己酮茶碱在马内毒素血症全血模型中抑制介质合成。

Circulatory shock Pub Date : 1994-12-01
M H Barton, J N Moore
{"title":"己酮茶碱在马内毒素血症全血模型中抑制介质合成。","authors":"M H Barton,&nbsp;J N Moore","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Whole blood from 10 healthy horses was aseptically collected into heparin or citrate anticoagulant and incubated in vitro for 6 hr in the absence (saline control) or presence of 1 ng endotoxin/ml blood. Pentoxifylline (0.1, 1, 10, or 100 micrograms/ml blood) was added 1 hr before, at the same time, or 1 hr after endotoxin. As compared to saline controls, pentoxifylline alone had no effect on mediator production, with the exception of significantly increasing 6-ketoprostaglandin F1 alpha concentration. Pentoxifylline inhibited endotoxin-induced increases in tumor necrosis factor (TNF) and interleukin-6 (IL-6) activity in a dose-related fashion, whether added before, at the same time, or after endotoxin. Pentoxifylline significantly inhibited tissue factor activity, but only when added before endotoxin. Pentoxifylline had no effect on endotoxin-induced 6-keto-prostaglandin F1 alpha production, but significantly inhibited thromboxane B2 (TxB2) production. The results of this study indicate that pentoxifylline, at blood concentrations consistent with those achieved in vivo, has effects that may be beneficial in the treatment of endotoxemia.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 4","pages":"216-20"},"PeriodicalIF":0.0000,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Pentoxifylline inhibits mediator synthesis in an equine in vitro whole blood model of endotoxemia.\",\"authors\":\"M H Barton,&nbsp;J N Moore\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Whole blood from 10 healthy horses was aseptically collected into heparin or citrate anticoagulant and incubated in vitro for 6 hr in the absence (saline control) or presence of 1 ng endotoxin/ml blood. Pentoxifylline (0.1, 1, 10, or 100 micrograms/ml blood) was added 1 hr before, at the same time, or 1 hr after endotoxin. As compared to saline controls, pentoxifylline alone had no effect on mediator production, with the exception of significantly increasing 6-ketoprostaglandin F1 alpha concentration. Pentoxifylline inhibited endotoxin-induced increases in tumor necrosis factor (TNF) and interleukin-6 (IL-6) activity in a dose-related fashion, whether added before, at the same time, or after endotoxin. Pentoxifylline significantly inhibited tissue factor activity, but only when added before endotoxin. Pentoxifylline had no effect on endotoxin-induced 6-keto-prostaglandin F1 alpha production, but significantly inhibited thromboxane B2 (TxB2) production. The results of this study indicate that pentoxifylline, at blood concentrations consistent with those achieved in vivo, has effects that may be beneficial in the treatment of endotoxemia.</p>\",\"PeriodicalId\":10280,\"journal\":{\"name\":\"Circulatory shock\",\"volume\":\"44 4\",\"pages\":\"216-20\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1994-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Circulatory shock\",\"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":"Circulatory shock","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

取10匹健康马全血,无菌放入肝素或柠檬酸抗凝剂中,在不含(生理盐水对照)或内毒素1 ng /ml血液的情况下体外培养6小时。内毒素检测前1小时、同时1小时或内毒素检测后1小时加入己酮茶碱(0.1、1、10、100微克/毫升血)。与生理盐水对照相比,除了显著增加6-酮前列腺素F1 α浓度外,单独的己酮茶碱对介质的产生没有影响。己酮茶碱以剂量相关的方式抑制内毒素诱导的肿瘤坏死因子(TNF)和白细胞介素-6 (IL-6)活性的升高,无论是在内毒素之前、同时添加还是在内毒素之后添加。己酮茶碱对组织因子活性有显著抑制作用,但仅在内毒素前添加。己酮茶碱对内毒素诱导的6-酮-前列腺素F1 α的产生没有影响,但显著抑制血栓素B2 (TxB2)的产生。本研究结果表明,在与体内浓度一致的血液浓度下,己酮茶碱可能对内毒素血症的治疗有益。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Pentoxifylline inhibits mediator synthesis in an equine in vitro whole blood model of endotoxemia.

Whole blood from 10 healthy horses was aseptically collected into heparin or citrate anticoagulant and incubated in vitro for 6 hr in the absence (saline control) or presence of 1 ng endotoxin/ml blood. Pentoxifylline (0.1, 1, 10, or 100 micrograms/ml blood) was added 1 hr before, at the same time, or 1 hr after endotoxin. As compared to saline controls, pentoxifylline alone had no effect on mediator production, with the exception of significantly increasing 6-ketoprostaglandin F1 alpha concentration. Pentoxifylline inhibited endotoxin-induced increases in tumor necrosis factor (TNF) and interleukin-6 (IL-6) activity in a dose-related fashion, whether added before, at the same time, or after endotoxin. Pentoxifylline significantly inhibited tissue factor activity, but only when added before endotoxin. Pentoxifylline had no effect on endotoxin-induced 6-keto-prostaglandin F1 alpha production, but significantly inhibited thromboxane B2 (TxB2) production. The results of this study indicate that pentoxifylline, at blood concentrations consistent with those achieved in vivo, has effects that may be beneficial in the treatment of endotoxemia.

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
期刊最新文献
Comparison of binding specificity and the function of two human IgM anti-lipid A monoclonal antibodies. Hypertonic saline/dextran versus lactated Ringer's treatment for hemorrhage in dehydrated swine. Lysozyme regulates LPS-induced interleukin-6 release in mice. Liver oxygen uptake dependence and mitochondrial function in septic rats. Efficacy of continuous arteriovenous hemofiltration in endotoxic shock.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1