[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Jiang, Xiaosi; Wu, Dan; Jiang, Zichao; Ling, Weiwei; Qian, Geng

doi:10.1155/2021/4665632

Cited by 18 publications

(15 citation statements)

References 126 publications

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“…Likewise, the antioxidant activity of melatonin in reducing the adverse effects of I/R injury was also shown to be related to its inhibitory action on the mitochondrial permeability transition pore opening as well as up-regulation of cytochrome c oxidase activity [ 127 , 128 ]. In addition, nicorandil, a mitochondrial ATP-sensitive potassium channel opener, has been demonstrated to prevent I/R-induced injury to the myocardium, alleviate cardiomyocyte necrosis, attenuate endothelial dysfunction, and improve blood flow as well as cardiac function [ 129 ]. These experimental observations indicate that several cardiac alterations induced by I/R injury are prevented by treatment with a wide variety of pharmacological agents including antioxidants; however, extensive research work needs to be carried out to establish if these interventions are able to reverse the I/R-induced myocardial abnormalities.…”

Section: Pharmacotherapy Of I/r Injury To the Heartmentioning

confidence: 99%

Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury

et al. 2022

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Ischemia-reperfusion (I/R) injury is well-known to be associated with impaired cardiac function, massive arrhythmias, marked alterations in cardiac metabolism and irreversible ultrastructural changes in the heart. Two major mechanisms namely oxidative stress and intracellular Ca2+-overload are considered to explain I/R-induced injury to the heart. However, it is becoming apparent that oxidative stress is the most critical pathogenic factor because it produces myocardial abnormalities directly or indirectly for the occurrence of cardiac damage. Furthermore, I/R injury has been shown to generate oxidative stress by promoting the formation of different reactive oxygen species due to defects in mitochondrial function and depressions in both endogenous antioxidant levels as well as regulatory antioxidative defense systems. It has also been demonstrated to adversely affect a wide variety of metabolic pathways and targets in cardiomyocytes, various resident structures in myocardial interstitium, as well as circulating neutrophils and leukocytes. These I/R-induced alterations in addition to myocardial inflammation may cause cell death, fibrosis, inflammation, Ca2+-handling abnormalities, activation of proteases and phospholipases, as well as subcellular remodeling and depletion of energy stores in the heart. Analysis of results from isolated hearts perfused with or without some antioxidant treatments before subjecting to I/R injury has indicated that cardiac dysfunction is associated with the development of oxidative stress, intracellular Ca2+-overload and protease activation. In addition, changes in the sarcolemma and sarcoplasmic reticulum Ca2+-handling, mitochondrial oxidative phosphorylation as well as myofibrillar Ca2+-ATPase activities in I/R hearts were attenuated by pretreatment with antioxidants. The I/R-induced alterations in cardiac function were simulated upon perfusing the hearts with oxyradical generating system or oxidant. These observations support the view that oxidative stress may be intimately involved in inducing intracellular Ca2+-overload, protease activation, subcellular remodeling, and cardiac dysfunction as a consequence of I/R injury to the heart.

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Section: Pharmacotherapy Of I/r Injury To the Heartmentioning

confidence: 99%

Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury

et al. 2022

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“… 29 The release of both pro-inflammatory mediators, such as TNF-α and IL-1β, and ROS plays an important role in the development and progression of MNR. 30 We found that nicorandil could improve inflammation and oxidative stress, which may participate in MNR, in addition to its effect on vasodilation in this trail. Thus, the suppression of MNR by nicorandil might occur through the inflammatory pathway.…”

Section: Discussionmentioning

confidence: 57%

Effects of nicorandil on systemic inflammation and oxidative stress induced by percutaneous coronary intervention in patients with coronary heart disease

Zong

et al. 2021

J Int Med Res

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Objective The present study investigated the effects of a bolus intracoronary injection of nicorandil on systemic inflammation and oxidative stress induced by percutaneous coronary intervention (PCI) in patients with coronary heart disease (CHD). Methods Patients undergoing coronary angiography (CAG) were enrolled into the CAG group (n = 30). Patients undergoing PCI were randomly divided into the PCI (n = 30) and PCI + nicorandil groups (n = 30). Results Blood taken from patients in the placebo group 24 hours after PCI exhibited significant increases in the expression of inflammatory indicators and mild increases in the expression of anti-inflammatory indicators. The intracoronary injection of nicorandil reversed the elevation of inflammatory indicators and significantly increased the levels of anti-inflammatory indicators in the blood of patients with PCI. Blood taken from patients in the placebo group 24 hours after PCI also displayed significant decreased superoxide dismutase levels and increased malondialdehyde levels. Nicorandil treatment reversed these changes of oxidative stress marker levels. Conclusions These results indicated the possible medical application of intracoronary injections of nicorandil for reducing systemic inflammation and oxidative stress in the peripheral blood of patients undergoing PCI.

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“…In addition, nicorandil dilates the microvasculature to improve cardiac perfusion by activating potassium ATP channels ( 19 ). Nicorandil also protects cardiomyocytes by opening the mitochondrial potassium ATP channels in ischemia-reperfusion conditions ( 20 ). In patients with ST-segment elevation myocardial infarction, intracoronary or intravenous administration of nicorandil during primary PCI improved myocardial microcirculation and reduced infarct size ( 21 – 23 ).…”

Section: Discussionmentioning

confidence: 99%

Nicorandil Improves Left Ventricular Myocardial Strain in Patients With Coronary Chronic Total Occlusion

Chen

Feng

et al. 2022

Front. Cardiovasc. Med.

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BackgroundNicorandil is recommended as a second-line treatment for stable angina; however, randomized-controlled trials to evaluate the benefit of nicorandil for patients with chronic total occlusion (CTO) are lacking.ObjectiveTo determine whether nicorandil can improve left ventricular (LV) myocardial strain in patients with CTO.MethodsPatients with CTO were included and randomized to the nicorandil group (n = 31) and the control group (n = 30). Nicorandil was given orally at 15 mg/day for 3 months in the nicorandil group. Three-dimensional speckle-tracking echocardiography and the Seattle Angina Questionnaire (SAQ) survey were performed at baseline and at 3 months. The primary study endpoint was the LV global area strain (GAS) at 3 months.ResultsThe nicorandil and the control groups were well-matched at baseline, including the mean GAS and SAQ scores. At 3 months, GAS in the nicorandil group was significantly higher than that in the control group (−23.7 ± 6.3% vs. −20.3 ± 5.6%, respectively; p = 0.033). There were no significant differences in LV global longitudinal strain, global circumferential strain, global radial strain, LV ejection fraction, LV end-diastolic volume, and LV end-systolic volume at 3 months between the two groups. At 3 months, the SAQ scores for angina stability, angina frequency, and treatment satisfaction in the nicorandil group were significantly higher than those in the control group.ConclusionNicorandil treatment can improve GAS and angina symptoms in patients with CTO.Clinical Trial Registrationwww.ClinicalTrials.gov, identifier: NCT05087797.

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[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Cited by 18 publications

References 126 publications

Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury

Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury

Effects of nicorandil on systemic inflammation and oxidative stress induced by percutaneous coronary intervention in patients with coronary heart disease

Nicorandil Improves Left Ventricular Myocardial Strain in Patients With Coronary Chronic Total Occlusion

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