scholarly journals Correction to “Specific Lowering of Asymmetric Dimethylarginine by Pharmacological Dimethylarginine Dimethylaminohydrolase Improves Endothelial Function, Reduces Blood Pressure and Ischemia-Reperfusion Injury”

2021 ◽  
Vol 376 (3) ◽  
pp. 463-463
Keyword(s):  
Blood Pressure ◽  
Endothelial Function ◽  
Reperfusion Injury ◽  
Asymmetric Dimethylarginine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Dimethylarginine Dimethylaminohydrolase

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.

scholarly journals Influence of Hypoxic and Hyperoxic Preconditioning on Endothelial Function in a Model of Myocardial Ischemia-Reperfusion Injury with Cardiopulmonary Bypass (Experimental Study)

2020 ◽  
Vol 21 (15) ◽  
pp. 5336
Author(s):  
Irina A. Mandel ◽  
Yuri K. Podoksenov ◽  
Irina V. Suhodolo ◽  
Darya A. An ◽  
Sergey L. Mikheev ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiopulmonary Bypass ◽  
Endothelial Function ◽  
Light Microscopy ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Endothelin 1 ◽  
Nitric Oxide Metabolites

The aim of the experiment was to evaluate the effect of preconditioning based on changes in inspiratory oxygen fraction on endothelial function in the model of ischemia-reperfusion injury of the myocardium in the condition of cardiopulmonary bypass. The prospective randomized study included 32 rabbits divided into four groups: hypoxic preconditioning, hyperoxic preconditioning, hypoxic-hyperoxic preconditioning, and control group. All animals were anesthetized and mechanically ventilated. We provided preconditioning, then started cardiopulmonary bypass, followed by induced acute myocardial infarction (ischemia 45 min, reperfusion 120 min). We investigated endothelin-1, nitric oxide metabolites, asymmetric dimethylarginine during cardiopulmonary bypass: before ischemia, after ischemia, and after reperfusion. We performed light microscopy of myocardium, kidney, lungs, and gut mucosa. The endothelin-1 level was much higher in the control group than in all preconditioning groups after ischemia. The endothelin-1 even further increased after reperfusion. The total concentration of nitric oxide metabolites was significantly higher after all types of preconditioning compared with the control group. The light microscopy of the myocardium and other organs revealed a diminished damage extent in the hypoxic-hyperoxic preconditioning group as compared to the control group. Hypoxic-hyperoxic preconditioning helps to maintain the balance of nitric oxide metabolites, reduces endothelin-1 hyperproduction, and enforces organ protection.

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 Asymmetric dimethylarginine accumulates in the kidney during ischemia/reperfusion injury

2014 ◽  
Vol 85 (3) ◽  
pp. 570-578 ◽  
Author(s):  
Yosuke Nakayama ◽  
Seiji Ueda ◽  
Sho-ichi Yamagishi ◽  
Nana Obara ◽  
Kensei Taguchi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Asymmetric Dimethylarginine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

Shear Stress Induced by Acute Heat Exposure Is Not Obligatory to Protect Against Endothelial Ischemia-reperfusion Injury in Humans

2021 ◽  
Author(s):  
Holden W. Hemingway ◽  
Rauchelle E. Richey ◽  
Amy M. Moore ◽  
Austin M. Shokraeifard ◽  
Gabriel C. Thomas ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Reperfusion Injury ◽  
Brachial Artery ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heat Exposure ◽  
Body Core Temperature ◽  
Whole Body ◽  
Flow Mediated Dilatation

Acute heat exposure protects against endothelial ischemia-reperfusion (I/R) injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We tested the hypothesis that inhibiting the increase in shear stress induced by acute heat exposure would attenuate the protection of endothelial function following I/R injury. Nine (3 women) young healthy participants were studied under 3 experimental conditions: 1) thermoneutral control; 2) whole-body heat exposure to increase body core temperature by 1.2 °C; 3) heat exposure + brachial artery compression to inhibit the temperature-dependent increase in shear stress. Endothelial function was assessed via brachial artery flow-mediated dilatation before (pre-I/R) and after (post-I/R) 20 min of arm ischemia followed by 20 min of reperfusion. Brachial artery shear rate was increased during heat exposure (681 ± 359 s-1), but not for thermoneutral control (140 ± 63 s-1; P < 0.01 vs. heat exposure) nor heat + brachial artery compression (139 ± 60 s-1; P < 0.01 vs. heat exposure). Ischemia-reperfusion injury reduced flow-mediated dilatation following thermoneutral control (pre-I/R, 5.5 ± 2.9 % vs. post-I/R, 3.8 ± 2.9 %; P = 0.06), but was protected following heat exposure (pre-I/R, 5.8 ± 2.9 % vs. post-I/R, 6.1 ± 2.9 %; P = 0.5) and heat + arterial compression (pre-I/R, 4.4 ± 2.8 % vs. post-I/R, 5.8 ± 2.8 %; P = 0.1). Contrary to our hypothesis, our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury in humans.

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