantly higher in the control group than in the study group.ConclusionsN-Acetylcysteine decreased pump-induced oxidoinflammatory response during CPB, suggesting that it could be a novel therapy for assisting in the prevention of CBP-induced oxidoinflammatory damage.

Effects of trimetazidine on tissue damage in kidney after hindlimb ischemia-reperfusion.

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, 8h 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.

Effects of Daflon on oxidative stress induced by hindlimb ischemia/reperfusion.

The objective of this study was to investigate the effects of Daflon 500 mg on tissue damage in kidney after ischemia/reperfusion hindlimb, by assessing blood biochemical assay and histopathological analysis. Rats were given Daflon 80 mg x kg(-1) x day(-1) for 10 days. On 11th day of treatment, 4h ischemia followed by 4 h 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<0.01, for all). On the other hand, serum myeloperoxidase and malondialdehyde levels were significantly lower in the Daflon-received rats (P<0.01, for all). Histopathological studies demonstrated that, there was a prominent tubulointerstitial injury with loss of brush border and this degeneration was accompanied by segmental glomerular degeneration also for both control and Daflon group. Daflon-received group animals displayed significantly less periglomerular and perivascular leukocytic infiltration (P=0.015). These overall results suggest that Daflon contributes renal protection from hind limb ischemia/reperfusion injury in some degree, by decreasing systemic oxidative stress.

The effect of ethylenediaminetetraacetic acid on calcific degeneration in bovine pericardium

Calcification is the most frequent cause of the clinical failure of bovine pericardium bioprosthetic valves, preventing their widespread application for surgical treatment. The aim of this study was to minimize calcific degeneration in bovine pericardium by using a chelating agent, ethylenediaminetetraacetic acid (EDTA). Freshly excised bovine pericardium was dissected free from adhering fat tissue and cut into 1-cm2 pieces that were rinsed in phosphate-buffered saline solution (PBS) and transferred into 4°C PBS containing 1% glutaraldehyde (GA) for initial fixation, then allocated into two groups. Group I received the same treatment in a fresh solution for 5 more days. Group II underwent an additional fixation step in PBS solution (pH 7.4, 37°C) containing 11% EDTA for a period of 48 h (30 ml/g tissue) and was then transferred into freshly prepared PBS + 1% GA solution at 37°C for another 3 days. To investigate the calcification rate, pericardial patches were inserted into the dorsal pouches of 25 male Wistar rats for 21 days. Calcium levels were measured with an atomic absorption spectrophotometer and examined histo-pathologically. The calcium content of EDTA-treated pericardium (Group II), 21 ± 3.8 µg/mg, was significantly lower than that of Group I, 43.3 ± 9.2 µg/mg. Assessment of the degree of calcification in the histological sections generally agreed well with the results of the chemical analyses. Calcium deposition in Group I samples were found to be solid mineral depositions, whereas in the Group II pericardial samples, only smaller traces of calcium were found. Calcific degeneration in bovine pericardium can be reduced by using chelates such as EDTA.