2015/01/19 by Jilin Bai, Patrick D. Lyden · 2 citations
Medicine · Neuroscience · #Acute Ischemic Stroke Management #Neuroinflammation and Neurodegeneration Mechanisms #Traumatic Brain Injury and Neurovascular Disturbances #Medicine #Reperfusion injury #Neurovascular bundle #Ischemia #Thrombolysis #Penumbra #Ischemic preconditioning #Cardiology #Reperfusion therapy #Blood–brain barrier #Intracerebral hemorrhage #Subarachnoid hemorrhage #Internal medicine #Pathology #Central nervous system #Myocardial infarction
paper · doi:10.1111/ijs.12434
openalex publication_date 2015/01/19 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/15
Cerebral postischemic reperfusion injury is defined as deterioration of ischemic brain tissue that parallels and antagonizes the benefits of restoring cerebral circulation after therapeutic thrombolysis for acute ischemic stroke. To understand the paradox of injury caused by treatment, we first emphasize the phenomenon in which recanalization of an occluded artery does not lead to tissue reperfusion. Additionally, no-reflow after recanalization may be due to injury of the neurovascular unit, distal microthrombosis, or both, and certainly worsens outcome. We examine the mechanism of molecular and subcellular damage in the neurovascular unit, notably oxidative stress, mitochondrial dysfunction, and apoptosis. At the level of the neurovascular unit, which mediates crosstalk between the damaged brain and systemic responses in blood, we summarize emerging evidence demonstrating that individual cell components play unique and cumulative roles that lead to damage of the blood-brain barrier and neurons. Furthermore, we review the latest developments in establishing a link between the immune system and microvascular dysfunction during ischemic reperfusion. Progress in assessing reperfusion injury has also been made, and we review imaging studies using various magnetic resonance imaging modalities. Lastly, we explore potential treatment approaches, including ischemic preconditioning, postconditioning, pharmacologic agents, and hypothermia.