过氧化甲乙酮烧伤对新西兰大白兔肾损伤的实验性研究

目的：观察过氧化甲乙酮( methyl ethyl ketone peroxide, MEKP)烧伤对新西兰大白兔肾功能的影响及肾组织的病理变化,探讨MEKP烧伤致肾损伤的机制。方法将30只新西兰大白兔随机分为普通火焰烧伤组( A组)、MEKP烧伤组( B组)及对照组,每组10只。分别于0、1、2、4 h采集血液,观察3组血清肌酐( Scr)、尿素( BUN)水平的变化情况及肾组织形态学变化。结果3组伤后0 h Scr和BUN比较差异无统计学意义(P>0．05)。伤后1、2、4 h A、B组Scr、BUN均高于对照组,且B组高于A组(P<0．05,P<0．01)。 B组肾组织病理表现为肾小管(尤其近端小管)上皮细胞变性坏死,肾小球结构破坏。结论 MEKP烧伤后肾损伤的机制为组织缺血缺氧及再灌注损伤等,同时MEKP吸收入血代谢产生大量自由基及有机酸,导致肾小管上皮细胞及肾小球基底细胞膜脂质过氧化,细胞代谢发生障碍,造成肾小管上皮细胞及肾小球进一步损伤。

A Experimental Study on Renal Injury Caused By Methyl Ethyl Ketone Peroxide Burns in Zelanian White Rabbits

Objective To observe effect of Methyl ethyl ketone peroxide ( MEKP) burns on renal function and pathological changes of renal tissues, and to study mechanisms of renal injury induced by methyl ethyl ketone peroxide burns in Zelanian white rabbits. Methods A total of 30 Zelanian white rabbits were randomly divided into common flame burning group (Group A, n=10), MEKP burns group (Group B, n=10) and control group (n=10). Blood samples were collected 0, 1, 2 and 4 h after burning respectively, and level changes of serum creatinine (Scr) and blood urea nitrogen ( BUN) , and morphological changes of renal tissues were detected in three groups. Results There were no significant differences in Scr and BUN levels at 0 h after burning among three groups (P>0. 05);at 1, 2 and 4 h after burning, the Scr and BUN levels in group A and B were significantly higher than those in control group, and the levels in group B were higher than those in group A (P<0. 05, P<0. 01). Pathological signs of renal tissues included epithelial cell degeneration and necrosis of kidney tubule ( especially proximal tubule) and structural damage of renal glomerulus in group B. Conclusion The kidney injury mechanisms after MEKP burns are tissue ischemia and hypoxia and reperfusion injury. Meanwhile, methyl ethyl ketone peroxide was absorbed into a large amount of free radicals and organic acids pro-duced by blood metabolism, and it can induce lipid peroxidation of renal tubular epithelial cell and glomerular basal cell membranes, cellular metabolism disorder, which can cause further damage to renal tubular epithelial cell and renal glomer-ulus.