[Translocation of intestinal endotoxin and bacteria induced by the apoptosis of enterocytes in scald rats after delayed resuscitation].

OBJECTIVE

To investigate the role of enterocyte apoptosis in translocation of intestinal endotoxin and bacteria after delayed resuscitation in scalded rats.

METHODS

One hundred and ten male Wistar rats were divided randomly into two groups: group A, early resuscitation, n=60; group B, delayed resuscitation, n=50. All animals were subjected to 30% total body surface area (TBSA) full-thickness scald. In group A, saline resuscitation was begun immediately after the injury. Saline resuscitation later than 6 hours after scalding was referred as delayed resuscitation. Apoptosis of enterocytes was identified by DNA fragmentation (ap%), DNA agarose gel electrophoresis, TdT-mediated dUTP nick end labeling (TUNEL) method and electron microscope (EM). The levels of endotoxin in portal vein and systemic circulation were determined by limulus amebocyte lysate technique. The amount of bacteria in mesenteric lymph nodes (MLN) was detected by a quantitative bacteria culture of biopsy.

RESULTS

The ap% of enterocytes was increased significantly in groups A and B, peaking at 12 hours postburn. The increased ap% in the group B occurred much earlier and higher than in group A from 3 hours to 48 hours postburn (P<0.05 or P<0.01). This was corroborated by the results observed in electrophoresis, TUNEL method and EM. The portal endotoxin was much higher in group B than in group A at the same postburn timepoints. So were the endotoxin levels in systemic circulation. A significant positive relationship existed between the portal endotoxin levels and the ap% of intestinal epithelial cells in groups A and B (group A: r=0.936, P<0.01; group B: r=0.899, P<0.05). The frequency of bacteria translocation of MLN in group B was higher than that in group A.

CONCLUSION

Significant pathologic apoptosis of enterocytes is induced by delayed resuscitation after thermal injury in rats. This may lead to a compromise of intestinal barrier. It may be one of the major causes of translocation of endotoxin and bacteria postburn.