Myocardial protection of MCI-186 in rabbit ischemia–reperfusion

Wu, Tai-Wing; Zeng, Ling-Hua; Wu, Jun; Fung, Kwok‐Pui

doi:10.1016/s0024-3205(02)01965-3

Cited by 124 publications

(79 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Wu et al have shown a protective effect of edaravone on the myocardium when it was administered during coronary occlusion or after reperfusion (27). Thus, we presumed that preservation of endothelial function by edaravone may also be observed if it is administered during occlusion or after reperfusion.…”

Section: Myocardial Protection By Edaravonementioning

confidence: 82%

Edaravone Preserves Coronary Microvascular Endothelial Function After Ischemia/Reperfusion on the Beating Canine Heart In Vivo

et al. 2007

View full text Add to dashboard Cite

Abstract. We examined whether edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, exerts its protective effect on coronary microvessels after ischemia / reperfusion (I/ R) in vivo. Ninety-minute coronary occlusion followed by reperfusion was performed in 16 open-chest dogs with and without edaravone administration. Coronary small artery (≥100 µm in size) and arteriolar (<100 µm) vasodilation, in the presence of endothelium-dependent (acetylcholine) or -independent (papaverine) vasodilators, was directly observed using intravital microscopy before and after I / R. I / R impaired microvascular vasodilation in response to acetylcholine, whereas administration of edaravone preserved the response in microvessels of both sizes, but to a greater extent in the coronary small arteries. No significant changes were noted with papaverine administration. In the edaravone group, the fluorescent intensity from reactive oxygen species (ROS) was lower, whereas nitric oxide (NO) intensity was higher relative to controls in the microvessels of the ischemic area. In conclusion, edaravone preserves coronary microvascular endothelial function after I / R in vivo. These effects, which were NOmediated, were attributed to the ROS scavenging properties of edaravone.

show abstract

Section: Myocardial Protection By Edaravonementioning

confidence: 82%

Edaravone Preserves Coronary Microvascular Endothelial Function After Ischemia/Reperfusion on the Beating Canine Heart In Vivo

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Edaravone reduced the myocardial necrotic area following myocardial I/R in rats (21) and in rabbits (22). Edaravone also prevented lethal ventricular tachyarrhythmias upon reperfusion and deteriorations in cardiac function following ischemia and I/R in rats, by inhibiting lipid peroxidation (23).…”

Section: Myocardial Injurymentioning

confidence: 99%

Beyond neurological disease: New targets for edaravone (Review)

Kikuchi¹,

Uchikado²,

Miyagi³

et al. 2011

Int J Mol Med

View full text Add to dashboard Cite

show abstract

“…16 Previous experimental studies have reported that the administration of edaravone just before reperfusion reduced reperfusion injuries and myocardial damage in myocardial ischemia-reperfusion animal models. 17,18 Edaravone has been shown to attenuate pressure overload-induced LV hypertrophy via its antioxidant function according to a recent report. 19 With these effects, edaravone has been recognized as both a potent cardioprotective and a cytoprotective agent.…”

mentioning

confidence: 99%

Long-Term Efficacy of Edaravone in Patients With Acute Myocardial Infarction

Tsujita

Shimomura

Kaikita

et al. 2006

Circ J

View full text Add to dashboard Cite

yocardial reperfusion is necessary for the salvage and recovery of the ischemic myocardium. Early reperfusion therapy has improved the clinical outcomes of patients with acute myocardial infarction (AMI), but these benefits are limited in some patients by reperfusion injuries. 1 There is now increasing evidence that reactive oxygen species (ROS) lead to reperfusion injuries in the ischemic myocardium and that they are related to subsequent left ventricular (LV) dysfunction. 2,3 Recent investigations have shown that increased vascular oxidative stress predicts the risk of cardiovascular events in patients with coronary artery disease. 4 Various different radical scavengers and antioxidants have been shown to effectively reduce reperfusion injury in experimental models. 5,6 In these ischemia-reperfusion models, it was demonstrated that radical scavengers such as superoxide dismutase and vitamin E analog reduced infarct size by limiting reperfusion-induced oxidative stress and by attenuating the inflammatory response. On the basis of this established scientific rationale, several randomized controlled trials were designed to prove or disprove the causative effects for antioxidant supplements. 7-10 Unfortunately, results of these studies on antioxidants and cardiovascular event risks have been disappointing, especially in regards to the studies investigating primary prevention. Namely, each study has several limitations to test therapeutic agents in clinical practice, mainly because of their low accessibility to tissue or rapid clearance from the body. 11,12 In contrast, edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), has a low molecular weight (174.20 kD), is lipophilic, and is readily accessible to tissue. 13,14 Edaravone has the ability to scavenge toxic free radicals; moreover, it has been shown to inhibit vascular endothelial cell injury and to inhibit the aggravation of brain edema caused by free radical-induced lipid peroxidation. 15 Recently, edaravone has been officially approved for the treatment of acute ischemic stroke in Japan. 16 Previous experimental studies have reported that the administration of edaravone just before reperfusion reduced reperfusion injuries and myocardial damage in myocardial ischemia-reperfusion animal models. 17,18 Edaravone has been shown to attenuate pressure overload-induced LV hypertrophy via its antioxidant function according to a recent report. 19 With these effects, edaravone has been recognized as both a potent cardioprotective and a cytoprotective agent. We have recently demonstrated that the administration of edaravone just prior to myocardial reperfusion attenuated both enzymatic infarct size and reperfusion arrhythmia in patients with AMI; 20 however, its effects on long-term clinical outcomes in AMI patients have not yet been clarified. The purpose of the present study was to clarify the efficacy of edaravone on the long-term prognosis in patients with AMI. Long-Term Efficacy of Edaravone in Patients With Acute Myocardial InfarctionKenichi Tsujita, MD; Hideki Shimo...

show abstract

Myocardial protection of MCI-186 in rabbit ischemia–reperfusion

Cited by 124 publications

References 12 publications

Edaravone Preserves Coronary Microvascular Endothelial Function After Ischemia/Reperfusion on the Beating Canine Heart In Vivo

Edaravone Preserves Coronary Microvascular Endothelial Function After Ischemia/Reperfusion on the Beating Canine Heart In Vivo

Beyond neurological disease: New targets for edaravone (Review)

Long-Term Efficacy of Edaravone in Patients With Acute Myocardial Infarction

Contact Info

Product

Resources

About