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PURPOSE: To investigate the effects of bradykinin on reperfusion injury in an experimental intestinal ischemia reperfusion model. METHODS: We used 32 Wistar-Albino rats. We composed 4 groups each containing 8 rats. Rats in sham group were sacrified at 100 minutes observation after laparotomy. Thirty minutes reperfusion was performed following 50 minutes ischaemia in control group after observing 20 minutes. Ischaemic preconditioning was performed in one group of the study. We performed the other study group pharmacologic preconditioning by infusional administration of 10 µg/kg/minute bradykinin intravenously. We sacrified all of the rats by taking blood samples to evaluate the lactate and lactate dehydrogenase (LDH) after resection of jejunum for detecting tissue myeloperoxidase (MPO) activity. RESULTS: Lactate and LDH levels were significantly higher in control and study groups than the sham group (P<0.001). There is no difference between the study groups statistically. (P>0.05). The results were the same for MPO levels. Although definitive cell damage was determinated in the control group by hystopatological evaluation, the damage in the study groups observed was lower in different levels. However, there was no significant difference between the study groups statistically (P>0.05). CONCLUSION: Either ischeamic preconditioning or pharmacologic preconditioning made by bradykinin reduced the ischemia reperfusion injury at jejunum.

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Purpose To investigate the effects of bradykinin on reperfusion injury in an experimental intestinal ischemia reperfusion model. Methods We used 32 Wistar-Albino rats. We composed 4 groups each containing 8 rats. Rats in sham group were sacrified at 100 minutes observation after laparotomy. Thirty minutes reperfusion was performed following 50 minutes ischaemia in control group after observing 20 minutes. Ischaemic preconditioning was performed in one group of the study. We performed the other study group pharmacologic preconditioning by infusional administration of 10 g/kg/minute bradykinin intravenously. We sacrified all of the rats by taking blood samples to evaluate the lactate and lactate dehydrogenase (LDH) after resection of jejunum for detecting tissue myeloperoxidase (MPO) activity. Results Lactate and LDH levels were significantly higher in control and study groups than the sham group (P 0.001). There is no difference between the study groups statistically. (P>0.05). The results were the same for MPO levels. Although definitive cell damage was determinated in the control group by hystopatological evaluation, the damage in the study groups observed was lower in different levels. However, there was no significant difference between the study groups statistically (P>0.05). Conclusion Either ischeamic preconditioning or pharmacologic preconditioning made by bradykinin reduced the ischemia reperfusion injury at jejunum.(AU)

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Abstract Background In this study, we aimed to investigate the effect of dexmedetomidine on colistin nephrotoxicity in rats. Methods Thirty-two Wistar albino rats were allocated into four groups. Intraperitoneal (ip) saline at 1 mL.kg-1 was administered to the control group and 10 mg.kg-1 ip colistin was given to the colistin group. In the DEX10 group 10 mcg.kg-1 dexmedetomidine ip was given 20 min before the injection of 10 mg.kg-1 ip colistin. In the DEX20 group ip 20 mcg.kg-1 dexmedetomidine was injected 20 min before the administration of 10 mg.kg-1 ip colistin. These treatments were continued twice a day for seven days. Samples were taken on the eighth day. BUN, Cr, KIM-1, TAS, and TOS were examined in blood samples and caspase-3 was examined in kidney tissue samples. Results The values for BUN, Cr and TOS were significantly higher in the colistin group than in the control group. BUN, Cr and TOS changes in the DEX10 and DEX20 groups were not significant compared with the control group but they were significantly lower compared with the colistin group. TAS values in the DEX10 group were significantly lower than in the control group. Apoptotic activity was significantly higher in the colistin group compared with the control group, but there was no significant difference in terms of caspase-3 staining activity when DEX10 and DEX20 groups were compared with the control group. Conclusion Oxidative damage and apoptosis played roles in colistin nephrotoxicity, and colistin nephrotoxicity could be prevented by treatment with dexmedetomidine.

Resumo Justificativa Neste estudo, buscamos investigar o efeito da dexmedetomidina sobre a nefrotoxicidade da colistina em ratos. Métodos Trinta e dois ratos Wistar albinos foram alocados em quatro grupos: o grupo controle recebeu 1 mL.kg-1 de solução salina intraperitoneal (ip); o grupo colistina recebeu 10 mg.kg-1 de colistina ip; o grupo DEX10 recebeu 10 mcg.kg-1 de dexmedetomidina ip 20 minutos antes da injeção de 10 mg.kg-1 de colistina ip; o grupo DEX20 recebeu 20 mcg.kg-1 de dexmedetomidina ip 20 minutos antes da administração de 10 mg.kg-1 de colistina ip. Estes tratamentos foram continuados duas vezes ao dia durante sete dias. As amostras foram colhidas no oitavo dia. BUN, Cr, KIM-1, TAS e TOS foram examinados nas amostras de sangue e caspase-3 foi examinada nas amostras de tecido renal. Resultados Os valores de BUN, Cr e TOS foram significativamente maiores no grupo colistina do que no grupo controle. As alterações em BUN, Cr e TOS nos grupos DEX10 e DEX20 não foram significativas em comparação com o grupo controle, mas foram significativamente menores em comparação com o grupo colistina. Os valores de TAS no grupo DEX10 foram significativamente menores do que no grupo controle. A atividade apoptótica foi significativamente maior no grupo colistina em comparação com o grupo controle, mas não houve diferença significativa em termos de atividade na coloração da caspase-3 quando os grupos DEX10 e DEX20 foram comparados com o grupo controle. Conclusão O dano oxidativo e a apoptose desempenharam papéis na nefrotoxicidade da colistina e a nefrotoxicidade de colistina pode ser prevenida pelo tratamento com dexmedetomidina.

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BACKGROUND: In this study, we aimed to investigate the effect of dexmedetomidine on colistin nephrotoxicity in rats. METHODS: Thirty-two Wistar albino rats were allocated into four groups. Intraperitoneal (ip) saline at 1mL.kg-1 was administered to the control group and 10mg.kg-1 ip colistin was given to the colistin group. In the DEX10 group 10mcg.kg-1 dexmedetomidine ip was given 20min before the injection of 10mg.kg-1 ip colistin. In the DEX20 group ip 20mcg.kg-1 dexmedetomidine was injected 20min before the administration of 10mg.kg-1 ip colistin. These treatments were continued twice a day for seven days. Samples were taken on the eighth day. BUN, Cr, KIM-1, TAS, and TOS were examined in blood samples and caspase-3 was examined in kidney tissue samples. RESULTS: The values for BUN, Cr and TOS were significantly higher in the colistin group than in the control group. BUN, Cr and TOS changes in the DEX10 and DEX20 groups were not significant compared with the control group but they were significantly lower compared with the colistin group. TAS values in the DEX10 group were significantly lower than in the control group. Apoptotic activity was significantly higher in the colistin group compared with the control group, but there was no significant difference in terms of caspase-3 staining activity when DEX10 and DEX20 groups were compared with the control group. CONCLUSION: Oxidative damage and apoptosis played roles in colistin nephrotoxicity, and colistin nephrotoxicity could be prevented by treatment with dexmedetomidine.