Expansion
Oxygen returns to injured tissue and generates free radicals
Expansion
Four mechanisms, all triggered by the return of oxygen to injured tissue:
- Free radical generation, as xanthine oxidase and damaged mitochondria meet returning oxygen
- Calcium overload, worsening mitochondrial injury and opening the permeability transition pore
- Neutrophil influx, releasing proteases and further radicals
- Complement activation, against neoantigens exposed by ischaemia
“The oxygen that saves the tissue also injures it.”
Clinical consequences
- Myocardial stunning: reversible contractile dysfunction lasting days after successful reperfusion, with viable myocardium
- No reflow phenomenon: capillary obstruction means tissue perfusion fails even with a patent epicardial artery
- Reperfusion arrhythmias after thrombolysis or angioplasty
- Compartment syndrome and systemic effects after revascularising an ischaemic limb, with hyperkalaemia, acidosis and myoglobinuria
Hibernating myocardium is the counterpart: chronically underperfused but viable myocardium with reduced contractility, which recovers after revascularisation. Distinguishing it from scar is the purpose of viability imaging.