相似文献

1

Post-conditioning restores pre-ischaemic receptor coupling in rat isolated hearts.

Br J Pharmacol. 2009 Mar;156(6):901-8. doi: 10.1111/j.1476-5381.2008.00053.x.

2

Modulation of receptor sensitivity: possible therapeutic target?

Br J Pharmacol. 2009 Mar;156(6):899-900. doi: 10.1111/j.1476-5381.2009.00115.x.

3

Ischaemic post-conditioning protects both adult and aged Sprague-Dawley rat heart from ischaemia-reperfusion injury through the phosphatidylinositol 3-kinase-AKT and glycogen synthase kinase-3beta pathways.

Clin Exp Pharmacol Physiol. 2009 Aug;36(8):756-63. doi: 10.1111/j.1440-1681.2009.05148.x. Epub 2009 Jan 17.

4

Adverse Effects on β-Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long-Term Cardiac Function.

J Am Heart Assoc. 2017 Dec 22;6(12):e006809. doi: 10.1161/JAHA.117.006809.

5

Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK.

Cardiovasc Drugs Ther. 2006 Feb;20(1):13-25. doi: 10.1007/s10557-006-6257-7.

6

Loss of ischaemic preconditioning in ovariectomized rat hearts: possible involvement of impaired protein kinase C epsilon phosphorylation.

Cardiovasc Res. 2008 Aug 1;79(3):387-94. doi: 10.1093/cvr/cvn086. Epub 2008 Apr 4.

7

The significance of the washout period in preconditioning.

Cardiovasc Ther. 2017 Jun;35(3). doi: 10.1111/1755-5922.12252.

8

The infarct size-limiting effect of ischemic postconditioning (IPOC) is suppressed in isolated hyperhomocysteinemic (Hhcy) rat hearts: the reasonable role of PKC-delta.

Biomed Pharmacother. 2009 Dec;63(10):787-91. doi: 10.1016/j.biopha.2009.06.012. Epub 2009 Oct 14.

9

Inhibition of the malate-aspartate shuttle by pre-ischaemic aminooxyacetate loading of the heart induces cardioprotection.

Cardiovasc Res. 2010 Nov 1;88(2):257-66. doi: 10.1093/cvr/cvq205. Epub 2010 Jun 18.

10

Role of phosphoinositide 3-kinase IA (PI3K-IA) activation in cardioprotection induced by ouabain preconditioning.

J Mol Cell Cardiol. 2015 Mar;80:114-25. doi: 10.1016/j.yjmcc.2014.12.021. Epub 2015 Jan 7.

引用本文的文献

1

Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Deletion but Not Inhibition of Extracellular PCSK9 Reduces Infarct Sizes Ex Vivo but Not In Vivo.

Int J Mol Sci. 2022 Jun 10;23(12):6512. doi: 10.3390/ijms23126512.

2

Autocrine effects of PCSK9 on cardiomyocytes.

Basic Res Cardiol. 2020 Nov 10;115(6):65. doi: 10.1007/s00395-020-00824-w.

3

Adverse Effects on β-Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long-Term Cardiac Function.

J Am Heart Assoc. 2017 Dec 22;6(12):e006809. doi: 10.1161/JAHA.117.006809.

4

Specific Mechanisms Underlying Right Heart Failure: The Missing Upregulation of Superoxide Dismutase-2 and Its Decisive Role in Antioxidative Defense.

Antioxid Redox Signal. 2015 Nov 20;23(15):1220-32. doi: 10.1089/ars.2014.6139. Epub 2015 Jun 18.

5

Modulation of receptor sensitivity: possible therapeutic target?

Br J Pharmacol. 2009 Mar;156(6):899-900. doi: 10.1111/j.1476-5381.2009.00115.x.

本文引用的文献

1

Protein kinase C protects preconditioned rabbit hearts by increasing sensitivity of adenosine A2b-dependent signaling during early reperfusion.

J Mol Cell Cardiol. 2007 Sep;43(3):262-71. doi: 10.1016/j.yjmcc.2007.05.016. Epub 2007 May 24.

2

Vasodilatory effect of tuberoinfundibular peptide (TIP39): requirement of receptor desensitization and its beneficial effect in the post-ischemic heart.

Peptides. 2007 Apr;28(4):878-86. doi: 10.1016/j.peptides.2006.12.010. Epub 2006 Dec 20.

3

Reperfusion injury: does it exist?

J Mol Cell Cardiol. 2007 Jan;42(1):12-8. doi: 10.1016/j.yjmcc.2006.09.009. Epub 2006 Oct 27.

4

Trafficking of G protein-coupled receptors.

Circ Res. 2006 Sep 15;99(6):570-82. doi: 10.1161/01.RES.0000242563.47507.ce.

5

Attenuated cardioprotection by ischemic preconditioning in coronary stenosed heart and its restoration by carvedilol.

Cardiovasc Res. 2006 Aug 1;71(3):537-47. doi: 10.1016/j.cardiores.2006.05.011. Epub 2006 May 10.

6

Bringing preconditioning and postconditioning into focus.

Cardiovasc Res. 2006 May 1;70(2):167-9. doi: 10.1016/j.cardiores.2006.03.009. Epub 2006 Mar 20.

7

Survival kinases in ischemic preconditioning and postconditioning.

Cardiovasc Res. 2006 May 1;70(2):240-53. doi: 10.1016/j.cardiores.2006.01.017. Epub 2006 Mar 20.

8

Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade.

Cardiovasc Res. 2006 May 1;70(2):308-14. doi: 10.1016/j.cardiores.2006.02.014. Epub 2006 Feb 23.

9

Clinical applicability of preconditioning and postconditioning: the cardiothoracic surgeons's view.

Cardiovasc Res. 2006 May 1;70(2):174-80. doi: 10.1016/j.cardiores.2006.01.020. Epub 2006 Mar 9.

10

Postconditioning the human heart.

Circulation. 2005 Oct 4;112(14):2143-8. doi: 10.1161/CIRCULATIONAHA.105.558122. Epub 2005 Sep 26.

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍。

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

文档翻译

学术文献翻译模型，支持多种主流文档格式。

后适应可恢复大鼠离体心脏缺血前的受体偶联。

Post-conditioning restores pre-ischaemic receptor coupling in rat isolated hearts.

作者信息

Schreckenberg Rolf, Maier Thorsten, Schlüter Klaus-Dieter

机构信息

Justus-Liebig-University, Institute of Physiology, Aulweg, Giessen, Germany.

出版信息

Br J Pharmacol. 2009 Mar;156(6):901-8. doi: 10.1111/j.1476-5381.2008.00053.x.

DOI:10.1111/j.1476-5381.2008.00053.x

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2697714/

Abstract

BACKGROUND AND PURPOSE

Ischaemic preconditioning (IPC) and ischaemic post-conditioning (IPoC) activate signal transduction pathways that are also involved in receptor de- and re-sensitization such as phosphatidylinositol (PI) 3-kinase. Therefore, IPC and IPoC may affect post-infarct receptor coupling.

EXPERIMENTAL APPROACH

Rat isolated hearts (Langendorff mode, constant flow) were exposed to 45 min flow arrest followed by 120 min reperfusion, including IPC or IPoC. Control hearts were perfused without a 45 min flow arrest. Left ventricular developed pressure (LVdevP) was determined. Thirty min after reperfusion, hearts were exposed to parathyroid hormone-related peptide (PTHrP) or isoprenaline for 10 min to monitor receptor responsiveness. Reperfusion injury was quantified by enzyme release.

KEY RESULTS

IPC and IPoC significantly reduced enzyme release compared with ischaemia and reperfusion alone by 75% and 62% respectively. Wortmannin or chelerythrine inhibiting either PI 3-kinase or protein kinase C, respectively, attenuated protection. Application of PTHrP 30 min after reperfusion did not change LVdevP in hearts exposed to ischaemia (+1 +/- 11%), but IPoC restored the normal and non-ischaemic response to PTHrP characterized by a negative inotropism (-8.3 +/- 3.9% and -12.9 +/- 6.1%). IPC restored a small negative inotropic effect (-4.4 +/- 4.7%). Application of a PTHrP receptor antagonist during the 45 min flow arrest attenuated receptor desensitization (DeltaLVdevP: -6.1 +/- 1.7%). Wortmannin but not chelerythrine attenuated the re-sensitizing effect of IPoC on post-ischaemic receptor coupling (DeltaLVdevP: +6.2 +/- 10.5 and -15.0 +/- 7.7%). As observed with PTHrP receptors, IPoC restored beta-adrenoceptors (DeltaLVdevP: +9.3 +/- 11.8% vs. 62.3 +/- 15.8%).

CONCLUSIONS AND IMPLICATIONS

IPoC restores PTHrP receptor coupling in a PI 3-kinase-dependent way. A similar mechanism may allow beta-adrenoceptor re-sensitization.

摘要

背景与目的

缺血预处理（IPC）和缺血后处理（IPoC）激活的信号转导通路也参与受体的失敏和再敏化过程，如磷脂酰肌醇（PI）3激酶。因此，IPC和IPoC可能影响梗死后的受体偶联。

实验方法

将大鼠离体心脏（Langendorff模式，恒流灌注）进行45分钟的停流处理，随后进行120分钟的再灌注，其中包括IPC或IPoC处理。对照组心脏不进行45分钟的停流处理。测定左心室舒张末压（LVdevP）。再灌注30分钟后，将心脏暴露于甲状旁腺激素相关肽（PTHrP）或异丙肾上腺素10分钟，以监测受体反应性。通过酶释放量来量化再灌注损伤。

主要结果

与单纯缺血再灌注相比，IPC和IPoC分别使酶释放量显著降低75%和62%。渥曼青霉素或白屈菜红碱分别抑制PI 3激酶或蛋白激酶C后，减弱了保护作用。再灌注30分钟后应用PTHrP对经历缺血的心脏的LVdevP无影响（+1±11%），但IPoC恢复了对PTHrP的正常非缺血反应，其特征为负性肌力作用（-8.3±3.9%和-12.9±6.1%）。IPC恢复了较小的负性肌力作用（-4.4±4.7%）。在45分钟停流期间应用PTHrP受体拮抗剂可减弱受体失敏（ΔLVdevP：-6.1±1.7%）。渥曼青霉素而非白屈菜红碱减弱了IPoC对缺血后受体偶联的再敏化作用（ΔLVdevP：+6.2±10.5和-15.0±7.7%）。与PTHrP受体情况相同，IPoC恢复了β肾上腺素能受体功能（ΔLVdevP：+9.3±11.8%对62.3±15.8%）。

结论与意义

IPoC以PI 3激酶依赖的方式恢复PTHrP受体偶联。类似机制可能使β肾上腺素能受体再敏化。