• 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

低钙和/或高钾减轻再灌注损伤的机制。

Mechanisms of reduced reperfusion injury by low Ca2+ and/or high K+.

作者信息

Tani M, Neely J R

机构信息

Weis Center for Research, Geisinger Clinic, Danville, Pennsylvania 17822.

出版信息

Am J Physiol. 1990 Apr;258(4 Pt 2):H1025-31. doi: 10.1152/ajpheart.1990.258.4.H1025.

DOI:10.1152/ajpheart.1990.258.4.H1025
PMID:2330991
Abstract

Mechanisms of the protective effects of low Ca2+ (0.15 mM) and/or high K+ (20 mM) concentrations in the buffer on reperfusion injury were investigated. Intracellular Na+ (Nai+) increased fourfold during 25 min of ischemia. When hearts were reperfused with the standard buffer (1.25 mM Ca2+, 5.9 mM K+), Nai+ increased further during the 1st 2 min (5-fold) and then declined by 30% at 10 min of reperfusion. Ca2+ uptake increased 6- and 12-fold at 10 and 30 min of reperfusion, respectively. Function, which was assessed as the product of developed pressure and heart rate, recovered to 45% of the preischemic value and end-diastolic pressure was elevated (EDP: 31 mmHg). Reperfusion for 10 min with low Ca2+ buffer abolished the increase in Ca2+ uptake during this period, but it increased 10-fold when the perfusate was switched back to the standard buffer. Accelerated Ca2+ influx at this time was probably through Na(+)-Ca2+ exchange because Nai+ did not decline during low Ca2+ reperfusion. Elevation of EDP was suppressed (12 mmHg), but development of pressure did not increase. Reperfusion for 10 min with high K+ buffer accelerated the decline in Nai+ by 70% and reduced the increase in Ca2+ uptake (8-fold). Recovery of function improved (67%, EDP: 18 mmHg). Further improvement in function (78%, EDP: 10 mmHg) was obtained along with less Ca2+ uptake (7-fold) when low Ca2+ and high K+ were combined. Recovery of energy metabolites at 10 and 30 min of reperfusion was not different among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了缓冲液中低钙(0.15 mM)和/或高钾(20 mM)浓度对再灌注损伤的保护作用机制。在25分钟的缺血期间,细胞内钠离子(Nai+)增加了四倍。当心脏用标准缓冲液(1.25 mM钙,5.9 mM钾)进行再灌注时,Nai+在最初2分钟内进一步增加(5倍),然后在再灌注10分钟时下降30%。在再灌注10分钟和30分钟时,钙摄取分别增加了6倍和12倍。功能通过收缩压和心率的乘积来评估,恢复到缺血前值的45%,舒张末期压力升高(EDP:31 mmHg)。用低钙缓冲液再灌注10分钟消除了在此期间钙摄取的增加,但当灌注液换回标准缓冲液时,钙摄取增加了10倍。此时加速的钙内流可能是通过钠-钙交换,因为在低钙再灌注期间Nai+没有下降。EDP的升高受到抑制(12 mmHg),但压力的升高没有增加。用高钾缓冲液再灌注10分钟使Nai+的下降加速了70%,并减少了钙摄取的增加(8倍)。功能恢复得到改善(67%,EDP:18 mmHg)。当低钙和高钾联合使用时,功能进一步改善(78%,EDP:10 mmHg),同时钙摄取减少(7倍)。在再灌注10分钟和30分钟时,各组能量代谢产物的恢复没有差异。(摘要截断于250字)

相似文献

1
Mechanisms of reduced reperfusion injury by low Ca2+ and/or high K+.低钙和/或高钾减轻再灌注损伤的机制。
Am J Physiol. 1990 Apr;258(4 Pt 2):H1025-31. doi: 10.1152/ajpheart.1990.258.4.H1025.
2
Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart.钠离子蓄积会增加钙离子超载,并损害缺氧大鼠心脏的功能。
J Mol Cell Cardiol. 1990 Jan;22(1):57-72. doi: 10.1016/0022-2828(90)90972-5.
3
Intermittent perfusion of ischemic myocardium. Possible mechanisms of protective effects on mechanical function in isolated rat heart.缺血心肌的间歇性灌注。对离体大鼠心脏机械功能的保护作用的可能机制。
Circulation. 1990 Aug;82(2):536-48. doi: 10.1161/01.cir.82.2.536.
4
Deleterious effects of digitalis on reperfusion-induced arrhythmias and myocardial injury in ischemic rat hearts: possible involvements of myocardial Na+ and Ca2+ imbalance.洋地黄对缺血大鼠心脏再灌注诱导的心律失常和心肌损伤的有害作用:心肌钠和钙失衡的可能参与。
Basic Res Cardiol. 1991 Jul-Aug;86(4):340-54. doi: 10.1007/BF02191531.
5
Vascular washout reduces Ca2+ overload and improves function of reperfused ischemic hearts.
Am J Physiol. 1990 Feb;258(2 Pt 2):H354-61. doi: 10.1152/ajpheart.1990.258.2.H354.
6
[The reversal of the protective effects of intermittent perfusion on ischemic myocardium by hypoxic, no-substrates, zero-K+ perfusate].[缺氧、无底物、零钾灌注液对间歇性灌注缺血心肌保护作用的逆转]
Kokyu To Junkan. 1991 Feb;39(2):157-61.
7
[Mechanism of myocardial protection with potassium arrest in isolated ischemic rat hearts].[离体缺血大鼠心脏钾停搏心肌保护机制]
Kokyu To Junkan. 1991 Nov;39(11):1151-7.
8
[Enhancement of susceptibility to ouabain in ischemic rat heart].[缺血大鼠心脏对哇巴因敏感性的增强]
Kokyu To Junkan. 1991 Jan;39(1):37-43.
9
Cicletanine and reperfusion injury: is there any correlation between arrhythmias, 6-keto-PGF1 alpha, thromboxane B2, and myocardial ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia/reperfusion in isolated rat heart.西氯他宁与再灌注损伤:在离体大鼠心脏中,缺血/再灌注诱导的心律失常、6-酮-前列腺素F1α、血栓素B2和心肌离子转移(Na+、K+、Ca2+和Mg2+)之间是否存在关联?
J Cardiovasc Pharmacol. 1991 Apr;17(4):551-9.
10
Effects of Na-K-2Cl cotransport inhibition on myocardial Na and Ca during ischemia and reperfusion.缺血再灌注期间钠-钾-2氯协同转运抑制对心肌钠和钙的影响。
Am J Physiol. 1996 Feb;270(2 Pt 1):C608-18. doi: 10.1152/ajpcell.1996.270.2.C608.

引用本文的文献

1
Controlling Reperfusion Injury With Controlled Reperfusion: Historical Perspectives and New Paradigms.控制性再灌注防治再灌注损伤:历史观点与新范例。
J Cardiovasc Pharmacol Ther. 2021 Nov;26(6):504-523. doi: 10.1177/10742484211046674. Epub 2021 Sep 17.
2
Transplantation of Hearts Donated after Circulatory Death.循环性死亡后捐献心脏的移植
Front Cardiovasc Med. 2018 Feb 13;5:8. doi: 10.3389/fcvm.2018.00008. eCollection 2018.
3
Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis.
再灌注期间O-连接的N-乙酰葡糖胺水平升高可导致功能恢复改善和钙蛋白酶蛋白水解减少。
Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1391-9. doi: 10.1152/ajpheart.00285.2007. Epub 2007 Jun 15.
4
Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.暴露于缺血再灌注的心脏线粒体中的生化功能障碍。
Biochem J. 2005 Sep 1;390(Pt 2):377-94. doi: 10.1042/BJ20042006.
5
Myocardial recovery during post-ischemic reperfusion: optimal concentrations of Na+ and Ca2+ in the reperfusate and protective effects of amiloride added to cardioplegic solution.缺血后再灌注期间的心肌恢复:再灌注液中Na⁺和Ca²⁺的最佳浓度以及添加到心脏停搏液中的氨氯地平的保护作用。
Heart Vessels. 1995;10(6):310-7. doi: 10.1007/BF02911389.
6
Role of controlled cardiac reoxygenation in reducing nitric oxide production and cardiac oxidant damage in cyanotic infantile hearts.控制性心脏复氧在减少青紫型婴儿心脏一氧化氮生成及心脏氧化损伤中的作用
J Clin Invest. 1994 Jun;93(6):2658-66. doi: 10.1172/JCI117279.
7
Role of catalase in myocardial protection against ischemia in heat shocked rats.过氧化氢酶在热休克大鼠心肌缺血保护中的作用。
Mol Cell Biochem. 1993 Dec 22;129(2):187-94. doi: 10.1007/BF00926367.
8
Deleterious effects of digitalis on reperfusion-induced arrhythmias and myocardial injury in ischemic rat hearts: possible involvements of myocardial Na+ and Ca2+ imbalance.洋地黄对缺血大鼠心脏再灌注诱导的心律失常和心肌损伤的有害作用:心肌钠和钙失衡的可能参与。
Basic Res Cardiol. 1991 Jul-Aug;86(4):340-54. doi: 10.1007/BF02191531.
9
Participation of calcium ions in the molecular mechanism of cardioprotective action of exogenous phosphocreatine.
Basic Res Cardiol. 1991 Jul-Aug;86(4):327-39. doi: 10.1007/BF02191530.