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Multiple organ parenchymal cell apoptosis and its induction early after ischemia-reperfusion in rats and mice / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 792-793, 2001.
Artigo em Chinês | WPRIM | ID: wpr-410249
ABSTRACT

AIM:

To determine the evolutionary pattern of parenchymal cell apoptosis in multiple organs early after intestinal ischemia-reperfusion(I/R) and its induction mechanisms and the role of apoptosis in triggering SIRS/MODS.

METHODS:

An I/R model was reproduced by clipping and releasing the superior mesenteric artery in rats and mice. Flow cytometry, electron microscope, DNA agarose gel electrophoresis, TUNEL method, fluorescent and Gomori's silver-HE staining were used to detect apoptosis. Distribution features of apoptotic parenchymal cells in multiple organs were observed. Immunohistochemical staining of HSP 70 and Bcl-2 were performd to study the induction mechanisms of apoptosis.RESULTS and

CONCLUSION:

1. Damage of the liver, lung, gut and kidney was appeared in early phase of I/R. The percentages of apoptosis in parenchyma organs increased progressively. The percentages of cell necrosis increased with the prolonged I/R duration. 2. Percentages of apoptosis were much higher near the central veins of liver lobules, in the outer medulla of the kidney, and the antimescenteric border of intestinal mucosal epithelium because of ischemia. 3. The expression of HSP 70 increased and Bcl-2 reduced in the areas mentioned above because of hypoperfusion. 4. Apoptosis of I/R hepatocytes, splenocytes and thymocytes was obviously increased after Kupffer cell blockage with GdCl3, showing the functional state of Kupffer cells may play an important role in SIRS/MODS.
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2001 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2001 Tipo de documento: Artigo