What is Ischemia?

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The term, ischemia, denotes inadequate blood supply to tissues due to blockage of the arterial inflow, while, reperfusion injury is defined as the injury caused by the restitution of blood flow after an ischemic peroid, leading to death of cells that were only reversibly injured at the time of blood flow restitution. [63]. The final infarct size after an MI event is therefore the result of the ischemic and reperfusion damage. For this reason, the term that best describes this process of myocyte death in reperfused MI is myocardial ischemia/reperfusion (I/R) injury [64]. In the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which activate the G protein signaling pathways therefore promoting myocardial survival. While in the late phase, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF and SDF-1, in the injured myocardium, hence promoting a cardio-protective state. The liver also participates in cardioprotection through the up regulation and release of secretory proteins, including FGF21 and TFF3, which also promote cardiomyocyte survival. [65]. Foundational studies performed about three decades ago with animal models demonstrated that an early reperfusion was able to limit infarct size [66]. Then fibrinolysis was indisputably associated with a decrease in mortality in patients with STEMI [67].A decade later; primary angioplasty was shown to be more superior than fibrinolysis [68]. Currently primary coronary angioplasty (PCI) has been established as the backbone treatment for STEMI patients. The period from the onset of symptoms of MI (representative of the time of coronary occlusion) and reperfusio... ... middle of paper ... ... of the need of duplicate revascularization over balloon angioplasty [75]. Both pre- and post -conditioning appears to protect cardiomyocytes at the time of reperfusion therapy. Ischemic post-conditioning is a chain of repetitive intermissions of coronary blood flow administered after a period of ischemia. Inhibition of ONOO−-induced nitro-oxidative stress might pay a critical role in postcon-mediated cardioprotection [76]. Iliodromitis et al also reported that postcon-mediated cardioprotection was in cohorts with reduced nitro-oxidative stress in vivo. The acknowledgment that iNOS activation in cardiac myocytes could be advantageous and that nitriate/NO could have both beneficial and detrimental effects, lead to the dose of 1400W iNOS inhibitor being chosen to significantly inhibit, but not restrict, increase in the level of myocardial iNOS activity after MI [77]

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