Reperfusion injury

Reperfusion injury has been defined as myocardial tissue blood supply after a period of ischemia. Whether reperfusion merely  accelerates the damage that would have occurred during the initial ischemia  or whether there is a additional injury caused by reperfusion itself is still researched. Although the crucial role of reperfusion injury in revascularization procedures has bees recognized, the etiology and pathogenesis of this phenomenon remain unknown.
Myocardial ischemia accompanied by reperfusion injury followed by complete normalization if it took 5 minutes, by diastolic and systolic dysfunction if ischemia took 15-20 minutes and without return contractile function if ischemia took more than one hour.
The most common cause found in patients who died after reperfusion is hemorrhagic infarction. In myocardial infarction of less than 3 days the cellular response is present throughout the myocardial infarction, in contrast to the distinct zones seen in the non- reperfused myocardial infarctions. Reperfusion itself may produce injury.

The mediators of reperfusion injury

Reperfusion injury

One of the mediators of reperfusion injury is oxygen free radicals. The possible role of reactive oxygen species in reperfusion injury has evolved from our knowledge. They elaborate enzyme systems that rapidly detoxify superoxide and peroxide. The metabolism of reactive oxygen also has damaging effects. The investigators of this event have suspected that even physiological quantities of peroxide may inhibit the aerobic oxidation of pyruvate and thus restrict cellular ATP formation.
Another mediator of reperfusion injury is endothelial dysfunction and microvascular injury. Recent reports indicate that endothelium-dependent relaxation  of coronary microvessels is markedly impaired after ischemia with reperfusion. This microvascular endothelium dysfunction may be caused by blood products or myocardial metabolites that are released during the reperfusion period or by oxygen free radicals.
One of the oldest hypotheses about reperfusion injury involved calcium overload. Other mediators involved in reperfusion injury are altered myocardial metabolism and endogenous protective mechanisms.
There are some cardiovascular risk factors influence reperfusion injury. This are  hypercholesterolemia, very high glucose and hypertension.

Pharmacological methods to attenuate reperfusion injury

There are a number of pharmacological methods for attenuate reperfusion injury. In the treatment of myocardial infarction, restoration of coronary flow as soon as possible is a very important thing to prevent and reduce myocardial necrosis and ischemia. By this treatment ensure a reduction of mortality,  complications and a good prognosis in infarction. Early myocardial reperfusion injury prevent necrosis; in this way systolic and diastolic functions are established and are preventable fatal arrhythmias. In the early hours of  infarction,  reperfusion injury offers the greatest benefits: higher thrombus lysis.
Anti-ischemic therapy and lytic therapy has an important role to reduce myocardial energy demand. There are three revascularizations methods: trombembolitic treatment,  coronary angioplasty and coronary bypass. To thrombolytic treatment add anticoagulant and antithrombotic treatment and GP IIb/IIIa blockers. Thrombolytic agents currently used are streptokinase, tissue plasminogen activator and urokinase.

Conclusion for reperfusion injury

In conclusion the beneficial effect of fast recanalization may be offset by reperfusion injury.