On the role of oxidative stress and neutrophils in myocardial reperfusion injury.

1. Apart from ‘no-reflow’ phenomenon/microvascular injury and myocardial injury/stunning, both of which undoubtedly constitute the MRI, one cannot ignore the reperfusion arrhythmias that considerably contribute to myocardial dysfunction observed in this setting [2]. 2. It is prudent to acknowledge that various problems in the experimental study of MRI still exist and sometimes provoke confusion [3,4]. The duration of ischemia, the timing of drug administration, the drug delivery method and the selection of end-points for cardioprotection, are some of them. For example, it is highly possible that intravenous (and not intracoronary) administration of drugs during ischemia may not reach the ischemic area in the absence of collaterals. 3. It is well established that repetitive short periods of ischemia may be cardioprotective due to induction of ischemic preconditioning [5]. On the other hand, repetitive stunning may lead to chronic stunning which is believed to be a form of myocardial hibernation [5,6]. Consequently, the concept of MRI has currently become more complex and subtle manipulations are needed in order to alleviate its detrimental effects and potentate its potential favorable effects.