Disease relevance of Myocardial Reperfusion Injury

• Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury [1].
• Both in experiments (acute) and in chronic models, resveratrol attenuates myocardial ischemic reperfusion injury, atherosclerosis, and reduces ventricular arrhythmias [2].

High impact information on Myocardial Reperfusion Injury

• Effects of the angiotensin AT1 receptor blocker candesartan on myocardial ischemic/reperfusion injury [3].
• Time window of nitroxide effect on myocardial ischemic-reperfusion injury potentiated by iron [4].
• Therapeutic potential of vitamin E against myocardial ischemic-reperfusion injury [5].
• Early treatment with deferoxamine limits myocardial ischemic/reperfusion injury [6].
• Recombinant soluble P-selectin glycoprotein ligand-1 protects against myocardial ischemic reperfusion injury in cats [7].

Chemical compound and disease context of Myocardial Reperfusion Injury

• The fact that rabbit hearts do not contain detectable xanthine oxidase activity would seem to preclude an obligatory role of this enzyme both in the generation of myocardial ischemic/reperfusion injury and in the protective actions of allopurinol [8].
• The results of the present study suggest a protective role of icatibant in myocardial ischemic-reperfusion injury [9].
• Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat [9].
• Augmentation of endogenous adenosine levels is associated with decreased myocardial ischemic-reperfusion injury [10].
• Calcium (Ca2+) overload is an important pathophysiological factor in myocardial ischemic/reperfusion injury [11].

Gene context of Myocardial Reperfusion Injury

• However, direct myocardial protection by hANP against myocardial ischemic reperfusion injury has been rarely investigated [12].
• The role of Cu/Zn-superoxide dismutase (SOD) in myocardial ischemic reperfusion injury was studied by using a mouse model with targeted disruption of the mouse Sod I gene [13].

References