Bhaskar L, Mathan M M, Balasubramanian K A
Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, Tamilnadu, India.
Mol Cell Biochem. 1995 Oct 4;151(1):9-14. doi: 10.1007/BF01076889.
Reperfusion injury following ischemia is thought to be the consequence of reactive oxygen species. Role of these free radicals on the damaging effects of ischemia in colon has been investigated. A rat experimental model was used in which colon was subjected to ischemia and reperfusion and mucosal damage was assessed by biochemical and histological studies. Activity of myeloperoxidase, a neutrophil marker, was increased after ischemia (I) and ischemia/Reperfusion (I/R). Lipid peroxidation products such as malonaldehyde and conjugated diene did not show any change in the experimental colonic mucosa as compared to control. Mucosal level of low molecular weight thiols were found to be altered after I/R. A decrease in alpha-tocopherol level was noticed after ischemia and the decrease was prominent after reperfusion. Histology indicated morphological changes in colon due to ischemia and reperfusion and the damage was more severe after reperfusion. These results suggest that colonic mucosal damage occurs during I/R and free radicals generated by the infiltrated neutrophils may play a role in this damaging process.
缺血后的再灌注损伤被认为是活性氧的结果。已经研究了这些自由基在结肠缺血损伤作用中的角色。使用了大鼠实验模型，其中结肠经历缺血和再灌注，并通过生化和组织学研究评估黏膜损伤。中性粒细胞标志物髓过氧化物酶的活性在缺血（I）和缺血/再灌注（I/R）后增加。与对照组相比，实验性结肠黏膜中的脂质过氧化产物如丙二醛和共轭二烯没有显示任何变化。发现I/R后低分子量硫醇的黏膜水平发生改变。缺血后α-生育酚水平降低，再灌注后降低更为明显。组织学表明结肠因缺血和再灌注而出现形态学变化，再灌注后损伤更严重。这些结果表明，I/R期间发生结肠黏膜损伤，浸润的中性粒细胞产生的自由基可能在这一损伤过程中起作用。
