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Avaliação morfológica e imunohistoquímica tardia do fígado e do pulmão após lesão de isquemia e reperfusão hepática seletiva com modulação pelo precondicionamento isquêmico ou pela N-acetilcisteina / Late morphological and immunohistochemical evaluation of liver and lung after seletive ischemia and reperfusion injury modulated by ischemic preconditioning or N-acetyl

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Previous issue date: 2007 / Este estudo teve como objetivo avaliar 0 papel do precondicionamento isquemico (IPC) e da N-acetilcisteina (NAC) no figado e no pulmao na fase tardia da lesao de isquemia e reperfusao hepatica. Foram usados 24 ratos Wistar EPM-1, distribuidos por randomizacao em quatro grupos: (IR) Isquemia hepatica por 40 minutos e reperfusao por 24 horas; (IPC) precondicionamento isquemico de 10 minutos de isquemia e 10 minutos de reperfusao antes da isquemia prolongada; (NAC) Animais receberam N-acetilcisteina 15 minutos antes da isquemia e 5 minutos antes da reperfusao e (SHAM) Animais foram operados e tiveram 0 pediculo hepatico manipulado sem serem submetidos a isquemia. Na reoperacao, apos 24 horas de reperfusao hepatica, foi colhido sangue para dosagem de aspartate aminotransferase (AST) e alanino aminotransferase (AL T) e retirados os lobos isquemicos do figado e 0 pulmao esquerdo para estudo histologico e imunohistoquimico com Caspase-3 e PCNA para avaliar a apoptose e a proliferacao celular, respectivamente. Foram usados 0 teste de Kruskal-Wallis e 0 teste de variancia com pos-teste de Tukey (p < 0,05). Os valores da AST foram similares entre os grupos (p=0,45); para a ALT houve aumento comparado ao grupo SHAM (p=0,036). Nos grupos IPC e NAC houve prevencao da necrose (p=0,027), apoptose (p=0,003) e esteatose microvesicular (p=0,0007); porem somente no grupo NAC houve reducao do infiltrado inflamatorio (p=0,004) no figado. Os grupos IPC e NAC reduziram a marcacao citoplasmatica de Caspase-3 (p=0,0001) e a marcacao nuclear do PCNA (p=0,0001) no figado. No pulmao, o IPC reduziu 0 espessamento da parede do alveolo (p=0,014), porem tanto 0 IPC quanto a NAC reduziram a Caspase-3 e 0 PCNA em relacao ao grupo IR. Em conclusao, o precondicionamento isquemico e a N-acetilcisteina reduzem a lesao de isquemia e reperfusao hepatica no figado e no pulmao na fase tardia / This study aimed to evaluate the effect of ischemic preconditioning (IPC) and Nacetylcysteine
(NAC) in hepatic and pulmonary damage in late phase after liver
ischemia-reperfusion injury. 24 male Wistar-EPM rats were randomized and
assigned into four groups: (IR) Hepatic ischemia-reperfusion; (IPC) IPC achieved
before hepatic ischemia; (NAC) Animals received NAC pre treatment; and (SHAM)
Sham operated group. After 24 hours of hepatic reperfusion, blood, ischemic liver
and pulmonary samples were collected. Aspartate aminotransferase (AST) and
alanine aminotransferase (ALT) activity were measured, histological and
immunohistochemical studies in liver and lung were also performed. Apoptosis was
evaluated by Caspase-3 while cell proliferation by proliferating cell nuclear antigen
(PCNA) in liver and pulmonary samples. Kruskal-Wallis and one-way ANOVA with
post-hoc Tukey's test for multiple comparisons were used (p ≤ 0.05). AST levels were
similar among experimental groups. ALT lower levels were observed in sham group
(p=0.04). IPC and NAC groups prevented from necrosis (p=0.027), apoptosis
(p=0.003) and microvesicular steatosis (p=0.0007), but just NAC group prevented
from neutrophil infiltration in liver tissue (p=0.004). SHAM, NAC and IPC groups
were lower than IR group in the caspase-3 activity (P=0,001) and quantitative
analysis showed that PCNA in IR group was higher than SHAM, NAC and IPC
groups (P=0,001). In lung tissue, just IPC treatment reduced alveolar septal edema
(p=0.014), but IPC and NAC groups didn’t prevent from neutrophil infiltration or
vascular congestion. The immunohistochemical study showed NAC and IPC groups
prevented apoptosis (P= 0,001) and cell proliferation (P=0,001). In conclusion, IPC
and NAC attenuated hepatic and pulmonary damage after hepatic ischemiareperfusion
injury in late phase. / BV UNIFESP: Teses e dissertações

Identiferoai:union.ndltd.org:IBICT/oai:repositorio.unifesp.br:11600/23633
Date January 2007
CreatorsSouza, Maria Aparecida Galhardo de [UNIFESP]
ContributorsUniversidade Federal de São Paulo (UNIFESP), Montero, Edna Frasson de Souza [UNIFESP]
PublisherUniversidade Federal de São Paulo (UNIFESP)
Source SetsIBICT Brazilian ETDs
LanguagePortuguese
Detected LanguageEnglish
Typeinfo:eu-repo/semantics/publishedVersion, info:eu-repo/semantics/doctoralThesis
Format81 f.
Sourcereponame:Repositório Institucional da UNIFESP, instname:Universidade Federal de São Paulo, instacron:UNIFESP
Rightsinfo:eu-repo/semantics/openAccess

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