In myocardial, the Reperfusion injury maximum effect is caused due to -
Reperfusion injury refers to myocardial vascular or electrophysiological dysfunction that is induced by the restoration of blood flow to previously ischemic tissue.
o Manifestation includes:

Reperfusion arrhythmias.
Endothelial cell damage leading to microvascular dysfunction,
Myocardial stunning.
Myocyte death and infarction.

PATHOPHYSIOLOGY-
When blood flow to cardiac myocytes is disrupted by occlusion of a coronary artery, a series of events is set in motion that results in cellular injury and death. These processes are largely related to energy production and utilization and include the following :

Reduced energy production with a fall in intracellular ATP levels,
A transition from aerobic to anaerobic energy utilization,
An accumulation of the products of anaerobic metabolism,
Reduced intracellular pH.

Factors that contribute to reperfusion injury include the following :

Damage to cellular and organelle membranes, including mitochondria,
Myocyte hypercontracture.
Free radical formation.
Aggregation of leukocytes and inflammatory mediators,
Platelet activation.
Complement activation.
Activation of the pro-apoptotic signalling cascade.
Endothelium damage and vasoconstriction.

Oxygen and other free radicals -

Free radicals are produced within a minute of reperfusion and continue to be generated for hours after the restoration of blood flow to ischemic tissue.
Superoxide anion (O2)
Hydrogen peroxide (H2O2)
Hypochlorous acid (HClO)
Nitric oxide-derived peroxynitrite.
Hydroxyl radical (OH)
Several mechanisms have been proposed for the development of these free radicals including xanthine oxidase, activated neutrophils, electron leakage from ischemic mitochondrion, catecholamine oxidation, as well as cyclooxygenase and lipoxygenase enzymes.
The relative importance of each of these pathways is not clear, but they are probably interrelated and may potentiate one another.
Free radicals damage myocytes directly by altering membrane proteins and phospholipids. Because these membrane constituents play crucial roles as receptors, enzymes, and ion channels, free radical injury can lead to fatal metabolic and structure derangements. As an example, oxygen radicals inure the sarcolemma and may impair the contractile function of the myocyte on this basis. The role for free radicals as a source of significant myocardial damage is further supported by studies showing that free radical scavengers, such as superoxide dismutase, administered during thrombolytic therapy help preserve myocardial function. Finally, reactive oxygen species stimulate leukocyte activation, chemotaxis, and leukocyte-endothelial adherence.
Neutrophil
Monocytes
Free radicals
Eosinophils