The aim of this study was to observe the effects of different types of fluid resuscitation on hepatic mitochondria and apoptosis in hemorrhagic shock, and the corresponding mechanisms. Forty rats were divided into five groups: Sham surgery (Sham group), shock (Shock group), Ringer's lactate resuscitation (RL group), hydroxyethyl starch resuscitation (HES group) and autologous blood resuscitation (BL group). A model of hemorrhagic shock was successfully induced in the latter four groups. The recovery objective was to maintain the mean arterial pressure (MAP) of the rats at 80 mmHg. Two hours after the end of the recovery experiment, fresh liver samples were examined in order to observe the changes in the morphology and mitochondrial membrane potential (ΔΨm). In addition, the levels of succinate dehydrogenase (SDH) activity were assessed, and a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was conducted to evaluate the level of apoptosis in the liver cells. In the Shock, RL, HES and BL groups, mitochondrial ultrastructural damage in the liver cells, significant reductions in liver cell function, liver ΔΨm and SDH activity, and the apoptosis of hepatocytes were more apparent compared with those in the Sham group. In the BL group, compared with the RL and HES groups, the injuries to the mitochondrial ultrastructure and liver cell function were significantly reduced, the hepatic ΔΨm and SDH activity were significantly increased and the hepatocyte apoptosis index (AI) was significantly reduced (P<0.05). In conclusion, in a rat model of hemorrhagic shock, different methods of fluid resuscitation may improve the liver cells with regard to mitochondrial ultrastructure and function, the stability of liver ΔΨm, the activity of SDH and the inhibition of liver cell apoptosis. The results indicate that infusion with autologous blood followed by RL solution is a preferable method of fluid resuscitation compared with HES.
Keywords: apoptosis; fluid resuscitation; hemorrhagic shock; mitochondrial membrane potential; succinate dehydrogenase.