Urocortin Protects Coronary Endothelial Function During Ischemia-Reperfusion: A Brief Communication

2004 ◽  
Vol 229 (1) ◽  
pp. 118-120 ◽  
Author(s):  
Angel Luis García-Villalón ◽  
Elena Sanz ◽  
Luis Monge ◽  
Nuria Fernández ◽  
Belén Climent ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Ischemia Reperfusion ◽  
Coronary Endothelial Function

scholarly journals Mechanisms of the protective effects of urocortin on coronary endothelial function during ischemia-reperfusion in rat isolated hearts

2005 ◽  
Vol 145 (4) ◽  
pp. 490-494 ◽  
Author(s):  
Angel Luis García-Villalón ◽  
Yesika María Amezquita ◽  
Luis Monge ◽  
Nuria Fernández ◽  
Belén Climent ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Isolated Hearts ◽  
Coronary Endothelial Function

Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect

Surgery ◽  
1996 ◽  
Vol 120 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Hitoshi Yokoyama ◽  
David M. Lingle ◽  
Juan A. Crestanello ◽  
Joseph Kamelgard ◽  
Brian R. Kott ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Reperfusion Injury ◽  
Coenzyme Q10 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Effect ◽  
Coronary Endothelial Function

scholarly journals Protection of Coronary Endothelial Function during Cardiac Surgery: Potential of Targeting Endothelial Ion Channels in Cardioprotection

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Qin Yang ◽  
Cheuk-Man Yu ◽  
Guo-Wei He ◽  
Malcolm John Underwood
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cardiac Surgery ◽  
Ion Channels ◽  
Endothelial Function ◽  
Trp Channels ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Coronary Endothelial Function ◽  
Vasoactive Factors

Vascular endothelium plays a critical role in the control of blood flow by producing vasoactive factors to regulate vascular tone. Ion channels, in particular, K+channels and Ca2+-permeable channels in endothelial cells, are essential to the production and function of endothelium-derived vasoactive factors. Impairment of coronary endothelial function occurs in open heart surgery that may result in reduction of coronary blood flow and thus in an inadequate myocardial perfusion. Hyperkalemic exposure and concurrent ischemia-reperfusion during cardioplegic intervention compromise NO and EDHF-mediated function and the impairment involves alterations of K+channels, that is,KATPandKCa, and Ca2+-permeable TRP channels in endothelial cells. Pharmacological modulation of these channels during ischemia-reperfusion and hyperkalemic exposure show promising results on the preservation of NO and EDHF-mediated endothelial function, which suggests the potential of targeting endothelial K+and TRP channels for myocardial protection during cardiac surgery.

scholarly journals Regional coronary endothelial function is related to local coronary wall thickness in CAD patients using 3T MRI

2011 ◽  
Vol 13 (S1) ◽  
Author(s):  
Allison G Hays ◽  
Sebastian Kelle ◽  
Glenn A Hirsch ◽  
Jing Yu ◽  
Harsh K Agarwal ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Wall Thickness ◽  
3T Mri ◽  
Coronary Endothelial Function ◽  
Coronary Wall

scholarly journals Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning

2018 ◽  
Vol 315 (1) ◽  
pp. H150-H158 ◽  
Author(s):  
Marie Hauerslev ◽  
Sivagowry Rasalingam Mørk ◽  
Kasper Pryds ◽  
Hussain Contractor ◽  
Jan Hansen ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Glyceryl Trinitrate ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Myocardium ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Human Endothelium

Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. Because of overlapping mechanisms, this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. We investigated whether long-term GTN treatment modifies the protection by RIC in the rat myocardium and human endothelium. We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. In addition to allocated treatment, rats were coadministered with reactive oxygen species (ROS) or nitric oxide (NO) scavengers. Rats and humans were randomized to 1) control, 2) RIC, 3) GTN, and 4) GTN + RIC. In protocols 3 and 4, rats and humans underwent long-term GTN treatment for 7 consecutive days, applied subcutaneously or 2 h daily transdermally. In rats, RIC and long-term GTN treatment reduced mean IS (18 ± 12%, P = 0.007 and 15 ± 5%, P = 0.002) compared with control (35 ± 13%). RIC and long-term GTN treatment in combination did not reduce IS (29 ± 12%, P = 0.55 vs. control). ROS and NO scavengers both attenuated IS reduction by RIC and long-term GTN treatment. In humans, I/R reduced endothelial function ( P = 0.01 vs. baseline). Separately, RIC and long-term GTN prevented the reduction in endothelial function caused by I/R; given in combination, prevention was lost. RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO-dependent mechanisms. However, when given in combination, RIC and long-term GTN treatment fail to confer protection. NEW & NOTEWORTHY Remote ischemic conditioning (RIC) and long-term glyceryl trinitrate (GTN) treatment protect against ischemia-reperfusion injury in both human endothelium and rat myocardium. However, combined application of RIC and long-term GTN treatment abolishes the individual protective effects of RIC and GTN treatment on ischemia-reperfusion injury, suggesting an interaction of clinical importance.

Tackling endothelial dysfunction by modulating NOS uncoupling: new insights into its pathogenesis and therapeutic possibilities

2012 ◽  
Vol 302 (5) ◽  
pp. E481-E495 ◽  
Author(s):  
Rinrada Kietadisorn ◽  
Rio P. Juni ◽  
An L. Moens
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Therapeutic Interventions ◽  
Enos Uncoupling ◽  
Underlying Causes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide synthase (eNOS) serves as a critical enzyme in maintaining vascular pressure by producing nitric oxide (NO); hence, it has a crucial role in the regulation of endothelial function. The bioavailability of eNOS-derived NO is crucial for this function and might be affected at multiple levels. Uncoupling of eNOS, with subsequently less NO and more superoxide generation, is one of the major underlying causes of endothelial dysfunction found in atherosclerosis, diabetes, hypertension, cigarette smoking, hyperhomocysteinemia, and ischemia/reperfusion injury. Therefore, modulating eNOS uncoupling by stabilizing eNOS activity, enhancing its substrate, cofactors, and transcription, and reversing uncoupled eNOS are attractive therapeutic approaches to improve endothelial function. This review provides an extensive overview of the important role of eNOS uncoupling in the pathogenesis of endothelial dysfunction and the potential therapeutic interventions to modulate eNOS for tackling endothelial dysfunction.

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