The effect of taurolidine on experimental thrombus formation.

Venous thrombosis can be the source of emboli, a significant health risk encountered throughout surgical and medical clinics. Taurolidine is an antimicrobial agent used to prevent intraabdominal adhesion formation and sepsis in experimental and clinical trials. The aim of this study is to evaluate effect of taurolidine on experimental thrombus formation and make a comparison with low-molecular weight heparin. Four groups of ten Wistar-Albino rats (300-350 g) were used; with the first and second groups each being administered 10 and 20 mg of taurolidine, the third group low-molecular weight heparin and the fourth group saline solution (control group) respectively. Experimental thrombus formation was performed in rats in the area of the abdominal inferior vena cava by using a combination of stasis and hypercoagulability described by Wessler et al. [Wessler, S., Reimer, S.M., Sheps, M.C., 1959. Biologic assay of a thrombosis inducing activity in human serum. J. Appl. Physiol. 14:943-946.]. Thrombocyte count, the weight of thrombus, prothrombin time and activated partial thromboplastin time and activities of coagulation factors were measured and compared across groups. Thrombus weights in the taurolidine treated groups were lower than the control group and greater than the low-molecular weight heparin treated group. Taurolidine was found to decrease activities of coagulation factors V, VIII, IX, XI and XII. Taurolidine showed no effect on activated partial thromboplastin time and prothrombin time values; however, it decreased thrombus weight, but not as much as low-molecular weight heparin. The cause of these findings in our study may be related to the minimized effect of taurolidine on factor II, VII, and X activities. These effects likely render the agent ineffective in the prevention of venous thrombosis. Taurolidine was found to be less effective than low-molecular weight heparin in prevention of thrombus formation.

The role of simvastatin on postoperative peritoneal adhesion formation in an animal model.

AIM: The aim of this study is to show the effect of simvastatin on intra-abdominal adhesion formation. METHOD: Adhesion formation was achieved by scratching the cecum and anterior abdominal wall following median laparotomy. Three different groups of 10 rats each were formed. In group I, 0.57 mg/kg/day simvastatin was injected intraperitoneally right after the operation and for 5 days thereafter. In group II, an equal dose of simvastatin to that used in group I was given via gavage. A physiological saline solution was given to group III for the same period of time. On the 6th and 14th day, blood samples were taken and peritoneal lavage was performed to measure the tissue-type plasminogen activator (t-PA) activity. Adhesions were graded via re-laparotomies on the 14th day after the first operation. RESULTS: The adhesion scores were 1.40 +/- 0.22, 1.50 +/- 0.26, and 2.90 +/- 0.34 in groups I, II, and III, respectively (p = 0.007), and the score was higher in group III than in the other groups (p = 0.005, p = 0.011). CONCLUSION: Intraperitoneal simvastatin application decreases adhesion formation by increasing the t-PA level in abdominal surgery.

Role of glyceryl trinitrate, a nitric oxide donor, in the renal ischemia-reperfusion injury of rats.

BACKGROUND/AIMS: Ischemia-reperfusion injury is a serious clinical situation which can cause serious morbidity and mortality. An experimental renal ischemia-reperfusion injury model was designed to evaluate the role of glyceryl trinitrate (GTN) on renal function and histology. METHODS: 50 Wistar albino rats were used in our study. Five groups were formed: (1) sham-control group; (2) acute renal ischemia (ARI) group with placebo (0.9% NaCl) infusion; (3) GTN infusion with a 75 microg/kg/min dose prior to ARI was administered; (4) GTN infusion with a 150 microg/kg/min dose prior to ARI was given, and finally (5) 150 microg/kg/min GTN infusion after the ARI period was applied. Serum BUN and creatinine levels were measured for evaluation of renal function. T(max-sec), glomerular filtration rate (GFR), and T(max-min) results following a (99m)Tc-DTPA diuretic renal scintigraphy were used. Histological examination was performed on nephrectomy specimens. RESULTS: Groups 2 and 5 showed higher BUN, creatinine, and lower GFR values than the other groups (p = 0.0001). There was no difference in BUN, creatinine, and GFR levels between groups 2 and 5 (p = 0.971, p = 0.739, p = 0.393). Also the T(max-sec) values were higher in groups 2 and 5 compared with the other groups (p = 0.0001). The presence of tubular necrosis was different between groups and was higher in groups 2 and 5 (p = 0.002). CONCLUSION: The application of GTN, a nitric oxide donor, has caused significant improvement in renal function when applied prior to an experimentally designed renal ischemia-reperfusion model. But administration of GTN had no effect after occurrence of ischemia.

Effect of a selective cyclooxygenase-2 inhibitor on renal scarring.

BACKGROUND: Scarring is one of the steps of excessive wound healing, causing dysfunction of the involved tissues and clinically poor cosmetics. The aim of this study was to examine the effect of a highly selective cyclooxygenase-2 (COX-2) inhibitor on renal scar formation in experimental pyelonephritis. MATERIALS AND METHODS: Four groups of 10 Balb/C mice were formed. In groups I and II following the inoculation of lipopolysaccharide (LPS) into both kidneys, 0.18 and 0.36 mg/day of rofecoxib was given respectively via intraperitoneal route for 5 days. No medication was applied following physiological saline solution injection to both kidneys of the mice in group III (negative control group). After group IV's LPS inoculation on the first day, saline solution (1 ml/day) was given intraperitoneally for 5 days (positive control group). Following the exposure of both kidneys, LPS of Escherichia coli (5 mg/kg) was injected into the kidneys of groups I, II, and IV. In group III, saline solution (0.1 ml) was used instead of LPS. Three days after the inoculation of LPS, solutions containing 0.18 and 0.36 mg of COX-2 inhibitor were given intraperitoneally for 5 days in groups I and II. No medication was used for the mice in group III. Six weeks after the inoculation of LPS and saline solution, all mice were humanely euthanized. Bilateral nephrectomies were done on each group of mice, and histopathological examination was performed. RESULTS: Inoculation of LPS into the renal parenchyma caused pyelonephritis and scar formation in all groups. The degree of pyelonephritis and scar formation was lesser in groups in which COX-2 inhibitors were used. The degree of scar formation was lesser in group II, in which 0.36 mg more of COX-2 inhibitor was used than in group I (0.18 mg of COX-2 inhibitor). CONCLUSION: In our study model, direct inoculation of LPS to kidneys caused experimentally induced pyelonephritis. Renal scar formation was effectively prevented through the utilization of rofecoxib at 0.36-mg doses.

Effect of proton pump inhibitors on hepatic regeneration.

INTRODUCTION: The liver is critical in multiple processes, including the clearance of endogenous compounds, the synthesis of macromolecules, and organ-specific biotransformation processes. Therefore, the liver's regenerating capacity is of vital importance. Multiple pathways are activated in the complex process that leads to hepatic regeneration. In the present study, we aimed to evaluate the effect of proton pump inhibitors omeprozole, lansoprazole, and pantoprazole on hepatic regeneration following partial hepatectomy. MATERIALS AND METHODS: Four groups were formed with 32 rats in each. Partial liver resections were performed for all animals. Omeprazole (71.4 microg/day), lansoprazole (107 microg/day), pantoprazole (143 microg/day) and placebo (0.5 cm(3)) were administered to the groups respectively. A quarter of the rats in each group were sacrificed on the 1st postoperative day. The rest were sacrificed on the 3rd, 5th and 7th postoperative days. The remnant regenerating liver mass was removed and weighed, and Ki-67 monoclonal antibody levels were measured. RESULTS: There was no statistical difference between the four groups on the first day in evaluating the weight of the liver mass (p = 0.09) and Ki-67 (p = 0.268) levels. Only the omeprazole group showed a difference; the Ki-67 level was lower in the omeprazole group on the 3rd (p = 0.003, p = 0.0001, p = 0.003), 5th (p = 0.017, p = 0.001, p = 0.0001) and 7th (p = 0.0001) days compared to the other groups. Also the weight of the remnant liver mass was lower in the omeprazole group on the 3rd, 5th and 7th (p = 0.0001) days. CONCLUSION: We figured out that lansoprazole and pantoprazole have no effects on liver regeneration, whereas omeprazole showed a negative effect on hepatic regeneration.