重复性缺血的累积效应:病理生理学结果。

G Nagashima
{"title":"重复性缺血的累积效应:病理生理学结果。","authors":"G Nagashima","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The cumulative effect of ischemia on the brain was investigated in cats using a repetitive transient global ischemia model. The cats were submitted to three series of repetitive ischemia of 5.0, 7.5 and 10.0-minute durations at 1-hour intervals by intrathoracic clamping of the innominate and subclavian arteries. Pathophysiological changes during and after the ischemic episodes were evaluated by monitoring the electroencephalograms (EEG), cerebral blood flow (CBF), specific gravity and 31P-MR spectroscopy (MRS). Transient 5.0, 7.5, and 10.0-minute ischemias appeared to produce a slightly more severe energy failure on the 31P MRS measurement in the animals that had previously experienced an ischemic injury than those that had not. Additionally, repetition of ischemic episodes at 1-hour intervals led to a progressive lengthening of the duration of the spontaneous electrocortical suppression that followed each ischemic episode. However, preischemic hypoxia (5% O2 for 5 minutes) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate on the MRS measurement, otherwise the EEG activity declined progressively. This shut-down response of the EEG can be concluded to serve in preserving the energy state of the brain although it is not capable of preventing the development of postischemic brain edema and neuronal death.</p>","PeriodicalId":22311,"journal":{"name":"The Bulletin of Tokyo Medical and Dental University","volume":"41 2","pages":"23-36"},"PeriodicalIF":0.0000,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cumulative effect of repetitive ischemia: pathophysiological findings.\",\"authors\":\"G Nagashima\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The cumulative effect of ischemia on the brain was investigated in cats using a repetitive transient global ischemia model. The cats were submitted to three series of repetitive ischemia of 5.0, 7.5 and 10.0-minute durations at 1-hour intervals by intrathoracic clamping of the innominate and subclavian arteries. Pathophysiological changes during and after the ischemic episodes were evaluated by monitoring the electroencephalograms (EEG), cerebral blood flow (CBF), specific gravity and 31P-MR spectroscopy (MRS). Transient 5.0, 7.5, and 10.0-minute ischemias appeared to produce a slightly more severe energy failure on the 31P MRS measurement in the animals that had previously experienced an ischemic injury than those that had not. Additionally, repetition of ischemic episodes at 1-hour intervals led to a progressive lengthening of the duration of the spontaneous electrocortical suppression that followed each ischemic episode. However, preischemic hypoxia (5% O2 for 5 minutes) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate on the MRS measurement, otherwise the EEG activity declined progressively. This shut-down response of the EEG can be concluded to serve in preserving the energy state of the brain although it is not capable of preventing the development of postischemic brain edema and neuronal death.</p>\",\"PeriodicalId\":22311,\"journal\":{\"name\":\"The Bulletin of Tokyo Medical and Dental University\",\"volume\":\"41 2\",\"pages\":\"23-36\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1994-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Bulletin of Tokyo Medical and Dental University\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Bulletin of Tokyo Medical and Dental University","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

研究了猫脑缺血的累积效应,采用重复瞬态全脑缺血模型。通过胸内夹持无名动脉和锁骨下动脉,对猫进行5.0、7.5和10.0分钟的重复缺血,间隔1小时。通过监测脑电图(EEG)、脑血流量(CBF)、比重和31P-MR谱(MRS)评估缺血发作期间和之后的病理生理变化。在经历过缺血性损伤的动物中,短暂性缺血5.0分钟、7.5分钟和10.0分钟似乎比没有经历过缺血性损伤的动物产生更严重的31P MRS能量衰竭。此外,每隔1小时缺血发作的重复导致每次缺血发作后自发性皮层电抑制持续时间的逐渐延长。然而,缺血前缺氧(5% O2 5分钟)导致MRS测量中磷酸肌酸和细胞内无机磷酸盐水平的微小变化,否则脑电图活动逐渐下降。脑电图的这种关闭反应可以被推断为保存大脑的能量状态,尽管它不能阻止脑缺血后水肿和神经元死亡的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cumulative effect of repetitive ischemia: pathophysiological findings.

The cumulative effect of ischemia on the brain was investigated in cats using a repetitive transient global ischemia model. The cats were submitted to three series of repetitive ischemia of 5.0, 7.5 and 10.0-minute durations at 1-hour intervals by intrathoracic clamping of the innominate and subclavian arteries. Pathophysiological changes during and after the ischemic episodes were evaluated by monitoring the electroencephalograms (EEG), cerebral blood flow (CBF), specific gravity and 31P-MR spectroscopy (MRS). Transient 5.0, 7.5, and 10.0-minute ischemias appeared to produce a slightly more severe energy failure on the 31P MRS measurement in the animals that had previously experienced an ischemic injury than those that had not. Additionally, repetition of ischemic episodes at 1-hour intervals led to a progressive lengthening of the duration of the spontaneous electrocortical suppression that followed each ischemic episode. However, preischemic hypoxia (5% O2 for 5 minutes) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate on the MRS measurement, otherwise the EEG activity declined progressively. This shut-down response of the EEG can be concluded to serve in preserving the energy state of the brain although it is not capable of preventing the development of postischemic brain edema and neuronal death.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信