2005Zhongguo xiandai yixue/Zhongguo xiandai yixue zazhiRequires access

Effect of methylprednisolone on hemorrhagic shock in rats

Fulan Guan

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Abstract

Objective: To investigate the effect of methylprednisolone (MP) on hemorrhagic shock in rats and elucidate the underlying mechanisms. Method: Wistar rats were bled to induce the shock and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock+MP groups. Results: 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock+MP group was 80%, the difference was significant (P 0.01). 18 h after resuscitation, pathologic alterations of organs showed: in shock group, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration occurred. MP reduced these pathological alterations significantly. 18 h after resuscitation, creatine phosphokinase, transaminases and creatinin were elevated significantly in shock group, while these in shock+MP group were elevated slightly, the differences were significant (P 0.01). Increases in intracellular calcium and production of TNF-α by isolated kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by MP (P 0.01). Conclusion: Methylprednisolone reduces organ injury and mortality caused by hemorrhagic shock by blocking increase of intracellular calcium, activation and production of TNF-α of kupffer cells and preventing systemic progressive inflammation responses.

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Objective: To investigate the effect of methylprednisolone (MP) on hemorrhagic shock in rats and elucidate the underlying mechanisms. Method: Wistar rats were bled to induce the shock and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock+MP groups. Results: 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock+MP group was 80%, the difference was significant (P 0.01). 18 h after resuscitation, pathologic alterations of organs showed: in shock group, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration occurred. MP reduced these pathological alterations significantly. 18 h after resuscitation, creatine phosphokinase, transaminases and creatinin were elevated significantly in shock group, while these in shock+MP group were elevated slightly, the differences were significant (P 0.01). Increases in intracellular calcium and production of TNF-α by isolated kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by MP (P 0.01). Conclusion: Methylprednisolone reduces organ injury and mortality caused by hemorrhagic shock by blocking increase of intracellular calcium, activation and production of TNF-α of kupffer cells and preventing systemic progressive inflammation responses.

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Available abstract

Objective: To investigate the effect of methylprednisolone (MP) on hemorrhagic shock in rats and elucidate the underlying mechanisms. Method: Wistar rats were bled to induce the shock and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock+MP groups. Results: 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock+MP group was 80%, the difference was significant (P 0.01). 18 h after resuscitation, pathologic alterations of organs showed: in shock group, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration occurred. MP reduced these pathological alterations significantly. 18 h after resuscitation, creatine phosphokinase, transaminases and creatinin were elevated significantly in shock group, while these in shock+MP group were elevated slightly, the differences were significant (P 0.01). Increases in intracellular calcium and production of TNF-α by isolated kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by MP (P 0.01). Conclusion: Methylprednisolone reduces organ injury and mortality caused by hemorrhagic shock by blocking increase of intracellular calcium, activation and production of TNF-α of kupffer cells and preventing systemic progressive inflammation responses.

Key concepts: Medicine, Resuscitation, Shock (circulatory), Methylprednisolone, Edema, Internal medicine, Creatine kinase, Endocrinology

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