Postischemic

Postischemic describes events that occur after tissue has experienced ischemia, a period of reduced blood flow and oxygen supply. It is commonly used in reference to ischemia-reperfusion injury, where restoring circulation can paradoxically cause additional damage. Postischemic injury arises from reoxygenation-induced cascades, including reactive oxygen species generation, calcium overload, inflammation, endothelial dysfunction, and mitochondrial damage, potentially leading to cell death by necrosis or apoptosis and microvascular dysfunction (no-reflow).

Organs frequently affected include the heart, brain, kidney, and liver. In the heart, reperfusion after myocardial infarction or PCI can intensify injury and worsen functional recovery. In the brain, reperfusion after ischemic stroke may worsen edema and neuronal loss. Clinically, postischemic injury can present with arrhythmias, organ dysfunction, or failure, and may be monitored by tissue-specific biomarkers such as troponin or others.

Prevention and management focus on minimizing reperfusion injury during restoration of blood flow. Strategies include controlled reperfusion, ischemic preconditioning and postconditioning, and pharmacologic approaches aimed at reducing oxidative stress and inflammation, protecting mitochondria, and stabilizing calcium. Evidence for specific drugs remains mixed and management is tailored to the organ and clinical context.

See also reperfusion injury, postconditioning, no-reflow.