Durak I, Kurtipek O, Oztürk H S, Birey M, Güven T, Kavutcu M, Kaçmaz M, Dikmen B, Yel M, Canbolat O
Department of Biochemistry, Ankara University Medical Faculty, Turkey.
Can J Anaesth. 1997 Sep;44(9):1014-20. doi: 10.1007/BF03011975.
To investigate the effects of halothane and halothane plus vitamin E treatment on myocardial free radical metabolism in guinea pigs.
Four groups of seven animals were studied: control, halothane, halothane plus vitamin E and vitamin E groups. In the halothane group, halothane 1.5% in oxygen was given for 90 min over three days. In the halothane plus vitamin E group, 300 mg.kg-1.day-1 vitamin E im was started three days before the first halothane treatment and continued for three days. Following sacrifice, the hearts were assayed for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and malondialdehyde (MDA) level was determined. Electron spin resonance (ESR) analysis and electron microscopy (EM) were also performed.
In the halothane group, SOD activities and MDA concentrations were increased compared with control and GSH-Px and CAT activities were decreased. In the halothane plus vitamin E group, there were no differences in enzyme activity compared with halothane alone but the MDA level was decreased. In the vitamin E group, enzyme activities were increased compared with control. Mainly the CF3CHCl radical was identified by ESR analysis in heart tissues exposed to halothane and the concentration of this radical was reduced by vitamin E. Electron microscopy showed cytoplasmic vacuolisation and dilation in sarcoplasmic reticulum in the heart tissues exposed to halothane: both were prevented by vitamin E.
Although halothane causes impairment in enzymatic antioxidant defence potential, due to lowered GSH-Px and CAT activity, and accelerates peroxidative reactions in the tissues affected, no subcellular damage occurred. Vitamin E may protect tissues against free radical attack by scavenging toxic free radicals formed in heart tissue during halothane anaesthesia.
研究氟烷及氟烷加维生素E处理对豚鼠心肌自由基代谢的影响。
对四组动物（每组7只）进行研究：对照组、氟烷组、氟烷加维生素E组和维生素E组。氟烷组，在三天内给予含1.5%氟烷的氧气90分钟。氟烷加维生素E组，在首次氟烷处理前三天开始腹腔注射维生素E 300mg·kg-1·天-1，并持续三天。处死后，测定心脏的超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）活性及丙二醛（MDA）水平。还进行了电子自旋共振（ESR）分析和电子显微镜（EM）检查。
氟烷组与对照组相比，SOD活性和MDA浓度升高，GSH-Px和CAT活性降低。氟烷加维生素E组与单独使用氟烷组相比，酶活性无差异，但MDA水平降低。维生素E组与对照组相比，酶活性升高。ESR分析主要在暴露于氟烷的心脏组织中鉴定出CF3CHCl自由基，维生素E可降低该自由基的浓度。电子显微镜显示，暴露于氟烷的心脏组织中出现细胞质空泡化和肌浆网扩张：维生素E可预防这两种情况。
尽管氟烷由于GSH-Px和CAT活性降低而导致酶抗氧化防御能力受损，并加速受影响组织中的过氧化反应，但未发生亚细胞损伤。维生素E可通过清除氟烷麻醉期间心脏组织中形成的有毒自由基来保护组织免受自由基攻击。
