Tesis sobre el tema "Liver Ischemia Repercussion Injury"
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Winbladh, Anders. "Microdialysis in Liver Ischemia and Reperfusion injury". Doctoral thesis, Linköpings universitet, Kirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68651.
Texto completoBjörnsson, Bergþór. "Methods to Reduce Liver Ischemia/Reperfusion Injury". Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110318.
Texto completoDuarte, Sérgio Miguel Coelho. "Matrix-leukocyte interactions in liver ischemia-reperfusion injury". Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63694.
Texto completoDuarte, Sérgio Miguel Coelho. "Matrix-leukocyte interactions in liver ischemia-reperfusion injury". Tese, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63694.
Texto completoGeorgiev, Panco. "Normothermic ischemia reperfusion injury in the cholestatic mouse liver /". Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000256332.
Texto completoMüller, Christian. "α-Lipoic Acid Attenuates Ischemia Reperfusion Injury of the Rat Liver". Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-2394.
Texto completoHartkorn, Andreas. "Different approaches to influence the ischemia/reperfusion injury of the liver". Diss., kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/8918/.
Texto completoOkumura, Shinya. "Oral administration of polyamines ameliorates liver ischemia-reperfusion injury and promotes liver regeneration in rats". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225444.
Texto completoRichards, James Alexander. "The relative contribution of lymphocytes to hepatic ischemia reperfusion injury". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25856.
Texto completoBejaoui, Mohamed. "Polyethylene glycol conditioning: An effective strategy to protect against liver ischemia reperfusion injury". Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/385612.
Texto completoLa lesión por isquemia reperfusión (I/R) es un proceso complejo que tiene lugar cuando un órgano se ve privado del aporte sanguíneo (isquemia) y se manifiesta de forma predominante después del posterior restablecimiento del flujo sanguíneo (reperfusión). Existen numerosas situaciones en la práctica clínica en las que el hígado se ve sometido a una situación de I/R, entre ellas, la resección hepática y el trasplante hepático. Los polietilenglicoles (PEGs) son polímeros solubles en agua, no tóxicos y con diferentes pesos moleculares. Algunos de ellos, con un peso molecular de 20 kDa (PEG 20) y de 35 kDa (PEG 35) forman parte de la composición de soluciones de preservación de órganos (SCOT e IGL-1). Además, en varios modelos experimentales de in vivo e in vitro se ha reportado que varios PEGs ejercen efectos beneficiosos. Atendiendo a lo anteriormente expuesto, la utilización de PEGs puede constituir una excelente herramienta para prevenir el daño hepático por I/R. El objetivo de esta tesis es investigar los efectos beneficiosos del PEG 35 en diferentes modelos de lesión por I/R, que imitan una cirugía hepática. Nuestros resultados demuestran que: - EL PEG 35 administrado por vía intravenosa protege eficientemente el hígado de ratas contra la I/R caliente. Los mecanismos de protección están asociados con la activación de la supervivencia vía Akt y AMPK y la inhibición de la apoptosis. El PEG 35 también protege la morfología de los hepatocitos mediante el aumento de la F/G-actina y la activación de p-p38. - La administración intravenosa de PEG 35 protege los hígados esteatósicos en un modelo de I/R fría en ratas obesas. Los efectos protectores de PEG 35 están mediados por la preservación del estado mitocondrial, la estabilización del citoesqueleto y la regulación de las vías de señalización citoprotectoras AMPK y AKT. - La adición de PEG 35 a una nueva solucione de lavado aumenta la protección contra la lesión por I/R en un modelo de hígado de rata aislado y perfundido a través de la inhibición de las metaloproteinasas, la activación de vías de señalización citoprotectoras AMPK y eNOS y la preservación de la integridad del citoesqueleto.
Gerwig, Tobias. "Prevention of Ischemia-Reperfusion Injury in the Rat Liver by Atrial Natriuretic Peptide". Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-888.
Texto completoLi, Xianliang y 李先亮. "Insulin in UW solution exacerbates the ischemia/reperfusion injury in rat liver transplantation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B27785257.
Texto completoWada, Seidai. "CAAT/Enhancer Binding Protein-Homologous Protein Deficiency Attenuates Liver Ischemia/Reperfusion Injury in Mice". Kyoto University, 2018. http://hdl.handle.net/2433/235981.
Texto completoMiyachi, Yosuke. "Causes of liver steatosis influence the severity of ischemia reperfusion injury and survival after liver transplantation in rats". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263516.
Texto completoYamagami, Kazuhiko. "Heat shock preconditioning ameliorates liver injury following normothermic ischemia-reperfusion in steatotic rat livers". Kyoto University, 1999. http://hdl.handle.net/2433/181689.
Texto completoHirao, Hirofumi. "The Protective Function of Galectin-9 in Liver Ischemia and Reperfusion Injury in Mice". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225476.
Texto completoMiyauchi, Tomoyuki. "Preventive Effect of Antioxidative Nutrient‐Rich Enteral Diet Against Liver Ischemia and Reperfusion Injury". Kyoto University, 2019. http://hdl.handle.net/2433/242381.
Texto completoKageyama, Shoichi. "Graft Reconditioning With Nitric Oxide Gas in Rat Liver Transplantation From Cardiac Death Donors". Kyoto University, 2014. http://hdl.handle.net/2433/193570.
Texto completoHide, Alférez Diana. "Advances in ischemia and reperfusion injury: effects on liver microcirculation and therapeutic strategies for sinusoidal protection". Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/399454.
Texto completoEn la present tesi doctoral es demostren els efectes deleteris del dany per isquèmia-reperfusió sobre la microcirculació hepàtica tant en condicions de preservació en fred com d’isquèmia calenta. En particular, els efectes in vivo de l’isquèmia-reperfusió en calent inclouen dany microcirculatori agut associat amb un increment de la resistència vascular intrahepàtica, hipertensió portal i reducció de la perfusió hepàtica. Per prevenir aquests danys que afecten als diferents tipus cel·lulars del sinusoid hepàtic s’han avaluat dues estratègies terapèutiques: l’antioxidant rMnSOD en el context de la preservació en fred per transplantament i el vasoprotector simvastatina en un model d’isquèmia calenta. Els articles inclosos en la present tesi doctoral demostren com ambdós fàrmacs són efectius millorant la funció endotelial hepàtica. Aquests efectes es deuen, en part, al manteniment de les vies vasoprotectores derivades del factor de transcripció KLF2 , al manteniment de la biodisponibilitat d’òxid nítric i a la reducció dels nivells del radical lliure superòxid. Aquesta protecció de l’endoteli i la microcirculació hepàtica s’associa amb una prevenció de l’inflamació mitjançada per mol·lècules d’adhesió i finalment condueix a una reducció del dany hepàtic i una menor mort cel·lular.
Kavanagh, Dean Philip John. "Molecular events governing hematopoietic stem cell recruitment in Vivo in murine liver following Ischemia-reperfusion injury". Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/363/.
Texto completoHarada, Nobuko. "Inactivation of the small GTPase Rac1 protects the liver from ischemia/reperfusion injury in the rat". Kyoto University, 2004. http://hdl.handle.net/2433/145269.
Texto completoShimabukuro, Takashi. "Can Heat Shock Pretreatment Protect the Rat Liver with Carbon Tetrachrolide-induced Fibrosis form Ischemia-reperfusion Injury?" Kyoto University, 1998. http://hdl.handle.net/2433/182256.
Texto completoTamaki, Ichiro. "Hydrogen Flush After Cold Storage (HyFACS), as a new end-ischemic ex vivo treatment for liver grafts against ischemia/reperfusion injury". Kyoto University, 2019. http://hdl.handle.net/2433/242357.
Texto completoWang, Yuan y 王苑. "The effect of intravenous and intrathecal morphine preconditioning on hepatic ischaemia-reperfusion injury in normal and cirrhotic livers". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47849848.
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Okamura, Yusuke. "Impact of Subnormothermic Machine Perfusion Preservation in Severely Steatotic Rat Livers: A Detailed Assessment in an Isolated Setting". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225499.
Texto completoKusakabe, Jiro. "Complement 5 inhibition ameliorates hepatic ischemia/reperfusion injury in mice, dominantly via the C5a-mediated cascade". Kyoto University, 2020. http://hdl.handle.net/2433/254516.
Texto completoWestman, Bo. "Studies of ischemia and reperfusion in muscle and liver on glutathione and amino acid metabolism in man /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-406-8/.
Texto completoYonezawa, Kei. "Suppression of TNF-α production and neutrophil infiltration during ischemia-reperfusion injury of the liver after heat shock preconditioning". Kyoto University, 2002. http://hdl.handle.net/2433/149667.
Texto completoUchinami, Hiroshi. "Effect of heat shock preconditioning on NF-κB/I-κB pathway during ischemia-reperfusion injury of the rat liver". Kyoto University, 2002. http://hdl.handle.net/2433/149733.
Texto completoPantazi, Eirini. "New strategies to reduce liver ischemia – reperfusion injury in fatty and non-fatty livers: a focus on sirtuin 1 implication". Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/299797.
Texto completoLa lesión por isquemia-reperfusion (LIR) hepática es causa de una significativa mortalidad en caso de resecciones hepáticas y en el trasplante hepático. La LIR está relacionada con el desarrollo de fallo primario y con la disfunción primaria del injerto. Ella se está desarrollando por la privación del oxígeno durante la fase de isquemia y la nueva entrada de oxígeno, durante la reperfusión, la cual daña más el órgano sometido a isquemia. La LIR es un proceso muy complejo y varias investigaciones intensivas se han llevado a cabo para explorar los mecanismos de su patogénesis. Entre los más estudiados son el estrés oxidativo, la inflamación y la apoptosis. Además, debido a la gran demanda por órganos, muchos centros de trasplante se han visto obligados a utilizar injertos que anteriormente eran considerados inapropiados para trasplantar. Los hígados esteatósicos son un ejemplo; se caracterizan de una acumulación exagerada de lípidos y son más vulnerables frente la LIR. Además, están correlacionados con una incidencia elevada de disfunción después del trasplante. Consecuentemente, es necesario la identificación de nuevas estrategias que confieren una protección eficaz frente la LIR y especialmente en caso de hígados esteatósicos. La sirtuina 1 (SIRT1) es una enzima que elimina el grupo acetilo en varias proteínas y así regula varios procesos celulares, como la respuesta frente varios tipos de estrés, el ciclo celular y el metabolismo. Estudios recientes en el corazón y el cerebro han asociado la activación de la SIRT1 con una aumentada resistencia frente la LIR. No obstante, no se ha reportado todavía una posible implicación de la SIRT1 en la LIR hepática o en el trasplante. La presenta tesis tiene como objetivo investigar la implicación de la SIRT1 en la isquemia-reperfusión caliente en hígados esteatósicos de rata y su correlación con el precondicionamiento isquémico, una estrategia previamente reportada para prevenir la LIR. Además, se ha investigado la implicación de la SIRT1 en un modelo de trasplante ortotópico y en un modelo de trasplante con tamaño reducido en la rata. Así, el presente estudio demuestra que SIRT1 está involucrada en la LIR hepática y su activación podría ser una estrategia prometedora para disminuir los efectos adversos de la LIR.
Kume, Makoto. "Ischemic preconditioning of the liver in rats : Implications of heat shock protein induction to increase tolerance of ischemia-reperfusion injury". Kyoto University, 1999. http://hdl.handle.net/2433/181688.
Texto completoKadono, Kentaro. "Thrombomodulin Attenuates Inflammatory Damage Due to Liver Ischemia and Reperfusion Injury in Mice in Toll-Like Receptor 4-Dependent Manner". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225492.
Texto completoLevesque, Eric. "Interactions entre le foie et le poumon en transplantation hépatique : conséquences pulmonaires des lésions hépatiques d’ischémie/reperfusion : travaux expérimentaux et cliniques". Thesis, Paris Est, 2017. http://www.theses.fr/2017PESC0024.
Texto completoLiver and lung are two closely related organs. In liver transplantation, lung damage, complications, morbidity and mortality can be related to the liver disease of the recipient but also to the donor via the graft, its quality and its preservation. The aim of this manuscript was to study two aspects of these interactions: 1- the impact of acute respiratory failure (defined by the use of mechanical ventilation) on the post-transplantation outcome ii) the consequences of the ischemia-reperfusion injury of the graft on cardiopulmonary parameters in the recipient.In the first study, we investigated the impact of one or more organ failure (cerebral, lungs, kidney, circulation, hepatic and coagulation) on the 90-day mortality post LT. Patients with at least one organ failure had a significant decrease in post LT survival at 90-day (79% versus 96%) and 1 year (70% versus 91%) compared with cirrhotic patients without failure. In a second study, from the same cohort, we developed a model to predict short-term mortality. This model is composed of 6 factors including the existence of organ failure. In the third study, with a largest cohort (Agence de Biomedicine, PHRC “Optimatch”), we have confirmed these first results and we observe that the number at the LT influences the outcome. Decision tree-modeling identified 6 subgroups further classified in 4 increasing risk classes, highlighting the prognostic importance of respiratory failure and renal failure at the LT as well as complex interactions between donor and recipient features.In addition to the quality of the graft, its preservation has an impact on the graft function and on the cardiopulmonary parameters in the recipient. Indeed, in a model of LT in the large animal (pig) we show that the ischemia / reperfusion injuries, generated between the sampling and the implantation, have consequences on graft function, myocardium and lung. These lesions could be subdued according to the preservation technique.These studies demonstrate that during LT the recipient's pulmonary complications and its morbidity are related to the recipient’s pre-existing hepatic disease and to the donor via the graft through ischemia-reperfusion phenomena of the graft
Panisello, Roselló Arnau. "Noves estratègies en la prevenció de la lesió hepàtica per isquèmia reperfusió = New strategies in the prevention of liver ischemia reperfusion injury". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/664647.
Texto completoNowadays, the only solution for patients that are diagnosed with a terminal hepatic disease or that suffer from an acute hepatic injury is transplantation. However, the demand of organs for transplantation far exceeds the offer. In this context, the optimization of all the stages that englobes the process of transplantation is indispensable. In this case we mainly focus in three key concepts. One of the main reasons for which a liver transplant is not successful is due the complications derived from the ischemia-reperfusion injury. The ischemia-reperfusion injury (IRI) is a complex and multifactorial phenomenon that starts with the total or partial blood flow deprivation (ischemia) and its restoration after a more or less long time. As a consequence of blood flow deprivation, the organ suffers a series of reactions and metabolic changes which will affect its functional viability. For this reason, the understanding of the ischemia-reperfusion injury will supply us with the tools to counter its negative effects. In another vein, given the unbalanced ratio offer-demand of organs, it is mandatory to increase the available donor’s pool. Nowadays, and as a consequence of the occidental lifestyle, lots of possible donors are discarded due the presence of fat infiltration in their organs, that’s it, steatosis. The understanding and the improvement of this steatotic livers, opens a door to their usage and to increase the donor’s pool, with the derivative to increase the number of lives saved. Another key aspect in liver transplantation is the organ preservation prior to transplantation. In this sense, the improvement of the preservation solutions for livers is a crucial factor to increase livers viability, and therefore, achieving more availability with increased functionality. For this reason, the thesis entitled “new strategies in the prevention of liver ischemia reperfusion injury” uses the concepts IRI, liver steatosis and preservation solutions as fundamental axes in its studies to improve the quality and quantity of liver transplantation.
Kan, Chunyi [Verfasser], Uta [Gutachter] Dahmen, Jun Gutachter] Li y Silvio [Gutachter] [Nadalin. "Ischemia reperfusion injury of the marginal liver : identification and evaluation of novel therapeutic strategies / Chunyi Kan ; Gutachter: Uta Dahmen, Jun Li, Silvio Nadalin". Jena : Friedrich-Schiller-Universität Jena, 2018. http://d-nb.info/1170587232/34.
Texto completoKawasoe, Junya. "The lectin-like domain of thrombomodulin is a drug candidate for both prophylaxis and treatment of liver ischemia and reperfusion injury in mice". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263533.
Texto completoGringeri, Enrico. "Un nuovo sistema di perfusione parenchimale per la preservazione del graft epatico per trapianto: valutazione sperimentale sul piccolo e grande animale". Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425544.
Texto completoYERMEK, NIGMET. "Human Atrial Natriuretic Peptide in Cold Storage of Donation after Circulatory Death Rat Livers: An Old but New Agent for Protecting Vascular Endothelia?" Kyoto University, 2019. http://hdl.handle.net/2433/242391.
Texto completoBonsignore, Pasquale. "Sviluppo di biomarkers per la determinazione e la valutazione prognostica della ripresa funzionale epatica post trapianto, nel fegato marginale e nel non heart beating donor". Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423510.
Texto completoRiassunto Premesse generali Nell’ambito del trapianto di fegato, uno dei problemi più importanti non ancora risolti è la grande discrepanza tra la richiesta di organi e la risorsa di donazioni. Il ricorso ai così detti organi “marginali”, come quelli dei donatori a cuore non battente e con steatosi maggiore del 60%, potrebbe consentire di ampliare in maniera sensibile il pool degli organi disponibili per trapianto. L’impiego di questi fegati però è associato ad un’alta frequenza di Primary Disfunction postoperatoria a causa del danno che si sviluppa nel corso della preservazione in Cold Storage, nel contesto del processo di ischemia-riperfusione in ipotermia estrema (4°C). Si apre un’area di interesse di ricerca verso l’utilizzo di metodiche alternative nella conservazione del graft epatico come la Machine Perfusion, in grado di ridurre questo tipo di insulti e di consentire il dosaggio di biomarkers in grado di predire l’entità del danno da ischemia-riperfusione e la qualità della ripresa funzionale del graft dopo trapianto. Le grandi potenzialità di questo sistema nell’ambito della preservazione d’organo e i numerosi lavori in letteratura ci hanno spinto ad approfondire questa tematica. Scopo dello studio L’obiettivo del nostro lavoro è stato quello di realizzare un modello sperimentale di Machine Perfusion per la preservazione di fegati prelevati da donatore a cuore non battente, come valida alternativa alla preservazione tradizionale in Cold storage a 4°C. Ulteriore scopo del nostro progetto è stato quello di identificare eventuali biomarcatori in grado di predire l’entità del danno da ischemia-riperfusione e la qualità della ripresa funzionale del graft dopo trapianto di fegato da donatore a cuore non battente. Materiali e metodi Per questi esperimenti abbiamo utilizzato 10 maiali Landrace di circa 20 Kg ai quali abbiamo praticato, 60 minuti dopo l’arresto cardiaco, un’epatectomia totale, prelevando così il fegato. Gli animali sono stati suddivisi in due gruppi di 5 ciascuno: nel primo gruppo (Gruppo A) il fegato prelevato è stato perfuso in MP (Machine perfusion) per sei ore con soluzione di Celsior a 20°C. Nel secondo gruppo (Gruppo B) il fegato prelevato nei 5 animali è stato conservato per 6 ore in CS (Cold storage). In tutti i gruppi di studio il periodo di preservazione è stato seguito da un periodo di rewarming inteso come riperfusione dell’organo con sangue autologo in normotermia (37°) per due ore per valutare la risposta alla riperfusione. Durante tutte le otto ore dell’esperimento sono stati raccolti campioni ematici e istologici. Risultati Dal punto di vista biochimico (AST, ALT, LDH) e istologico (necrosi e congestione) la preservazione mediante perfusione a 20°C si è dimostrata superiore rispetto al Cold Storage. Il dosaggio di AST, ALT, Acido lattico ed LDH si è dimostrato essere un parametro attendibile per la valutazione del danno d’organo e della ripresa funzionale del graft epatico. Il dosaggio di citochine quali IL1, IL6, TNf alfa non ha mostrato alcuna significatività. Conclusioni Queste evidenze sperimentali mettono in rilievo l’efficacia di una preservazione con macchina a perfusione continua a 20°C sul grande animale. Sia dal punto di vista biochimico che istologico, infatti, abbiamo osservato che la Machine Perfusion in moderata ipotermia è di beneficio nella preservazione del graft ed offre il notevole vantaggio di poter testare, durante la perfusione, biomarcatori che possono predire l’eventuale ripresa funzione dell’organo, prima dell’esecuzione del trapianto, al fine di ridurre l’incidenza di disfunction del graft post trapianto.
Filho, Marco Antonio Corrêa Guimarães. "Efeito do pré-condicionamento isquêmico remoto em modelo de lesão hepática por isquemia-reperfusão em ratos". Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=7368.
Texto completoIschemia/Reperfusion (I/R) injury is an important pathophysiological mechanism in the postoperative liver failure. Different strategies to minimize the I/R liver injury have been developed during the last decades but the results had been disappointing. Recently, the remote ischemic preconditioning (RIPC), a method that involves a brief ischemic episode on an organ or tissue that subsequently affords protection to a remote organ or tissue, have been use in various experimental models with promising results. The precise pathway activated by the RIPC isnt clear, but cytokine release modulation has been proposed as a candidate mechanism. Thirty-six male rats (Rattus norvegicus) were divided in 3 groups: Sham; I/R injury, a 45 minutes lobar (70%) liver ischemia and reperfusion; and RIPC, 6 cycles of 4 minutes of ischemia and 4 minutes of reperfusion of the right hindlimb followed by a 45 minutes lobar (70%) liver ischemia and reperfusion. Liver tissue in the affected lobe and blood samples were collected after 60 minutes and 180 minutes of reperfusion for histopathological study of liver I/R, plasma cytokines (TNF-α, IL-6 and IL-10) and liver aminotransferases measurement (ALT). The histopathological study demonstrated a significant lesser degree of liver necrosis in the RIPC group (p <0,001). The aminotransferases levels followed the same pattern, with significant lower levels in the RIPC group (p <0,001). The cytokines assessment showed a reduction in the expression of IL-6 in the RIPC when compared with the I/R group (p <0,01). Interleukin-10 levels were higher in the RIPC group, but the difference wasnt significant. The TNF-α measurement didnt show any difference in the groups. The RIPC model presented consistently reduced the I/R injury to the liver and the IL-6 expression was similar to the reported in other studies.
Lehmann, Thorsten. "Die Bedeutung der toxischen Sauerstoffradikale beim Ischämie/Reperfusionsschaden nach Lebertransplantation in der Ratte". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/13953.
Texto completoBackground: Oxygen-derived free radicals play a central role in pathomechanisms of reperfusion injury after organ transplantation, and fatty livers are particularly susceptible. Endogenous radical scavenger systems such as superoxide dismutase (SOD) degrade toxic radicals; however, SOD is degraded rapidly when given exogenously. Therefore, the hypothesis that treatment of the donor liver with an adenoviral vector encoding the Cu/Zn-SOD gene (Ad.SOD1), or the Mn-SOD gene or the ec-SOD gene would lead to permanent gene expression and therefore protect the organ against injury and increase survival in a rat model of liver transplantation including fatty livers was tested. Transplantation of reduced-size livers may lead to a hypermetabolic state and increased production of oxygen radicals. Since oxygen radicals may cause liver injury and impair liver regeneration, we tested the hypothesis that overexpression of superoxide dismutase (SOD) in reduced-size livers (RSL) would accelerate regeneration and reduce injury in a rat model of transplantation of RSL. Methods: Donors received chow diet (untreated), high-fat diet, or ethanol-containing high-fat diet. Some donors were infected with Ad-SOD1, while untreated grafts and livers infected with the indicator gene lacZ encoding bacterial b-galactosidase (Ad.lacZ) served as controls. Some livers were harvested 72 hours later, reduced to 45% of weight, and transplanted. After liver transplantation, SOD activity and protein expression in liver, survival, histopathology, release of transaminases, free radical adducts in bile and activation of NF-kB, IkB kinase (IKK), Jun-N-terminal kinase (JNK) and TNFa were evaluated. Moreover, in transplanted split-livers regeneration was evaluated by Brdu-staining, and measurement of cyclinD1 and p21. Results: Approximately 80% of hepatocytes expressed b-galactosidase 72h after injection of Ad-lacZ. Moreover, SOD1 gene expression and activity were increased 3- and 10-fold in the Ad-SOD1 group, respectively. Following transplantation, 20-25% of rats treated with Ad.lacZ survived. In contrast, all SOD1-treated animals survived. Transaminases measured 8h after transplantation in Ad-SOD1 rats were only 40% of those in controls which increased 40-fold above normal values. Approximately 20% of hepatocytes in untreated and Ad.lacZ-infected organs were necrotic 8h after reperfusion, whereas necrosis was nearly undetectable in grafts from rats treated with Ad.SOD1. Free radical adducts were increased 2-fold in the ethanol group compared to untreated controls. Ad.SOD1 blunted this increase and reduced the activation of NF-kB, which was similar in untreated and ethanol-treated groups. Ad.SOD1 did not affect activity of IKK, but JNK activity was blunted. Release of TNFa was not affected. In recipients of Ad.SOD1-RSL survival was dramatically increased (100% vs. 20% in Ad.lacZ-RSL), and peak levels of AST/ALT and bilirubin levels were reduced by 75% and 87.5%, respectively (p
Glanemann, Matthias. "Mechanische und pharmakologische Organkonditionierung im Rahmen warmer Leberischämie". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/13969.
Texto completoThe present study analyses two strategies to protect from hepatic ischemia-reperfusion injury: ischemic preconditioning (IP) and pharmacologic administration of methylprednisolone (MP). First, the extent of hepatocellular damage after warm liver ischemia induced by cross clamping of the hepatic vessels in the hepatoduodenal ligament (Pringle manöver) was analysed demonstrating comparable tissue protection by both treatment modalities. After 70% partial hepatectomy including Pringle manöver however, the hepatocellular regerneration was markedly decreased after IP treatment, despite reduced ischemia-reperfusion injury. Moreover, MP treatment did not improve hepatic regeneration since it showed a comparable timing to untreated, ischemic controls. In conclusion, both IP and MP significantly reduced hepatic ischemia-reperfusion injury. However, no beneficial effects on hepatocellular regeneration after partial hepatectomy including pringle manöver were observed.
Morais, Lúcio Kenny. "Efeito do pré-condicionamento isquêmico remoto no transplante ortotópico de fígado de doadores em parada cardíaca. Estudo experimental em suínos". Universidade Federal de Goiás, 2012. http://repositorio.bc.ufg.br/tede/handle/tede/8061.
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Introduction: Improved liver function from non-heart-beating donors seems to be related to short periods of warm ischemia; hence ischemia-reperfusion injury is a critical unsolved issue. Remote Ischemic preconditioning (PC) has been shown to protect the liver from ischemia-reperfusion injury. However little is known about the usefulness of ischemic precondition as a strategy to improve tolerance of non-heart-beating liver grafts to warm ischemia. Therefore we designed an experimental study aiming the effects of ischemic preconditioning on liver transplantation from non-heart-beating donors. Methods: Protocol was approved by Federal University of Goias Ethics Committee. Twentyfour Landrace pigs were assigned into 4 groups: I: after cardiac arrest livers were procured and transplanted; II: after PC and cardiac arrest livers were procured and transplanted; III: after PC and cardiac arrest, a 15 minutes period of warm ischemia was observed before livers were procured and transplanted; IV: after PC and cardiac arrest, a 30 minutes period of warm ischemia was observed before livers were procured and transplanted. Donors: cardiac arrest was obtained by ligation of coronary arteries and interruption of ventilation. PC (10` x 10`) and warm ischemia waiting time were observed accordingly. Livers were flushed with 4°C HTK solution cooled and procured. Recipients: standard technique was used. After one hour of reperfusion, blood and liver samples were collected and euthanasia was carried out. Non-parametrical statistical tests were applied. Results were expressed as medians. A value of p<0.05 was considered statistically significant. Results: AST, ALT, lactic acid and factor V levels were similar for the different studied groups by the end of one hour of reperfusion. A trend towards a deteriorated liver function was observed in group IV. When histological variables were addressed, vacuolization of hepatocytes and cell dropout scores were similar in all groups. Congestion score, vacuolization of hepatocytes and cell dropout scores tended to be higher in animals from group IV, but with no statistical significance. Conclusions: Remote ischemic preconditioning showed no benefits to liver grafts from nonheart- beating donors. Even though it did not result in benefits, no prejudice could be noticed in this research, as well.
Introdução: A melhora na função hepática em doadores de coração parado parece estar relacionada a curtos períodos de isquemia normotérmica, logo a lesão de isquemia e reperfusão é uma questão crucial não resolvida. O pré-condicionamento isquémico remoto (PC), promove proteção ao fígado da lesão de isquemia e reperfusão. No entanto, pouco se sabe sobre a utilidade do PC como uma estratégia para melhorar a tolerância de enxertos de doadores em parada cardíaca frente à isquemia normotérmica. Portanto, foi desenvolvido um estudo experimental visando os efeitos do pré-condicionamento isquêmico no transplante de fígado de doadores em parada cardíaca.Métodos: O protocolo do estudo foi aprovado na Universidade Federal de Goiás pelo Comitê de Ética em Pesquisa. Vinte e quatro suínos da raça Landrace foram divididos em 4 grupos: I: após parada cardíaca, o fígado foi captado e transplantado; II: após o PC, promoveu-se a parada cardíaca, seguida de captação e transplante hepático; III: após o PC, promoveu-se a parada cardíaca, seguida de um período de 15 minutos de isquemia normotérmica, com captação e transplante hepático em seguida; IV: após o PC, promoveu-se a parada cardíaca, seguida de um período de 30 minutos de isquemia normotérmica, com captação e transplante hepático em seguida. Nos doadores, a parada cardíaca foi obtida pela ligadura das artérias coronárias e interrupção do suporte ventilatório. O PC (10 'x 10') e o tempo de isquemia normotérmica foram observados em conformidade com a padronização. O fígado foi perfundido com solução HTK resfriada a 4 ° C e posteriormente captado. Para o receptor foi utilizada a técnica padrão. Após uma hora de reperfusão, amostras de sangue e de tecido hepático foram coletadas, seguida da realização da eutanásia. Foram aplicados testes estatísticos não-paramétricos. Os resultados foram expressos em medianas. O valor de p <0,05 foi considerado estatisticamente significativo. Resultados: Os valores encontrados de AST, ALT, lactato e fator V foram semelhantes para os diferentes grupos estudados até o fim do experimento. No entanto, foi observado uma tendência para piora da função hepática no grupo IV. Em relação às variáveis histológicas, a vacuolização dos hepatócitos e a desestruturação celular foram semelhantes em todos os grupos; houve uma tendência de aumento da congestão no grupo IV, sem significância estatística. Conclusões: O pré-condicionamento isquêmico remoto não mostrou benefício para enxertos de fígado de parada cardíaca. Mesmo que o PC não tenha promovido benefícios nesta pesquisa, também não foram observados danos.
He, Zhong-De y 何鐘德. "PROTECTIVE EFFECT OF HONOKIOL ON RAT LIVER AGAINST ISCHEMIA- REPERFUSION INJURY". Thesis, 1996. http://ndltd.ncl.edu.tw/handle/94304226894410364954.
Texto completoChiu, En-Yu y 邱恩郁. "Protective Effect of KMUP-1 Against Ischemia-Reperfusion Injury In Liver". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/88699181037702214022.
Texto completo高雄醫學大學
藥理學研究所
98
Hepatic ischemia-reperfusion (I/R) -induced injury is a major cause of morbidity and mortality associated with liver transplantation and resectional surgery as well as septic and hemorrhagic shock. Indeed, there is a large body of experimental and clinical evidence suggesting that I/R induced by these surgical procedures or pathophysiological events injures the liver and may ultimately lead to tissue dysfunction and possibly liver failure. These surgical procedures or pathophysiological events usually results in oxidative stress, hepatocyte death, endothelial cell damage and microcirculatory disturbances, leading to liver dysfunction. Previous reports have defined this injury as bi-phasic, having both an acute and a sub-acute phase. The acute phase occurs within the first 6 h of reperfusion and is characterized by the activation of resident Kupffer cells, resulting in enhanced production of reactive oxygen species (ROS). Historically, enhanced ROS production has been thought to generate severe oxidative stress to the tissue by virtue of its ability to degrade membrane lipids and/or proteins. A growing body of experimental evidence suggests that nitric oxide (NO) may also modulate I/R-induced tissue injury in various organ systems. In vitro and in vivo data suggest that endothelial nitric oxide synthase (eNOS)-derived NO may act to protect tissue by virtue of its ability to react with and decompose ROS, and interfere with Caspase activation. Guanosine 3’,5’cyclic momnophosphate (cGMP), a key intracellular second messenger molecule, has been shown to up-regulate Bcl-2 expression in some cells. Phosphodiesterase 5 (PDE5) inhibition results in raising the intracellular cGMP concentration which subsequently activates cytosolic cGMP-dependent protein kinase (PKG). Previous studies demonstrated that PKG expression increased the protective effect against necrosis and apoptosis following simulated ischemia and reoxygenation. KMUP-1, a xanthine derivative, was demonstrated to promote vasodilation, inhibition of PDEs, enhancement of cGMP, and activation of K+ channels. In this study, we investigated the protective effects and pharmacological mechanism of action of KMUP-1 in liver after I/R. Male Wistar rats were randomly divided into five groups, as follows: Sham-operated group, I/R with Vehicle group, I/R with KMUP-1 0.25 mg/kg group, I/R with KMUP-1 0.5 mg/kg group, and I/R with KMUP-1 1 mg/kg group. They underwent 70% partial hepatic ischemia for 45 minutes and subsequent reperfusion for 240 miniutes. Sham-operated group underwent all surgical procedure except ligation of portal triad. All rats were treated by bolus injection via femoral vein (i.v.) 10 min before partial ischemia. They were sacrificed at 240 minutes after reperfusion. In a rat model of acute hepatic ischemia-reperfusion, administration of KMUP-1 inhibited I/R-induced apoptosis, as detected by ladder-pattern fragmentation of genomic DNA. KMUP-1 improved parameters of liver function, enhanced protein expressions of eNOS/ cGMP/ PKG pathway, and ratio of Bcl-2/ Bax and decreased ROS production and caspase-3 activation. In conclusion, these results suggest that KMUP-1 may protect liver from I/R-induced apoptosis by scavenging free radicals and regulating the protein expression of Bcl-2 family and eNOS/ cGMP/ PKG pathway. Thus, KMUP-1 will be useful clinically in the prevention of acute hepatic ischemia-reperfusion injury.
Pommey, Sandra Aude Isabelle. "Over-expression of human CD39 in mouse liver protects against ischemia reperfusion injury in a model of liver transplantation". 2009. http://repository.unimelb.edu.au/10187/5625.
Texto completoCD39 is an integral vascular and immune ectonucleotidase. CD39 hydrolyses extracellular nucleotides ATP and ADP into AMP, which is then hydrolysed into adenosine by CD73. Extracellular adenosine produced by the concerted action of CD39 and CD73 has potent anti-inflammatory and anti-coagulation effects acting principally via the purinergic adenosine receptor A2a.
NKT cells have only recently been recognised and constitute an important subset of T lymphocytes that display both effector and suppressive functions. NKT cells are found in high proportion in the liver of mice and are implicated by depletion studies in protection against hepatic IRI.
We have generated mice transgenic for human CD39 (hCD39) and have shown they have an anti-coagulant phenotype. As CD39 is also critical to immune regulation we hypothesised that transgenic expression of hCD39 would modify lymphocyte development and/or function and consequently impact on ischemia reperfusion injury.
Flow cytometric analysis was used to assess the number and phenotype of lymphocytes within the thymus and in the periphery of hCD39 transgenic mice. In vitro and in vivo assays were used to test the function of CD4+ T cells and invariant NKT cells from hCD39 transgenic mice. Bone marrow adoptive transfers experiments defined the role of hCD39 expression on bone marrow progenitor cells in comparison to tissue expression. The importance of adenosine signalling through the A2a receptor was studied by crossing hCD39 transgenic mice with A2a receptor knock-out (KO) mice. The effect of hCD39 expression on ischemia reperfusion injury was evaluated in a model of murine liver transplantation
A high level of hCD39 expression in the transgenic thymus resulted in lymphocyte maturation blockade and peripheral lymphopenia of CD4+ T cells and invariant NKT cells. Both lymphocyte populations were functionally deficient. The observed phenotype resulted from the expression of hCD39 on bone marrow progenitor cells but was independent of A2a receptor signalling. Over-expression of hCD39 in transgenic livers was protective against ischemia reperfusion injury induced by cold storage and liver transplantation.
Lin, Han-Chen y 林含貞. "The Protective Effects of Ischemic Postconditioning on Liver Ischemia-reperfusion Injury Among Rats". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/06248672235876015037.
Texto completo國立臺灣大學
解剖學暨生物細胞學研究所
98
Introduction: Ischemic postconditioning (iPoC), a repetitive, brief ischemia- reperfusion maneuver performed at or before the initiation of tissue reperfusion, has been shown to mitigate reperfusion injury in heart and brain. The aim of this study is to investigate the effects of iPoC on liver ischemia- reperfusion injury. Methods: Partial liver ischemia-reperfusion injury is induced by clamping the left lobes of liver for 45 minutes on male Wistar rats (160 g- 180 g). Three cycles of one-minute’s ischemia-reperfusion of the liver, performed by clamping and de-clamping of the liver, are applied before the commencement of reperfusion as the iPoC maneuver. Blood and liver samples are harvested at 240 minutes after reperfusion for end-point assessments which include serum GPT, H&E staining, TUNEL staining, and electron microscopy (EM) study. The results are compared between the sham, sham+ATR(atractyloside), control , postconditioning (iPoC) and postconditioning+ATR (iPoC+ATR) groups. Results: Our data shows that there are no differences in the basal GPT levels of the five groups, but ischemic postconditioning could reduce the elevation of serum GPT level after reperfusion for 240 minutes (174.0±28.3 U/L v.s 416.3±16.7 U/L, p <0.05), and decrease the percentage of apoptotic hepatocytes(44.9±9.9 % v.s 81.1±13.8 %,p<0.05). The co-treatment with iPoC and ATR (iPoC+ATR) could increase the elevation of serum GPT and the number of apoptotic hepatocytes. There are no differences between iPoC+ATR and control groups in serum GPT level after reperfusion for 240 minutes (557.0±86.7 U/L v.s 416.3±16.7 U/L, p=0.18) and the percentage of apoptotic hepatocytes ((63.2±4.0 % v.s 81.1±13.8 %,p=0.09). EM study showed the morphology of mitochondria is more intact after reperfusion when compared to those in control group. Western blot shows increased cytochrome c expression in cytosol portion after reperfusion injury of liver, and postconditioning decreased the expression of cytochrome c after reperfusion. The co-treatment with iPoC and ATR could increase the expression of cytochrome c after reperfusion. Conclusions: This study shows that ischemic postconditioning can attenuate cell deaths after reperfusion injury of liver. The mechanism of protection conferred by postconditioning is related to reduced cytochrome c release, and mediation of mitochondrial permeability transition pore (mPTP).
Hartkorn, Andreas [Verfasser]. "Different approaches to influence the ischemia, reperfusion injury of the liver / Andreas Hartkorn". 2008. http://d-nb.info/990802906/34.
Texto completoMüller, Christian. "Alpha-Lipoic acid attenuates Ischemia reperfusion injury of the Rat Liver : mechanisms of protection". 2002. http://edoc.ub.uni-muenchen.de/239/.
Texto completoTian, Yu-Feng y 田宇峯. "Effects of Antrodia camphorate precondition against ischemia-reperfusion injury of the liver in rats". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/14121268590174437433.
Texto completo南台科技大學
生物科技系
98
It has been found that in recent years the incidence of liver diseases has been increasing greatly in Taiwan. Chronic liver diseases and liver cirrhosis are at the sixth among the top ten causes of death recently. Furthermore, liver cancer is the leading cause of cancer mortality. Liver resection and liver transplantation are the main therapy. Ischemia-reperfusion injury plays an important role during liver resection or liver transplantation. Ischemia-reperfusion (I/R) injury of the liver may occur under many clinical conditions, such as hepatic trauma, hepatic transplantation, hypoperfusion shock or partial hepatectomy for liver tumors. Until now, the actual mechanisms remain unknown. There is evidenced that the sequence of hepatic I/R injury may cause severe liver injury. It was suggested that the increase of Kupffer cells activation induced reaction oxygen species involves the possible mechanisms. Activation of Kupffer cells results in production and release of proinflammatory cytokins, including tumor necrosis factor α (TNF-α) and interleukin 1(IL-1β), chemokines, and neutrophil activation, lead to sinusoid endothelial cell death and hepatic cell damage. The period of hepatic ischemia associated with this technique and the resultant reperfusion can lead to liver injury and dysfunction, which is the main cause of death after hepatectomy. Thus, hepatic I/R injury has been actively investigated, and recently, protective strategies consisting of surgical interventions, pharmacological agents, and gene therapy have been reported. Therefore, enhancing the safety of hepatic surgery and diminishing the significant rates of morbidity and mortality are the most important task in clinical therapy. In Taiwan, Antrodia camphorate(AC) is an exclusive fungus parasitic on the inner cavity of the endemic species Cinnamomum kanehirai Hayata and an important traditional Chinese medicinal fungus(Basidiomycetes) for the treatment of human disease such as food and drug intoxication, abdominal pain, hypertension and liver cancer. Recently, polysaccharides extracted from fruiting bodies and mycelial cultures of Antrodia camphorate are reported to provide several therapeutic benefits including anti-inflammation, antioxidation, vasorelaxation and anti-hepatitis B virus activities, but the underlying molecular mechanisms are obscure. Our study had four groups which included ischemia reperfusion group、0.2 g/kg AC + I/R group、AC sham group and normal control group. The I/R rats are treated with 0.2 g/kg Antrodia camphorate (AC) 30 minute before ischemia (IR, ischemia 30min + 0.2 g/kg A.C.), than reperfusion 6h or reperfusion 7 day. Rat serums which were assayed TNF-αquantity by ELISA were extrated before ischemia、after reperfusion 2h and 6h. The serums which were assayed IL-6 and IL-10 quantity by ELISA were extrated before ischemia、after reperfusion 1h, 2h, 3h, 4h, 5h and 6h. After reperfusion 6h the serums were also assayed glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) quantity. Liver tissue【left lateral lobe(ischemia liver) and right lateral lobe(nonischemia liver】will be taken for measuring lipid peroxidation(MDA assay).liver tissue will also be taken for paraffin-embedded tissue sections which were respectively stained by H&E or TUNEL, and observed histopathology and liver cell apoptosis. In these results, the ischemia reperfusion animal modal was successful,when MBP decreased at ischemia stage and increased gradually at reperfusion stage. Furthermore the liver was black and necrosis during reperfusion 6h. Pretreated Antrodia camphorate, we detected that rat GPT concentration was improved at reperfusion 6h stage, contrasted with IR control (P<0.05), but GOT concentration was decreased slighter in pretreated Antrodia camphorate. The paraffin-emmbedded tissue sections which were stained by H&E showed that AC could diminish hepatocyte vacuolar degeneration, vascular congestion and less severe hepatic necrosis in liver grafts at reperfusion 6 hours. The physiology monitory result showed : 1. After ischemia injury, AC could avoid high body temperature. 2. At ischemia stage, AC could maintain heart rate stability. 3. Contrasted with IR control, AC could maintain blood pressure stability at reperfusion 3~6 h. Under other hand, AC could reduce the TNF-α、IL-6 quantity of liver ischemia reperfusion injury rat serum, and suppress inflammation reaction. In AC therapy group, because inflammation reaction were be suppressed, IL-10 quantity range on the rise were be down regulating in serum. When we assayed MDA level., which was decreased at Antrodia camphorate pretreatment, compared with IR control after reperfusion 6h. In the result of TUNEL stain, AC reduced severe hapatic cell DNA fragmentation and apoptosis in liver at reperfusion 6 hours. At reperfusion 7 day, we found AC which could increase the survival rate to 80%。 In this study, we had established rat liver ischemia reperfusion modal. The results suggested, effect of Antrodia camphorate precondition to protect was good, which could reduce liver ischemia reperfusion injury. In the future, we will investigate the mechanism of protection with Antrodia camphorate, and add other medicine or therapy method which can increase the curative effect of liver ischemia reperfusion injury.