The effect of glycine on survival after hemorrhagic shock in the rats.
- Author:
Gang WANG
1
;
En-hua WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Disease Models, Animal; Glycine; pharmacology; therapeutic use; Kidney; drug effects; physiopathology; Kupffer Cells; drug effects; metabolism; Lung; drug effects; physiopathology; Random Allocation; Rats; Rats, Wistar; Shock, Hemorrhagic; drug therapy; mortality; physiopathology; Survival Rate; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Surgery 2004;42(5):296-301
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of glycine on survival after hemorrhagic shock in the rats and elucidate the underlying mechanisms.
METHODSWistar rats were bled to establish the shock model 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 + glycine group.
RESULTS(1) 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock + glycine group was 77.8%, the difference was significant (P < 0.05). (2) 18 h after resuscitation, pathologic alterations of organs showed, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration in shock group. Glycine reduced these pathological alterations significantly. (3) 18 h after resuscitation, creatine phosphokinase, transaminases and creatinine were elevated significantly in shock group, while these were elevated slightly in shock + glycine group, the differences were significant (P < 0.01). (4) Increases in intracellular calcium and production of TNF-alpha by isolated Kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by glycine (P < 0.01).
CONCLUSIONGlycine reduces organ injury and mortality caused by hemorrhagic shock by preventing increase of intracellular calcium and production of TNF-alpha of Kupffer cells and blocking systemic inflammation responses.