Abstract

To evaluate bladder histology in healing and biochemical analysis of rats with single kidney in ischemia/reperfusion, treated with tacrolimus. Fifty rats randomized into five groups. Three rats died in surgery, 47 rats divided in groups: Control (non-operated, n=10), Sham (operated without drugs, n=8), T1 (operated + tacrolimus 1mg/kg, n=10), T2 (operated + tacrolimus 0.1 mg/kg, n=10), T3 (operated + tacrolimus 10mg/kg, n=9). The surgery was: laparotomy, right nephrectomy, left kidney ischemia/reperfusion, cystotomy followed by bladder suture. After that, rats were submited to gavage daily (Control and Sham with saline solution. T1, T2, T3 with tacrolimus in doses already mentioned). On the 14th day, after death induction, cystectomy was performed and bladder was histologicaly analysed. The serum urea, creatinine and tacrolimus were analysed too. There was difference in serum tacrolimus in T3 compared to the other groups (p<0.05). There was higher doses of creatinine in T3 group and higher urea in groups with tacrolimus. There were significant differences among all histologic variables comparing groups with and without tacrolimus (p<0.05). Tacrolimus associated with ischemia/reperfusion is nephrotoxic, suppresses inflammation and seems to delay the healing bladder.

Highlights

  • The repair process of wounds can be basically divided in three phases: Inflammatory with platelet accumulation, coagulation, and leukocyte migration; Proliferative which is the reparative process with re-epithelialization, neovascularization and matrix synthesis; Remodeling phase which is the period of scar contraction and collagen production[1]

  • The values of tacrolimus showed that administration of different doses produced serum levels differents between groups

  • Concluded that Cyclosporin A had a protective effect on renal function and reduced the severity of tissue damage in kidneys subjected to normothermic ischemia and 40 minutes later reperfusion

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Summary

Introduction

The repair process of wounds can be basically divided in three phases: Inflammatory with platelet accumulation, coagulation, and leukocyte migration; Proliferative which is the reparative process with re-epithelialization, neovascularization and matrix synthesis; Remodeling phase which is the period of scar contraction and collagen production[1].Several factors affect healing, slowing the process, for example infections, hypoxia, diabetes, ionizing radiation, aging and malnutrition[1]. The repair process of wounds can be basically divided in three phases: Inflammatory with platelet accumulation, coagulation, and leukocyte migration; Proliferative which is the reparative process with re-epithelialization, neovascularization and matrix synthesis; Remodeling phase which is the period of scar contraction and collagen production[1]. Some studies have shown that exogenous drugs inhibit healing. Chemotherapeutic agents such as adriamycin, nitrogen mustard, methotrexate, doxorubicin to inhibit cellular proliferation, the number of platelets, inflammatory cells and growth factors. The tamoxifen, an estrogen receptor modulator used for breast cancer, appears to reduce cell proliferation and the tensile strength of the wound. Glucocorticoids affect fibroblast proliferation and collagen synthesis, and reduce the amount of granulation tissue[2]

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