We examined the hypothesis that mild hypothermia (rectal temperature 34 degrees C) results in the same survival time, whether induced spontaneously or intentionally, during untreated, lethal, uncontrolled hemorrhagic shock in rats. Sixty-four Sprague-Dawley male rats were randomly assigned to normothermia (Nth) (n=19), spontaneous mild hypothermia (Sp.Hth) (n=25) or controlled mild hypothermia (Con.Hth) (n=20) groups. After blood withdrawal of 3 mL/100 g over 15 minutes, followed by 75% tail amputation under spontaneous breathing and light anesthesia by i.p. injection of pentobarbital sodium, rats were observed without fluid resuscitation or hemostasis for 180 minutes or until death. The initial temperature of the Nth group was artificially maintained throughout the experiment. For the mild hypothermia groups, the Sp.Hth group was exposed to ambient temperature while the Con. Hth group was actively cooled to a target rectal temperature of 34 degrees C. In the Con.Hth group, all rats except one died before 180 minutes. All rats in the Nth group died within 38 minutes, and within 67 minutes in the Sp.Hth group. The average survival time was shortest in the Nth group at 20.3 +/- 5.3 minutes, followed by the Sp.Hth group at 30.1 +/- 13.5 minutes, and the Con.Hth group at 81.9 +/- 39.8 minutes (p 0.01). Tail bleed out volume was 0.51 +/- 0.19, 0.26 +/- 0.15 and 0.19 +/- 0.12 mL/100 g in the Nth, Sp.Hth and Con.Hth groups, respectively (p 0.05). In conclusion, spontaneous mild hypothermia did not prolong the survival time as much as controlled mild hypothermia in the rat model for untreated, lethal, uncontrolled hemorrhagic shock.
Animal ; Blood Pressure ; Body Temperature ; Hypothermia/*physiopathology ; *Hypothermia, Induced ; Male ; Rats ; Rats, Sprague-Dawley ; Shock, Hemorrhagic/*mortality/physiopathology/therapy

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.

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