Kamiński M, Wiaderkiewicz R, Siekierska E
Department of Histology and Embryology, Silesian Medical Academy in Katowice.
Przegl Lek. 1997;54(10):693-701.
The study was performed on rats divided into 9 groups. Groups 1-3 served as controls. In groups 4 and 5 rat livers were subjected to 90-min ischemia followed by 12- or 24-hour reperfusion. In groups 6 and 7 rats were injected with intraperitoneal chlorfenvinphos (2 mg/kg b.w.) and sacrificed after 12 or 24 hours. In groups 8 and 9 rat livers were subjected to 90-min ischemia, 12- or 24-hour reperfusion and then rats were injected with chlorfenvinphos (2 mg/kg b.w.). Liver sections were evaluated morphologically, histochemically (SDH, LDH, G6Pase, glycogen, Mg2+ ATPase and AcP). The microsomal fraction of the liver was evaluated for cytochrome P450 content and NADPH-cytochrome P-450 reductase activity. It has been found that liver ischemia and reperfusion result in extensive necrosis, enzymatic disturbances, particularly in acinar zone 3. Ischemia as well as reperfusion decrease the cytochrome P450 content of hepatocytic microsomes and the activity of NADPH-cytochrome P-450 reductase. Intraperitoneal injection of chlorfenvinphos during ischemia and reperfusion dramatically intensifies damage to the liver, although chlorfenvinphos alone produces only mild nonspecific effects on the morphological and enzymatic structure of the liver.
该研究在分为9组的大鼠身上进行。第1 - 3组作为对照组。第4组和第5组大鼠肝脏经历90分钟缺血,随后再灌注12或24小时。第6组和第7组大鼠腹腔注射毒虫畏(2毫克/千克体重),并在12或24小时后处死。第8组和第9组大鼠肝脏经历90分钟缺血、12或24小时再灌注,然后大鼠注射毒虫畏(2毫克/千克体重)。对肝脏切片进行形态学、组织化学(琥珀酸脱氢酶、乳酸脱氢酶、葡萄糖-6-磷酸酶、糖原、镁离子-ATP酶和酸性磷酸酶)评估。对肝脏微粒体部分评估细胞色素P450含量和NADPH - 细胞色素P - 450还原酶活性。已发现肝脏缺血和再灌注导致广泛坏死、酶紊乱,尤其是在腺泡3区。缺血以及再灌注降低肝细胞微粒体的细胞色素P450含量和NADPH - 细胞色素P - 450还原酶活性。在缺血和再灌注期间腹腔注射毒虫畏会显著加剧对肝脏的损伤,尽管单独使用毒虫畏对肝脏的形态和酶结构仅产生轻微的非特异性影响。