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The Effects of Lidocaine on Kidney Injury Induced by Intestinal Ischemia-Reperfusion in Yong Rats

Author: LiuQingWen
Tutor: WuXueDong
School: Dali University
Course: Pediatrics
Keywords: Intestinal Ischemia-reperfusion kidney injury immunohistochemistry lidocaine young rats
CLC: R965
Type: Master's thesis
Year: 2011
Downloads: 7
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Abstract


Objectives: An intestinal ischemia reperfusion (Ⅱ/R) young rat model was established and the lidocaine was used to intervene for kidney injury in the model. The aim of this study was to evaluate the therapeutic effect and mechanism of pretreatment with lidocaine on Ischemia/reperfusion-induced acute kidney injury and pave reference of animal experiment, by the way of detecting the levels of the serum of creatinine (Scr) and BUN, the expression of malondialdehyde (MDA), myeloperoxidase (MPO), intercellular adhesion molecule-1 (ICAM-1),Tumor Necrosis Factor alpha (TNF-a) and nuclear factor of kappa B (NF-κB) in the kidney tissue of the young rats.Methods:Eighty Sprague Dawley (SD) young rats at 4 weeks old were randomly assigned into 4 groups:①Sham-operated group (Sham group,10 rats),only exposure to the superior mesenteric artery (SMA), no intestinal ischemia-reperfusion, an hour later, animals were killed.②Intestinal Ischemia group (Ⅱgroup,10 rats) expose the abdominal cavity, clamping the SMA, animals were killed after an hour later.③Intestinal Ischemia-reperfusion group (Ⅱ/R group.30 rats), the SMA were blocked lasting for an hour, before reperfusion of femoral vein injection of 0.5ml physiologic saline, after reperfusion 0.5 hour，1 hour.2 hour，10 animals were sacrificed at each time point.④Lidocaine intervention group (Lid group,30 rats), the SMA were blocked lasting for an hour, reperfusion after femoral vein before the injection of lidocaine 2mg/kg (diluted in 0.5 ml of physiologic saline), after reperfusion 0.5 hour,l hour,2 hour,10 animals were sacrificed at each time point. Animals were sacrificed then obtained kidney and venous blood samples. The samples of kidney were used for pathological study. The serum concentration of Cr and BUN were measured. MDA and MPO in renal tissue were measured by spectrophotometer. The expression of ICAM-1 in renal tissue was measured by enzyme-linked immunosorbent assay (ELISA). The expression of TNF-a and NF-κB in renal tissue were measured by the immunohistochemistry method. One-factor analysis of variance was used to analyse the data of measurement.Results:(1) Pathological change of renal tissue:the general HE staining showed that there were no significant pathological changes in renal tissue of sham-operated group; renal tissue of Intestinal Ischemia group became edema; renal tissue of Intestinal Ischemia-reperfusion group became hyperemia and edema, and renal proximal tubular epithelial cell became vacuolar degeneration; the longer ischemia time, the more significantly pathological damaged. The injury degree of renal tissue in lidocaine intervention group was less than that of sham-operated group’s. Immunohistochemical staining of TNF-a and NF-κB showed that there were buff granule in renal proximal tubular epithelial cell cytoblastema and nucleus.(2) Change condition of Scr and BUN:at 1h and 2h of reperfusion, Scr in Intestinal Ischemia-reperfusion group were higher than those of sham-operated group, Intestinal Ischemia group and lidocaine intervention group. Scr in lidocaine intervention group were higher than sham-operated group’s (P<0.05). At each corresponding time in 1 h and 2h of reperfusion, Scr in Ischemia-reperfusion group were higher than that that of lidocaine intervention group (P<0.01). If BUN in the four groups compared with each other, there were no statistical significance (P>0.05).(3) Change condition of MDA and MPO:MDA and MPO in Intestinal Ischemia-reperfusion group and lidocaine intervention group began to rise at 0.5h of reperfusion. In comparison with sham-operated group and Intestinal Ischemia group, MDA and MPO in Intestinal Ischemia-reperfusion group and lidocaine intervention group were both statistically higher, only except that there was no statistical significance at 0.5h in lidocaine intervention group compared with Intestinal Ischemia group. At each corresponding time in 1h and 2h of reperfusion, MDA and MPO in Intestinal Ischemia-reperfusion group were dramatically higher than lidocaine intervention group’s (P<0.01).(4) Change condition of ICAM-1:ICAM-1 reached peak at 1h in Intestinal Ischemia-reperfusion group and then declined. At each time point of reperfusion, ICAM-1 in Intestinal Ischemia-reperfusion group and lidocaine intervention group were dramatically higher than sham-operated group’s (P<0.01). At 1h and 2h of reperfusion, ICAM-1 in Intestinal Ischemia-reperfusion group were dramatically higher than Intestinal Ischemia group’s (P<0.01). At each corresponding time point in 1h and 2h of reperfusion, ICAM-1 in Intestinal Ichemia-reperfusion group were dramatically higher than lidocaine intervention group’s (P<0.01).(5) Change condition of TNF-a and NF-κB:TNF-a and NF-κB in Intestinal Ischemia-reperfusion group and lidocaine intervention group began to rise, at 0.5h of reperfusion. At each time point of reperfusion, TNF-a and NF-kB in Intestinal Ischemia-reperfusion group and lidocaine intervention group were dramatically higher than those of sham-operated group and Intestinal Ischemia group (P<0.01). At each time of reperfusion, TNF-a and NF-κB in Intestinal Ischemia-reperfusion group were dramatically higher than lidocaine intervention group’s (P<0.01).Conclusions:The Intestine Ischemia-reperfusion of young SD rats might cause the levels of Scr and that of MDA, MPO, ICAM-1, TNF-a and NF-κB increased. Lidocaine might have a protective effect on ischemia/reperfusion-induced acute kidney injury, by the way of reduceing the levels of Scr, MDA and MPO, and reduceing the renal expression of ICAM-1, TNF-αand NF-κB. The mechanism of it needs further study.

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