Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model

Sarcopenia and heart failure are common features of chronic liver disease (CLD). The loss of skeletal muscle (SM) and its function contributes to morbidity and mortality. Its prevalence in patients with CLD is estimated at 40-70%. Hepatic encephalopathy\n(HE) has a similar prevalence and, in additio...

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Autor principal: Grimaldi, Santiago Fernando
Otros Autores: Hilgendorf, Ingo
Formato: Tesis de maestría acceptedVersion
Lenguaje:Inglés
Publicado: Facultad de Farmacia y Bioquímica 2019
Materias:
Hiperamonemia
Mínima encefalopatía hepática
Hyperammonemia
Minimum hepatic encephalopathy
Ciencias de la vida
Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=afamaster&cl=CL1&d=HWA_5931
http://repositoriouba.sisbi.uba.ar/gsdl/collect/afamaster/index/assoc/HWA_5931.dir/5931.PDF
Aporte de:
Repositorio Digital de la Universidad de Buenos Aires (UBA) de Universidad de Buenos Aires
id I28-R145-HWA_5931
record_format dspace
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-145
collection Repositorio Digital de la Universidad de Buenos Aires (UBA)
language Inglés
orig_language_str_mv eng
topic Hiperamonemia
Mínima encefalopatía hepática
Hyperammonemia
Minimum hepatic encephalopathy
Ciencias de la vida
spellingShingle Hiperamonemia
Mínima encefalopatía hepática
Hyperammonemia
Minimum hepatic encephalopathy
Ciencias de la vida
Grimaldi, Santiago Fernando
Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
topic_facet Hiperamonemia
Mínima encefalopatía hepática
Hyperammonemia
Minimum hepatic encephalopathy
Ciencias de la vida
description Sarcopenia and heart failure are common features of chronic liver disease (CLD). The loss of skeletal muscle (SM) and its function contributes to morbidity and mortality. Its prevalence in patients with CLD is estimated at 40-70%. Hepatic encephalopathy\n(HE) has a similar prevalence and, in addition, there is a correlation between the two.\nThe CLD decreases the detoxification capacity of ammonia, so SM and astrocytes become the main route of ammonia, mainly through glutamine synthetase (GS). We\nhypothesized that a model of subclinical hepatic encephalopathy (MHE) showing moderate hyperammonemia and almost normal liver could show a starting point for\nearly events in myocardial (HM) damage. The Wistar rats were divided into 2 groups, (i) simulated surgery and (ii) group with stenosed portal vein, MHE. GS, oxygen consumption, nitric oxide production, light microscopy, high resolution light microscopy (HRLM) and electron transmission microscopy (ETM) were evaluated, after 14 days of surgery, in left HM. The results showed focal areas of fibrosis with Sirius red staining and a significant increase in GS (p <0.01) in the MHE group.\nHRLM showed that the HM triad (T-tubules and sarcoplasmic reticulum) was widely dilated with a convergent structure. This membrane traffic system was undulated with\nan increased surface, to the detriment of the fibrillar structure. ETM, confirmed these, showing subcellular edema, with detachment of fibrillar structures, swollen\nmitochondria with loss of ridges and matrix density, disruption of the nuclear\nmembrane and an increase in the number and size of subsarcolemal vacuoles. The triad was also altered showing the dilatation of this system and the focal interruption.\nThe most relevant ETM data were focal myofibrillolysis and wide alterations in\nmitochondria. These results suggest that under these conditions, in early stages of\nHE, hyperammonemia could induce myocardial cell damage, with or without CLD.
author2 Hilgendorf, Ingo
author_facet Hilgendorf, Ingo
Grimaldi, Santiago Fernando
format Tesis de maestría
Tesis de maestría
acceptedVersion
author Grimaldi, Santiago Fernando
author_sort Grimaldi, Santiago Fernando
title Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
title_short Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
title_full Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
title_fullStr Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
title_full_unstemmed Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
title_sort myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model
publisher Facultad de Farmacia y Bioquímica
publishDate 2019
url http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=afamaster&cl=CL1&d=HWA_5931
http://repositoriouba.sisbi.uba.ar/gsdl/collect/afamaster/index/assoc/HWA_5931.dir/5931.PDF
work_keys_str_mv AT grimaldisantiagofernando myocardialeffectsofhyperammonemiainaminimumhepaticencephalopathyanimalmodel
_version_ 1766017554567921664
spelling I28-R145-HWA_59312022-04-12 Sarcopenia and heart failure are common features of chronic liver disease (CLD). The loss of skeletal muscle (SM) and its function contributes to morbidity and mortality. Its prevalence in patients with CLD is estimated at 40-70%. Hepatic encephalopathy\n(HE) has a similar prevalence and, in addition, there is a correlation between the two.\nThe CLD decreases the detoxification capacity of ammonia, so SM and astrocytes become the main route of ammonia, mainly through glutamine synthetase (GS). We\nhypothesized that a model of subclinical hepatic encephalopathy (MHE) showing moderate hyperammonemia and almost normal liver could show a starting point for\nearly events in myocardial (HM) damage. The Wistar rats were divided into 2 groups, (i) simulated surgery and (ii) group with stenosed portal vein, MHE. GS, oxygen consumption, nitric oxide production, light microscopy, high resolution light microscopy (HRLM) and electron transmission microscopy (ETM) were evaluated, after 14 days of surgery, in left HM. The results showed focal areas of fibrosis with Sirius red staining and a significant increase in GS (p <0.01) in the MHE group.\nHRLM showed that the HM triad (T-tubules and sarcoplasmic reticulum) was widely dilated with a convergent structure. This membrane traffic system was undulated with\nan increased surface, to the detriment of the fibrillar structure. ETM, confirmed these, showing subcellular edema, with detachment of fibrillar structures, swollen\nmitochondria with loss of ridges and matrix density, disruption of the nuclear\nmembrane and an increase in the number and size of subsarcolemal vacuoles. The triad was also altered showing the dilatation of this system and the focal interruption.\nThe most relevant ETM data were focal myofibrillolysis and wide alterations in\nmitochondria. These results suggest that under these conditions, in early stages of\nHE, hyperammonemia could induce myocardial cell damage, with or without CLD. Fil: Grimaldi, Santiago Fernando. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Buenos Aires, Argentina Hilgendorf, Ingo Facultad de Farmacia y Bioquímica Rodríguez, Manuel Grimaldi, Santiago Fernando 2019-03-06 La sarcopenia y la insuficiencia cardíaca son características comunes de la enfermedad hepática crónica (EHC). La pérdida de músculo esquelético (ME) y de su\nfunción, contribuyen a la morbilidad y la mortalidad. Su prevalencia en pacientes con\nEHC se estimula en 40-70%. La encefalopatía hepática (EH) tiene una prevalencia similar y, además, existe una correlación entre las dos. La EHC disminuye la\ncapacidad de desintoxicación del amonio, por lo que el ME y los astrocitos se convierten en la ruta principal de metabolización del amonio, principalmente a través\nde la glutamina sintetasa (GS). Planteamos la hipótesis de que un modelo de encefalopatía hepática mínima (EHM) mostró hiperamonemia moderada y el hígado casi normal podría mostrar un punto de partida para eventos tempranos en el daño del miocardio (MC). Las ratas Wistar se dividieron en 2 grupos, (i) cirugía simulada y\n(ii) grupo con vena porta estenosada, EHM. GS, consumo de oxígeno, producción de óxido nítrico, microscopía óptica, microscopía de luz de alta resolución (MLAR) y\nmicroscopía electrónica (ME) se evaluaron después de 14 días de cirugía, en\nmiocardio ventricular izquierdo. Los resultados mostraron áreas focales de fibrosis con tinción de Sirius red y un aumento significativo de GS (p <0.01) en el grupo de EHM. La MLAR mostró que las tríadas miocárdicas (túbulos T y retículo sarcoplásmico) estaban ampliamente dilatadas con una estructura convergente. Este sistema de tráfico de membrana presentaba ondulación con superficie aumentada,\nen detrimento de la estructura fibrilar. En la ME, se confirmaron las presunciones vistas en la MLAR, mostrando edema subcelular con desprendimiento de estructuras fibrilares, mitocondrias edematizadas con pérdida de crestas y de densidad de la matriz, rotura de la membrana nuclear, y aumento en el número y tamaño de las vacuolas subsarcolemales. Las tríadas también estaban alteradas mostrando\ndilatación de este sistema e interrupción focal. Los datos de ME más relevantes\nfueron miofibrilolisis focal y las variadas alteraciones mitocondriales. Estos resultados sugieren que, en estas condiciones, las etapas iniciales de la EH, la hiperamonemia podría inducir daño celular miocárdico, con o sin EHC. application/pdf D´Annunzio, Verónica Eizayaga, Francisco Mertelsmann, Roland Hiperamonemia Mínima encefalopatía hepática Hyperammonemia Minimum hepatic encephalopathy eng Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/2.5/ar/ Ciencias de la vida Myocardial effects of hyperammonemia in a minimum hepatic encephalopathy animal model info:eu-repo/semantics/masterThesis info:ar-repo/semantics/tesis de maestría info:eu-repo/semantics/acceptedVersion http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=afamaster&cl=CL1&d=HWA_5931 http://repositoriouba.sisbi.uba.ar/gsdl/collect/afamaster/index/assoc/HWA_5931.dir/5931.PDF

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