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1.
Arch. esp. urol. (Ed. impr.) ; 66(10): 945-955, dic. 2013. ilus
Artigo em Espanhol | IBECS | ID: ibc-118676

RESUMO

OBJETIVO: La isquemia renal da lugar a la pérdida de función del órgano, en mayor o menor medida, dependiendo del tiempo de la misma como consecuencia del agotamiento de las reservas energéticas que la célula utiliza para sus funciones vitales. El aporte externo de una fuente de energía en forma de un precursor de ATP, como es la INOSINA, ha demostrado ser un método protector desde el punto de vista funcional. Pretendemos en éste trabajo poner de manifiesto las bases histológicas ultraestructurales en las que se basa dicho efecto protector. MÉTODO: Se estudian básicamente dos grupos de ratas y se comparan los hallazgos histològicos de las distintas partes de la nefrona después de perfundirlos con suero fisiológico ó inosina y someter los riñones a distintos tiempos de isquemia normotérmica. Dichos hallazgos se comparan a su vez con la morfología normal de un tercer grupo testigo. RESULTADOS: Los hallazgos histológicos se concretan en: 1- Ausencia de lesiones significativas en los animales perfundidos con inosina a los 60 y 120 min. de isquemia normotérmica. 2- Lesiones glomerulares y tubulares a partir de los 60 min de isquemia normotérmica en los animales perfundidos con suero fisiológico. CONCLUSIONES: Los animales perfundidos con suero fisiológico mostraron lesiones muy importantes a nivel glomerular y tubular a los 60 y 120 min de isquemia normotérmica. Dichas lesiones no se aprecian en los animales perfundidos con inosina. La similitud de los hallazgos morfológicos del grupo perfundido con inosina y el grupo testigo, permite atribuir a la inosina un efecto protector de la morfología de la nefrona de rata bajo condiciones de isquemia normotérmica en periodos inferiores a 120 min (AU)


OBJECTIVES: Renal ischemia, depending on its duration, results in organ function loss to a greater or lesser extent, due to the depletion of the energy cells need for their vital functions. The method of supplying an external energy source that may act as a precursor of ATP, such as inosine, has proved to be protective from a functional point of view. In this work, we aim to reveal the histological ultrastructural bases that underlie this protective effect. METHODS: We studied two groups of rats subjecting the kidneys to different durations of warm ischemia, and compared the histological findings at various parts of the nephron after perfusion with saline or inosine. These findings were compared, in turn, with the normal morphology of a third control group. RESULTS: The histological findings were: 1 ) No significant lesions after 60 and 120 min of warm ischemia in animals perfused with inosine; and 2) Glomerular and tubular injury after 60 min of warm ischemia in animals perfused with saline. CONCLUSIONS: The saline-perfused animals showed very significant injury at the glomerular and tubular levels after 60 and 120 min of warm ischemia. These lesions were not seen in animals perfused with inosine. The similarity of the morphological findings between the inosine-infused group and the control group suggests that inosine has a protective effect on the morphology of the rat nephron under conditions of warm ischemia for periods shorter than 120 min (AU)


Assuntos
Animais , Ratos , Isquemia/fisiopatologia , Inosina/uso terapêutico , Rim/ultraestrutura , Substâncias Protetoras/uso terapêutico , Modelos Animais de Doenças , Glomérulos Renais/fisiopatologia
2.
J. physiol. biochem ; 66(3): 189-196, sept. 2010.
Artigo em Inglês | IBECS | ID: ibc-122824

RESUMO

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During prolonged maximal exercise, oxygen deficits occur in working muscles. Progressive hypoxia results in the impairment of the oxidative resynthesis of ATP and increased degradation of purine nucleotides. Moreover, ATP consumption decreases the conversion of UDP to UTP, to use ATP as a phosphate donor, resulting in an increased concentration of UDP, which enhances pyrimidine degradation. Because the metabolism of pyrimidine nucleotides is related to the metabolism ofpurines, in particular with the cellular concentration of ATP, we decided to investigate the impact of a standardized exercise with increasing intensity on the concentration of uridine, inosine,hypoxanthine, and uric acid. Twenty-two healthy male subjects volunteered to participate in this study. Blood concentrations of metabolites were determined at rest, immediately after exercise, and after 30 min of recovery using high-performance liquid chromatography. We also studied the relationship between the levels of uridine and indicators of myogenic purine degradation. The results showed that exercise with increasing intensity leads to increased concentrations of inosine,hypoxanthine, uric acid, and uridine. We found positive correlations between blood uridine levels and indicators of myogenic purine degradation (hypoxanthine), suggesting that the blood uridine level is related to purine metabolism in skeletal muscles (AU)


Assuntos
Humanos , Masculino , Uridina/sangue , Nucleotídeos de Pirimidina/biossíntese , Exercício Físico/fisiologia , Hipóxia Celular/fisiologia , Purinas/biossíntese , Hipoxantinas/sangue , Inosina/sangue , Ácido Úrico/sangue
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