I finished a recent paper and though I would add this part of it to the forum......................

Reperfusion Injury
Prolonged ischemia from cessation of blood flow results in a core region of cell death surrounded by a penumbral region of susceptible tissue engaged in an intracellular battle between survival and demise. Overall, a switch to anaerobic glycolysis occurs in response to anoxia. Simultaneously, there is a corresponding rise in intracellular lactate and hydrogen ions. As this continues, glycolysis halts and ATP levels, which are essential in maintaining ionic pumps, plummet. Cells attempt to correct the acidosis by restoring ionic gradients with the Na+/H+ exchanger. However, the Na+/H+ exchanger depends on intracellular ATP, further consuming this scarce resource. Na+ removal from the cell is further hindered, as the Na+/K+-ATPase is also dependent on ATP. Concurrently, the Na+/Ca2+ exchanger works to assist in Na+ removal but this causes cytosolic Ca2+ to rise. As the duration of ischemia continues, ion pumps fail and this exacerbates the rise of intracellular ions. The influx of ions increases intracellular osmotic pressure and cellular swelling. As the anoxic cells move towards their inevitable necrotic death, cell membranes lyse. Ions, proteins, and neurotransmitters are released to the surrounding area causing damage and inflammation in neighboring cells. It is at this necrotic endpoint that no intervention will rescue cells from death (reviewed in Lipton, 1999; Gateau-Roesch, Argaud, and Ovize, 2006).
While the restoration of blood flow is imperative to prevent irreversible necrotic or apoptotic injury of cells surrounding the necrotic core, abrupt reperfusion may extend the irreversible injury into the penumbral region. In general, abrupt reperfusion 1) precipitously increases oxygen tensions promoting the rapid and persistent generation of ROS, 2) activates the Na+/H+ exchanger and the Na+/Ca2+ exchanger, 3) increases cytosolic and mitochondrial calcium levels, 5) opens the mitochondrial Permeability Transition Pore (mPTP), 6) creates broad endothelial dysfunction & general cell lysis and 7) generates microvascular flow defects (no-reflow phenomenon) (reviewed in Vinten-Johansen et al., 2007). Clinical profiles of the manifestations associated with reperfusion injury are described by Eltzschig and Collard (2004). “Stunning” takes place in myocardial tissue. ROS toxicity occurs and there is a decline in the re-synthesis of ATP. Also, there is an imbalance of cellular calcium uptake versus release. In patients undergoing revascularization procedures, arrhythmias are common and this correlates with an increase in the morbidity and mortality associated with stroke, head injury, circulatory arrest, and aneurysm repair. With gastrointestinal pathologies, abrupt reperfusion decreases intestinal barrier function. Finally, abrupt reperfusion increases the incidence of multiorgan systems failure in the critically ill patient. In total, clinical profiles establish that abrupt reperfusion amplifies cellular injury ubiquitously.