| Objective: Intestinal ischemia/reperfusion (I/R) injury is a common tissue and organ injury in surgery. Addition to intestinal regional injury, it can also induce endotoxemia, acute liver injury, acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). Recently, the mechanism of cytokines' effect on intestinal I/R injury has been gradually thought highly of. TNF- a has been seen as the pivotal mediator during cytokines'chain reaction of intestinal I/R injury. TNF- a , mainly secreted by macrophages, may be an important step in immunological disorder and early organic injury in intestinal I/R injury. This study is to detect the change of endotoxin in different time point of acute animal intestinal I/R injury, to assess the original cells of TNF- a in early intestinal I/R injury stage and the effect of kupffer cells different functional situation to TNF- a secret in intestinal I/R injury.Methode: Male SD rats are divided into two groups randomly, Gadolinium chloride(Gdcl3) treatment group and contrast group (ischemia/reperfusion group) . We occlude the rats'superior mesenteric artery(SMA) to produce intestinal I/R model. Two groups are disposed by before ischemia, ischemia 1 hour, ischemia/reperfusion 1 hour, 2 hours and 4 hours to assay:(1)endotoxin in plasm from portal vein and inferior vena cava(IVC) ;(2)TNF- a in serum from portal vein and inferior vena cava;(3)intestine and liver tissue immunohistochemical expression and distribution;(4)the intestinal mucosa tissue score.Results: This study successfully produce the model of intestinal I/R and we observed that intestinal I/R in rats can produce:(1) Endotoxin and TNF- a in blood:Contrast group: at ischemia 1 hour, the rats blood endotoxin and TNF-a begin to rise. The peak appears at I/R 1 hour and gradually drop till I/R 4 hours. Its value gets thesame level to the time before ischemia. Endotoxin and TNF- a in portal vein are higher than that in IVC, but no significant difference. Gdcb treatment group, endotoxin chang tendency is basically same to contrast group, but, I/R 2 hours is higher than v group(p<0.05). TNF- a , Gdcl3 treatment group is little higher than contrast group before ischemia, during ischemia/reperfusion, TNF- a has two peaks at I/R 1 hour and I/R 4 hours respectively. The value change tendency of portal vein and IVC have no significant difference.(2) The immunohistochemical expression and distribution of TNF- a in the intestine and liver:Contrast group: TNF- a positive material stained in intestinal mucosal cells in all the tissue and I/R 1 hour appears the strongest. TNF- a appears late in liver tissue and its expression is obviously weaker than that in intestinal mucosa.Gdcls treatment group: Two peaks are found in I/R 1 hour and I/R 4 hours. The expression of TNF- a in liver is no significant difference with contrast group (p>0.05).(3) The intestinal mucosal tissue score:Contrast group: The intestinal mucosa is weakly damaged with edema in ischemia 1 hour, more seriously with necrosis or hemorrhage in I/R 1 hour, I/R 2 hours, I/R 4 hours, but I/R 1 hour is the most seriously damaged.Gdcl3 treatment group s damage is similar to contrast group.Conclutions: Intestinal ischemia/reperfusion can result in the intestine becoming a cytokine-liberating organ. In the early stage, the transloction of endotoxin and bacteria from the intestine may be responsible for the TNF- a express and release, which would be a pivotal mediator and an important mechanism underlying pathophysiological alternations associated with intestinal I/R injury. Inactivation of Kupffer cells or not has no significant effect on TNF- a secreting in the early stage of Intestinal ischemia/reperfusion, but the normal functional states of Kupffer cells may protect the injury from intestinal I/R injury.
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