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超氧化物歧化酶对冷诱导水肿猫的影响。

Effect of superoxide dismutase in cats with cold-induced edema.

作者信息

Ikeda Y, Brelsford K L, Ikeda K, Bulkley G B, Long D M

机构信息

Department of Neurological Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

出版信息

Adv Neurol. 1990;52:203-10.

PMID:2168663
Abstract

We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.

摘要

我们评估了超氧化物歧化酶(SOD,一种氧自由基清除剂)作为一种探针来涵盖血管源性脑水肿损伤触发期和水肿发展延长阶段的潜在作用。通过标准化的皮质冷冻损伤在34只猫中制造血管源性脑水肿。通过SG测量和伊文思蓝扩散的平面测量法评估脑水肿和血脑屏障的破坏。通过在颅窗内局部应用NBT研究超氧自由基的检测。将动物分为两组:(a)对照组;(b)两个SOD治疗组——A组腹腔注射10000 U/kg聚乙二醇化超氧化物歧化酶(PEG-SOD)进行预处理,并在损伤后24小时和48小时处死,B组在损伤后先静脉推注游离超氧化物歧化酶(4 mg/kg),然后以1 mg/kg/分钟的速度持续给药20分钟,6小时后处死。我们的初步数据表明,在冷诱导损伤后大脑中检测到超氧自由基,但游离和PEG-SOD对冷诱导损伤产生的血管源性脑水肿没有有益作用。得出的结论是,超氧化物歧化酶的细胞内摄取可能是治疗冷诱导脑水肿产生效果所必需的。

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