Selective mitochondrial KATP channel activation results in antiarrhythmic effect during experimental myocardial ischemia/reperfusion in anesthetized rabbits

2002 ◽  
Vol 437 (3) ◽  
pp. 165-171 ◽  
Author(s):  
Biswadeep Das ◽  
Chayna Sarkar ◽  
K.Sudhakar Karanth
Keyword(s):  
Myocardial Ischemia ◽  
Katp Channel ◽  
Ischemia Reperfusion ◽  
Antiarrhythmic Effect ◽  
Channel Activation ◽  
Mitochondrial Katp Channel ◽  
Myocardial Ischemia Reperfusion ◽  
Experimental Myocardial Ischemia

Annexin 1 peptides protect against experimental myocardial ischemia‐reperfusion: analysis of their mechanism of action

2001 ◽  
Vol 15 (12) ◽  
pp. 2247-2256 ◽  
Author(s):  
Mylinh La ◽  
Michele D'Amico ◽  
Silvio Bandiera ◽  
Clara Di Filippo ◽  
Sonia M. Oliani ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Mechanism Of Action ◽  
Ischemia Reperfusion ◽  
Annexin 1 ◽  
Myocardial Ischemia Reperfusion ◽  
Experimental Myocardial Ischemia

scholarly journals Noninvasive Delayed Limb Ischemic Preconditioning Attenuates Myocardial Ischemia-Reperfusion Injury in Rats by a Mitochondrial KATP Channel-Dependent Mechanism

2011 ◽  
pp. 271-279 ◽  
Author(s):  
Y.-N. WU ◽  
H. YU ◽  
X.-H. ZHU ◽  
H.-J. YUAN ◽  
Y. KANG ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Katp Channel ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Dependent Mechanism

We previously demonstrated in rats that noninvasive delayed limb ischemic preconditioning (LIPC) induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb per day for three days confers the same cardioprotective effect as local ischemic preconditioning of the heart, but the mechanism has not been studied in depth. The aim of this project was to test the hypothesis that delayed LIPC enhances myocardial antioxidative ability during ischemia-reperfusion by a mitochondrial KATP channel (mito KATP)-dependent mechanism. Rats were randomized to five groups: ischemia-reperfusion (IR)-control group, myocardial ischemic preconditioning (MIPC) group, LIPC group, IR-5HD group and LIPC-5HD group. The MIPC group underwent local ischemic preconditioning induced by three cycles of 5-min occlusion and 5-min reperfusion of the left anterior descending coronary arteries. The LIPC and LIPC-5HD groups underwent LIPC induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb using a modified blood pressure aerocyst per day for three days. All rats were subjected to myocardial ischemia-reperfusion injury. The IR-5HD and LIPC-5HD groups received the mito KATP channel blocker 5-hydroxydecanoate Na (5-HD) before and during the myocardial ischemia-reperfusion injury. Compared with the IR-control group, both the LIPC and MIPC groups showed an amelioration of ventricular arrhythmia, reduced myocardial infarct size, increased activities of total superoxide dismutase, manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase, increased expression of Mn-SOD mRNA and decreased xanthine oxidase activity and malondialdehyde concentration. These beneficial effects of LIPC were prevented by 5-HD. In conclusion, delayed LIPC offers similar cardioprotection as local IPC. These results support the hypothesis that the activation of mito KATP channels enhances myocardial antioxidative ability during ischemia-reperfusion, thereby contributing, at least in part, to the anti-arrhythmic and anti-infarct effects of delayed LIPC.

The Antiarrhythmic Effect of 4-Methyl-2,6-Diisobornylphenol in Myocardial Ischemia/Reperfusion

2016 ◽  
Vol 683 ◽  
pp. 469-474 ◽  
Author(s):  
Tatyana Plotnikova ◽  
Mark Plotnikov ◽  
Galina Chernysheva ◽  
Vera Smol'yakova ◽  
Pyotr P. Shchetinin ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Antiarrhythmic Activity ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Antiarrhythmic Effect ◽  
Control Group ◽  
Acute Ischemia ◽  
Sterically Hindered Phenols ◽  
Myocardial Ischemia Reperfusion

We studied the antiarrhythmic activity of novel sterically hindered phenols – 4-methyl-2,6- diisobornylphenol (dibornol) in acute myocardial ischemia/reperfusion in male Wistar rats. Left coronary artery occlusion (10 min) in control group induced different ventricular arrhythmia and 23% mortality of animals. Dibornol (p.o. administration 100 mg/kg 24 and 3 hours before ischemia) did not change the frequency and kinds of arrhythmia in acute ischemia, but significantly reduced the frequency and the level of seriousness of arrhythmia in the reperfusion period, decreased the mortality of rats due to lethal arrhythmia.

Abstract 13107: Nitroglycerin Pretreatment Induces Metabolic Tolerance to Spinal Cord Ischemia-reperfusion Injury Through Nitric Oxide-mediated Mitochondrial Katp Channel Activation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yuki Ikeno ◽  
Christian V Ghincea ◽  
Gavriel Roda ◽  
Linling Cheng ◽  
Muhammad Aftab ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Reperfusion Injury ◽  
Motor Function ◽  
Katp Channel ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Channel Activation ◽  
Mitochondrial Katp Channel

Introduction: Pharmacologic induction of metabolic tolerance to spinal cord ischemia-reperfusion injury (SCI) after thoracoabdominal aortic intervention is not well established. We previously demonstrated that nicorandil pretreatment preserved motor function in a murine SCI model via direct mitochondrial ATP-sensitive potassium (KATP) channel activation and nitric oxide (NO) donation. However, the independent role of NO-mediated neuroprotection has not been elucidated. Hypothesis: Nitroglycerin pretreatment will induce neuroprotection through NO-mediated KATP channel activation. Methods: SCI was induced by 7 minutes of thoracic aortic cross-clamping in adult male C57BL/6 mice. Pretreatment constituted intraperitoneal injection 3 consecutive days before injury. Experimental groups: sham (no pretreatment or ischemia, n=10), SCI control (normal saline, n=20), nitroglycerin 1 mg/kg (n=18), nitroglycerin 1 mg/kg + 5-hydroxydecanonate 5 mg/kg (5HD, mitochondrial KATP channel blocker, n=13), 5HD 5 mg/kg (n=10), nitroglycerin 1 mg/kg + carboxy-PTIO (cPTIO) 1 mg/kg (NO scavenger, n=16), and cPTIO 1 mg/kg (n=10). Limb motor function and the number of viable neurons within the anterior horn of the spinal cord were evaluated. Results: Compared to SCI control, motor function was significantly preserved in the nitroglycerin pretreatment group at every time point after ischemia. In the nitroglycerin+5HD and nitroglycerin+cPTIO groups, motor preservation was significantly attenuated compared to nitroglycerin pretreatment (p<0.001). Histological analysis showed significant neuron preservation in the nitroglycerin pretreatment group compared with SCI control (p=0.011). This preservation was completely attenuated with 5HD or cPTIO co-administration (p=0.001). Conclusions: Nitroglycerin pretreatment significantly preserved motor function in a murine SCI model through NO-mediated KATP channel activation.

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