• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

在离体灌注大鼠心脏中,不同缺血时间后再灌注期间组织纤溶酶原激活物的释放。

Release of tissue plasminogen activator during reperfusion after different times of ischaemia in isolated, perfused rat hearts.

作者信息

Winnerkvist A, Wiman B, Valen G, Vaage J

机构信息

Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.

出版信息

Thromb Res. 1996 Jun 15;82(6):533-42. doi: 10.1016/0049-3848(96)00103-x.

DOI:10.1016/0049-3848(96)00103-x
PMID:8794525
Abstract

Tissue plasminogen activator (t-PA) is a potential marker of endothelial cell activation or injury. The relationship between duration of ischaemia and release of t-PA during reperfusion was investigated in isolated rat hearts exposed to either 5, 10, 20, 30, 40, or 60 min of global, normothermic ischaemia followed by 30 min of reperfusion (n = 8 in each group). t-PA activity was measured (chromogenic peptide substrate assay) in the effluent before ischaemia, and after 2.5, 5, 7.5, 10, 20, and 30 min of reperfusion. Release of lactate dehydrogenase (LD), a marker of myocyte injury, was measured before ischaemia and after 5 min reperfusion. Left ventricular pressures were measured by a balloon in the left ventricle. Ischaemia for 20 min or less had only minor effects on cardiac function. Thirty min or more of ischaemia induced ventricular fibrillation during reperfusion in most hearts. After ischaemia t-PA outflow increased, but without any significant difference between groups. Peak release occurred after either 2.5 or 5 min of reperfusion. After 10 min reperfusion the release was not different from the basal value. In contrast, postischaemic release of LD correlated to the length of ischaemia. To conclude, t-PA release from the ischaemic-reperfused rat heart is independent of the length of ischaemia. Thus the potential of t-PA to quantify endothelial injury appears to be limited.

摘要

组织型纤溶酶原激活剂(t-PA)是内皮细胞激活或损伤的一个潜在标志物。在暴露于5、10、20、30、40或60分钟全心、常温缺血然后再灌注30分钟的离体大鼠心脏中(每组n = 8),研究了缺血持续时间与再灌注期间t-PA释放之间的关系。在缺血前以及再灌注2.5、5、7.5、10、20和30分钟后,测量流出液中的t-PA活性(发色肽底物测定法)。在缺血前和再灌注5分钟后,测量乳酸脱氢酶(LD)的释放,LD是心肌细胞损伤的一个标志物。通过左心室内的球囊测量左心室压力。缺血20分钟或更短时间对心脏功能仅有轻微影响。30分钟或更长时间的缺血在大多数心脏的再灌注期间诱发心室颤动。缺血后t-PA流出增加,但各组之间无任何显著差异。在再灌注2.5或5分钟后出现峰值释放。再灌注10分钟后,释放与基础值无差异。相比之下,缺血后LD的释放与缺血时间长度相关。总之,缺血再灌注大鼠心脏中t-PA的释放与缺血时间长度无关。因此,t-PA量化内皮损伤的潜力似乎有限。

相似文献

1
Release of tissue plasminogen activator during reperfusion after different times of ischaemia in isolated, perfused rat hearts.在离体灌注大鼠心脏中,不同缺血时间后再灌注期间组织纤溶酶原激活物的释放。
Thromb Res. 1996 Jun 15;82(6):533-42. doi: 10.1016/0049-3848(96)00103-x.
2
Reactive oxygen intermediates and ischemia-reperfusion injury release tissue plasminogen activator from isolated rat hearts.活性氧中间体与缺血-再灌注损伤从离体大鼠心脏释放组织纤溶酶原激活物。
Thromb Res. 1993 Jul 15;71(2):113-21. doi: 10.1016/0049-3848(93)90177-p.
3
Mechanical conversion of post-ischaemic ventricular fibrillation: effects on function and myocyte injury in isolated rat hearts.
Scand J Clin Lab Invest. 1999 Feb;59(1):9-16. doi: 10.1080/00365519950185959.
4
Post-ischaemic dysfunction does not correlate with release of cardiac troponin T in isolated rat hearts.
Acta Physiol Scand. 1999 Sep;167(1):23-7. doi: 10.1046/j.1365-201x.1999.00562.x.
5
Brief perfusion with diluted whole blood after global myocardial ischaemia increases reperfusion injury.全心肌缺血后用稀释全血进行短暂灌注会增加再灌注损伤。
Cardiovasc Res. 1994 Aug;28(8):1157-65. doi: 10.1093/cvr/28.8.1157.
6
Transient beta adrenergic stimulation can precondition the rat heart against postischaemic contractile dysfunction.短暂的β肾上腺素能刺激可使大鼠心脏对缺血后收缩功能障碍产生预处理作用。
Cardiovasc Res. 1994 Nov;28(11):1726-34. doi: 10.1093/cvr/28.11.1726.
7
The influence of lactate, pyruvate and glucose as exogenous substrates on free radical defense mechanisms in isolated rat hearts during ischaemia and reperfusion.乳酸、丙酮酸和葡萄糖作为外源性底物对离体大鼠心脏缺血再灌注期间自由基防御机制的影响。
Mol Cell Biochem. 1995 May 24;146(2):147-55. doi: 10.1007/BF00944607.
8
Effects of landiolol on mechanical and metabolic changes in rat reperfused ischaemic hearts.兰地洛尔对大鼠再灌注缺血心脏机械和代谢变化的影响。
Clin Exp Pharmacol Physiol. 2007 Jan-Feb;34(1-2):55-60. doi: 10.1111/j.1440-1681.2007.04543.x.
9
Endothelin release during ischaemia and reperfusion of isolated perfused rat hearts.
J Mol Cell Cardiol. 1992 Nov;24(11):1291-305. doi: 10.1016/0022-2828(92)93095-2.
10
Histamine H3-receptor stimulation is unable to modulate noradrenaline release by the isolated rat heart during ischaemia-reperfusion.在缺血再灌注期间,组胺H3受体刺激无法调节离体大鼠心脏去甲肾上腺素的释放。
Fundam Clin Pharmacol. 1999;13(4):455-60. doi: 10.1111/j.1472-8206.1999.tb00003.x.

引用本文的文献

1
Prognostic role of tissue plasminogen activator in coronary artery disease with or without aortic valve sclerosis.组织型纤溶酶原激活物在合并或不合并主动脉瓣钙化的冠状动脉疾病中的预后作用。
ESC Heart Fail. 2023 Aug;10(4):2541-2549. doi: 10.1002/ehf2.14420. Epub 2023 Jun 12.
2
Histone deacetylase inhibitor treatment increases coronary t-PA release in a porcine ischemia model.组蛋白去乙酰化酶抑制剂治疗可增加猪缺血模型中冠状动脉组织型纤溶酶原激活物的释放。
PLoS One. 2014 May 12;9(5):e97260. doi: 10.1371/journal.pone.0097260. eCollection 2014.
3
Ischaemia-reperfusion injury impairs tissue plasminogen activator release in man.
缺血再灌注损伤可损害人体组织型纤溶酶原激活物的释放。
Eur Heart J. 2012 Aug;33(15):1920-7. doi: 10.1093/eurheartj/ehr380. Epub 2011 Oct 11.
4
The ADP receptor P2Y(1) mediates t-PA release in pigs during cardiac ischemia.ADP受体P2Y(1)介导猪心脏缺血期间组织型纤溶酶原激活物(t-PA)的释放。
J Thromb Thrombolysis. 2007 Oct;24(2):115-22. doi: 10.1007/s11239-007-0010-3. Epub 2007 Feb 10.
5
The plasminogen activator system modulates sympathetic nerve function.纤溶酶原激活物系统调节交感神经功能。
J Exp Med. 2006 Sep 4;203(9):2191-200. doi: 10.1084/jem.20060077. Epub 2006 Aug 28.