General pathology · Cell injury, adaptation and death
Hypoxia, ischemia and reperfusion injury !
- Mechanism
Blocked blood flow starves cells of oxygen. Restoring flow is essential, but it can briefly add damage of its own: reperfusion injury.
Updated 2026-11-01
What it is
Hypoxia is low oxygen; ischemia is low blood flow, which also cuts the supply of glucose and the removal of waste, so it injures faster. Restoring flow saves cells that are still reversibly injured, yet some cells that were alive before reperfusion die afterwards. That added damage comes from a burst of free radicals, calcium overload, recruited neutrophils and complement activation.
Key facts
- Brain neurons tolerate complete ischemia for only a few minutes; heart muscle for about twenty to thirty minutes.
- The ischemic penumbra in stroke is tissue that is still salvageable if flow returns.
- Myocardial stunning is reversible loss of contraction that lasts hours to days after reperfusion.
- Reperfusion arrhythmias can appear when a coronary artery is reopened.
Step by step
- Flow stops: oxygen and glucose delivery cease, metabolites accumulate.
- ATP falls, pumps fail, the cell swells and becomes acidic.
- Reversible injury: if flow returns quickly, most cells recover.
- On reperfusion, damaged mitochondria and returning oxygen create a burst of free radicals.
- Calcium floods the cells and opens mitochondrial pores; hypercontraction occurs in muscle.
- Neutrophils and complement arrive with the blood and add inflammatory damage.
- Some reperfused cells die (necrosis, apoptosis); the vessels may bleed into the infarct.
Clinical notes
- After revascularization of an acutely ischemic limb, swelling can cause compartment syndrome and release potassium and myoglobin.
- Hemorrhagic transformation is a feared complication when an ischemic stroke is reperfused.
Test yourself
Think of the answer, then tap the question to see it.
What are the main mechanisms of reperfusion injury?
Oxygen free radicals, intracellular calcium overload, neutrophil inflammation and complement activation.
What myocardial pattern is typical of reperfused infarcts?
Contraction band necrosis, caused by hypercontraction of myofibrils when calcium enters the cells.
Why is ischemia more harmful than hypoxia with preserved flow?
Without flow, glucose for anaerobic glycolysis is not delivered and acid metabolites are not removed.
Related
- Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNA
- Oxidative stress and free-radical injury
- Reversible vs irreversible cell injury: the point of no return
- Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous
- Infarction: red vs white, and what decides the damage
- The myocardial infarct over time: what the pathologist sees from hours to months
- Watershed areas and the organs most sensitive to ischemia
Related conditions
- Myocardial Infarction (Heart Attack)
- Ischaemic stroke
- Acute limb ischaemia
- Acute mesenteric ischaemia
- Acute compartment syndrome
- Acute kidney injury
- Perinatal asphyxia and hypoxic-ischaemic encephalopathy
- Cardiac arrest (VF, pulseless VT, asystole, PEA)
- Testicular torsion
- Ovarian torsion
Elsewhere in DurgiPedia
- Coronary circulation and myocardial ischemia
- Oxygen content, delivery and extraction
- The causes of hypoxemia
- Reactive oxygen species and antioxidants
- Lactate
- Complement: three pathways, MAC, regulators
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Heart Attack | Myocardial Infarction | MedlinePlus (MedlinePlus, US National Library of Medicine, 2024); Ischemic Stroke (StatPearls (NCBI Bookshelf), 2024); Acute Mesenteric Ischemia (StatPearls (NCBI Bookshelf), 2024).
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Representative model, for educational purposes only.