Carolina Ferreira Pinto

A sepse como causa de lesão renal aguda: modelo experimental

Sepsis associated with multiple organ failure such as acute kidney injury (AKI) shows a high mortality rate in critically ill patients. This study investigated the sepsis induced AKI in experimental models. Adult, males, Wistar rats divided into the following groups: Control-surgical control and Sepsis-sepsis induction for the cecal ligation and puncture (CLP). Physiological parameters (rectal temperature, mean arterial pressure-MAP, serum glucose and urinary flow); renal function (creatinine clearance); oxidative stress (urinary peroxides and thiobarbituric acid reactive substances-TBARS) and kidney histological analysis were evaluated. That study concludes that sepsis induces AKI by endothelial injury with hemodynamic dysfunction, release of inflammatory mediators and reactive oxygen species (ROS) generation by tubular cells, in an association of renal vasoconstriction due to hemodynamic and inflammatory disturbances.A sepse associada a falencia de multiplos orgaos como a lesao renal aguda (LRA) demonstra alta taxa de mortalidade no paciente critico. Este estudo investigou a LRA induzida pela sepse em modelo experimental. Foram utilizados ratos da raca Wistar, adultos e machos divididos nos seguintes grupos: Controle - controle cirurgico e Sepse - inducao da sepse pela ligadura e puncao do cecon (LPC). Foram avaliados os parâmetros fisiologicos (temperatura retal, pressao arterial media - PAM, glicemia serica e fluxo urinario); a funcao renal (clearance de creatinina); o estresse oxidativo (peroxidos urinarios e substâncias reativas com acido tiobarbiturico - TBARS) e realizada a analise histologica renal. O estudo conclui que a LRA induzida pela sepse caracteriza-se por lesao endotelial com disfuncao hemodinâmica, liberacao de mediadores inflamatorios e geracao de especies reativas de oxigenio (EROs) por celulas tubulares, caracterizando-se como uma associacao de vasoconstricao renal de origem hemodinâmica e inflamatoria.

The sepsis as cause of acute kidney injury: an experimental model

Sepsis associated with multiple organ failure such as acute kidney injury (AKI) shows a high mortality rate in critically ill patients. This study investigated the sepsis induced AKI in experimental models. Adult, males, Wistar rats divided into the following groups: Control-surgical control and Sepsis-sepsis induction for the cecal ligation and puncture (CLP). Physiological parameters (rectal temperature, mean arterial pressure-MAP, serum glucose and urinary flow); renal function (creatinine clearance); oxidative stress (urinary peroxides and thiobarbituric acid reactive substances-TBARS) and kidney histological analysis were evaluated. That study concludes that sepsis induces AKI by endothelial injury with hemodynamic dysfunction, release of inflammatory mediators and reactive oxygen species (ROS) generation by tubular cells, in an association of renal vasoconstriction due to hemodynamic and inflammatory disturbances.A sepse associada a falencia de multiplos orgaos como a lesao renal aguda (LRA) demonstra alta taxa de mortalidade no paciente critico. Este estudo investigou a LRA induzida pela sepse em modelo experimental. Foram utilizados ratos da raca Wistar, adultos e machos divididos nos seguintes grupos: Controle - controle cirurgico e Sepse - inducao da sepse pela ligadura e puncao do cecon (LPC). Foram avaliados os parâmetros fisiologicos (temperatura retal, pressao arterial media - PAM, glicemia serica e fluxo urinario); a funcao renal (clearance de creatinina); o estresse oxidativo (peroxidos urinarios e substâncias reativas com acido tiobarbiturico - TBARS) e realizada a analise histologica renal. O estudo conclui que a LRA induzida pela sepse caracteriza-se por lesao endotelial com disfuncao hemodinâmica, liberacao de mediadores inflamatorios e geracao de especies reativas de oxigenio (EROs) por celulas tubulares, caracterizando-se como uma associacao de vasoconstricao renal de origem hemodinâmica e inflamatoria.

Lesão renal aguda por glicerol: efeito antioxidante da Vitis vinifera L

BACKGROUND AND OBJECTIVES The Acute Kidney Injury (AKI) is the most serious complication of rhabdomyolysis. In this syndrome, the delivery of heme pigment induces an injury that distinguishes itself by glomerular vasoconstriction and direct cellular toxicity with oxidative component. The renoprotection with antioxidants has demonstrated satisfactory effect. The proanthocyanidins are natural antioxidants found in the grape seed extract. The aim of this study was to evaluate the antioxidant effect of Vitis vinifera (grape seed extract) on the renal function of rats submitted to the injury by rhabdomyolysis. METHODS Wistar rats, male, adults, weight ranging from 250-300g were used. The AKI was induced by intramuscular administration of glycerol 50%. The animals were distributed in 4 groups: Saline group (6 mL/kg of NaCl 0.9% intraperitoneal once a day), Glycerol group (6 mL/kg) of intramuscular glycerol each femoral region received 3 mL/kg of glycerol, once a day), Vitis vinifera group (3 mg/kg/day v.o by 5 days) and Glycerol + Vitis vinifera by 5 days before glycerol). RESULTS Renal function (RF-creatinine clearance) and oxidative profile (urinary peroxides-FOX-2 and MDA-TBARS) were evaluted. The Glycerol group treated with Vitis vinifera has shown improvements in RF and reduction levels of lipid peroxidation. CONCLUSION The results of this study have confirmed the antioxidant protection of Vitis vinifera in AKI induced by glycerol.BACKGROUND AND OBJECTIVES: The Acute Kidney Injury (AKI) is the most serious complication of rhabdomyolysis. In this syndrome, the delivery of heme pigment induces an injury that distinguishes itself by glomerular vasoconstriction and direct cellular toxicity with oxidative component. The renoprotection with antioxidants has demonstrated satisfactory effect. The proanthocyanidins are natural antioxidants found in the grape seed extract. The aim of this study was to evaluate the antioxidant effect of Vitis vinifera (grape seed extract) on the renal function of rats submitted to the injury by rhabdomyolysis. METHODS: Wistar rats, male, adults, weight ranging from 250-300g were used. The AKI was induced by intramuscular administration of glycerol 50%. The animals were distributed in 4 groups: Saline group (6 mL/kg of NaCl 0.9% intraperitoneal once a day), Glycerol group (6 mL/kg) of intramuscular glycerol each femoral region received 3 mL/kg of glycerol, once a day), Vitis vinifera group (3 mg/kg/day v.o by 5 days) and Glycerol + Vitis vinifera by 5 days before glycerol). RESULTS: Renal function (RF-creatinine clearance) and oxidative profile (urinary peroxides-FOX-2 and MDA-TBARS) were evaluted. The Glycerol group treated with Vitis vinifera has shown improvements in RF and reduction levels of lipid peroxidation. CONCLUSION: The results of this study have confirmed the antioxidant protection of Vitis vinifera in AKI induced by glycerol.

Proteção funcional da enzima heme-oxigenase-1 na lesão renal aguda isquêmica e tóxica

OBJETIVOS: Verificar la proteccion funcional de la heme-oxigenasa (HO-1), por medio del uso de su inductor (Hemin) y su inhibidor quimico (protoporfirina de zinc-ZnPP) en la lesion renal aguda isquemica y toxica producida por la Polimixina B (PmxB) en ratas. MATERIAL: Fueron utilizadas ratas Wistar, adultas y machos divididos en 8 grupos: SHAM (control), Isquemia (Isq), Isq+Hemin (indutor de HO-1), Isq+ZnPP (inibidor de HO-1), SALINA (control), Polimixina B (PmxB), PmxB+Hemin, PmxB+ZnPP. METODOS: Jaffe (clearance de creatinina, Clcr) y FOX-2 (peroxidos urinarios). RESULTADOS: La isquemia (30´) de los pediculos reales y la administracion de PmxB redujo el Clcr con manutencion del flujo urinario. Los peroxidos urinarios se elevaron en ambas lesiones. La administracion del Inductor de HO-1 determino mejora de la funcion renal y reduccion de los niveles de peroxidos urinarios. CONCLUSION: Los resultados de este estudio demuestran que la isquemia y la PmxB inducen AKL por la elevacion de los peroxidos urinarios. El inductor de HO-1 atenuo la lesion en ambos modelos por atenuacion del mecanismo redox.ABSTRACT Objective : To investigate the functional protection of heme-oxygenase-1 enzyme (HO-1) when using its inducer (Hemin) and inhibitor(zinc protoporphyrin-ZnPP) in ischemic and toxic acute kidney injury by Polymixin B in mice. Materials : Adult male Wistar mice dividedinto 8 groups were used: SHAM (control), Ischemic (Isq), Isq+Hemin (Inducer of H0-1), Isq+ZnPP (inhibitor of H0-1), SALINA(control), Polimyxin B (PmxB), PmxB+Hemin, PmxB+ZnPP. Method : Analysis consists of JaffO (creatinine clearance [crCl]) and FOX-2(urinary peroxides [UP]). Results : Thirty minutes renal ischemia and its treatment with PmxB reduced the crCl and maintained urinaryoutput. Urinary peroxide levels increased in both injuries. The administration of the inducer of H0-1 resulted in improvement in renalfunction and reduction in the levels of urinary peroxide. Conclusions : Findings indicated that ischemia and PmxB induce LAR (acutekidney injury [AKI]) by elevating the levels of urinary peroxide. The HO-1 inducer ameliorated the injury in both animal models throughredox mechanism.

Functional protection of heme-oxygenase-1 enzyme in ischemic and toxic acute kidney injury

OBJETIVOS: Verificar la proteccion funcional de la heme-oxigenasa (HO-1), por medio del uso de su inductor (Hemin) y su inhibidor quimico (protoporfirina de zinc-ZnPP) en la lesion renal aguda isquemica y toxica producida por la Polimixina B (PmxB) en ratas. MATERIAL: Fueron utilizadas ratas Wistar, adultas y machos divididos en 8 grupos: SHAM (control), Isquemia (Isq), Isq+Hemin (indutor de HO-1), Isq+ZnPP (inibidor de HO-1), SALINA (control), Polimixina B (PmxB), PmxB+Hemin, PmxB+ZnPP. METODOS: Jaffe (clearance de creatinina, Clcr) y FOX-2 (peroxidos urinarios). RESULTADOS: La isquemia (30´) de los pediculos reales y la administracion de PmxB redujo el Clcr con manutencion del flujo urinario. Los peroxidos urinarios se elevaron en ambas lesiones. La administracion del Inductor de HO-1 determino mejora de la funcion renal y reduccion de los niveles de peroxidos urinarios. CONCLUSION: Los resultados de este estudio demuestran que la isquemia y la PmxB inducen AKL por la elevacion de los peroxidos urinarios. El inductor de HO-1 atenuo la lesion en ambos modelos por atenuacion del mecanismo redox.ABSTRACT Objective : To investigate the functional protection of heme-oxygenase-1 enzyme (HO-1) when using its inducer (Hemin) and inhibitor(zinc protoporphyrin-ZnPP) in ischemic and toxic acute kidney injury by Polymixin B in mice. Materials : Adult male Wistar mice dividedinto 8 groups were used: SHAM (control), Ischemic (Isq), Isq+Hemin (Inducer of H0-1), Isq+ZnPP (inhibitor of H0-1), SALINA(control), Polimyxin B (PmxB), PmxB+Hemin, PmxB+ZnPP. Method : Analysis consists of JaffO (creatinine clearance [crCl]) and FOX-2(urinary peroxides [UP]). Results : Thirty minutes renal ischemia and its treatment with PmxB reduced the crCl and maintained urinaryoutput. Urinary peroxide levels increased in both injuries. The administration of the inducer of H0-1 resulted in improvement in renalfunction and reduction in the levels of urinary peroxide. Conclusions : Findings indicated that ischemia and PmxB induce LAR (acutekidney injury [AKI]) by elevating the levels of urinary peroxide. The HO-1 inducer ameliorated the injury in both animal models throughredox mechanism.

La sepsis como causa de la lesión renal aguda inducida: modelo experimental

Sepsis associated with multiple organ failure such as acute kidney injury (AKI) shows a high mortality rate in critically ill patients. This study investigated the sepsis induced AKI in experimental models. Adult, males, Wistar rats divided into the following groups: Control-surgical control and Sepsis-sepsis induction for the cecal ligation and puncture (CLP). Physiological parameters (rectal temperature, mean arterial pressure-MAP, serum glucose and urinary flow); renal function (creatinine clearance); oxidative stress (urinary peroxides and thiobarbituric acid reactive substances-TBARS) and kidney histological analysis were evaluated. That study concludes that sepsis induces AKI by endothelial injury with hemodynamic dysfunction, release of inflammatory mediators and reactive oxygen species (ROS) generation by tubular cells, in an association of renal vasoconstriction due to hemodynamic and inflammatory disturbances.A sepse associada a falencia de multiplos orgaos como a lesao renal aguda (LRA) demonstra alta taxa de mortalidade no paciente critico. Este estudo investigou a LRA induzida pela sepse em modelo experimental. Foram utilizados ratos da raca Wistar, adultos e machos divididos nos seguintes grupos: Controle - controle cirurgico e Sepse - inducao da sepse pela ligadura e puncao do cecon (LPC). Foram avaliados os parâmetros fisiologicos (temperatura retal, pressao arterial media - PAM, glicemia serica e fluxo urinario); a funcao renal (clearance de creatinina); o estresse oxidativo (peroxidos urinarios e substâncias reativas com acido tiobarbiturico - TBARS) e realizada a analise histologica renal. O estudo conclui que a LRA induzida pela sepse caracteriza-se por lesao endotelial com disfuncao hemodinâmica, liberacao de mediadores inflamatorios e geracao de especies reativas de oxigenio (EROs) por celulas tubulares, caracterizando-se como uma associacao de vasoconstricao renal de origem hemodinâmica e inflamatoria.

Protección funcional de la enzima heme-oxigenasa-1 en la lesión renal aguda isquémica y tóxica

OBJETIVOS: Verificar la proteccion funcional de la heme-oxigenasa (HO-1), por medio del uso de su inductor (Hemin) y su inhibidor quimico (protoporfirina de zinc-ZnPP) en la lesion renal aguda isquemica y toxica producida por la Polimixina B (PmxB) en ratas. MATERIAL: Fueron utilizadas ratas Wistar, adultas y machos divididos en 8 grupos: SHAM (control), Isquemia (Isq), Isq+Hemin (indutor de HO-1), Isq+ZnPP (inibidor de HO-1), SALINA (control), Polimixina B (PmxB), PmxB+Hemin, PmxB+ZnPP. METODOS: Jaffe (clearance de creatinina, Clcr) y FOX-2 (peroxidos urinarios). RESULTADOS: La isquemia (30´) de los pediculos reales y la administracion de PmxB redujo el Clcr con manutencion del flujo urinario. Los peroxidos urinarios se elevaron en ambas lesiones. La administracion del Inductor de HO-1 determino mejora de la funcion renal y reduccion de los niveles de peroxidos urinarios. CONCLUSION: Los resultados de este estudio demuestran que la isquemia y la PmxB inducen AKL por la elevacion de los peroxidos urinarios. El inductor de HO-1 atenuo la lesion en ambos modelos por atenuacion del mecanismo redox.ABSTRACT Objective : To investigate the functional protection of heme-oxygenase-1 enzyme (HO-1) when using its inducer (Hemin) and inhibitor(zinc protoporphyrin-ZnPP) in ischemic and toxic acute kidney injury by Polymixin B in mice. Materials : Adult male Wistar mice dividedinto 8 groups were used: SHAM (control), Ischemic (Isq), Isq+Hemin (Inducer of H0-1), Isq+ZnPP (inhibitor of H0-1), SALINA(control), Polimyxin B (PmxB), PmxB+Hemin, PmxB+ZnPP. Method : Analysis consists of JaffO (creatinine clearance [crCl]) and FOX-2(urinary peroxides [UP]). Results : Thirty minutes renal ischemia and its treatment with PmxB reduced the crCl and maintained urinaryoutput. Urinary peroxide levels increased in both injuries. The administration of the inducer of H0-1 resulted in improvement in renalfunction and reduction in the levels of urinary peroxide. Conclusions : Findings indicated that ischemia and PmxB induce LAR (acutekidney injury [AKI]) by elevating the levels of urinary peroxide. The HO-1 inducer ameliorated the injury in both animal models throughredox mechanism.