ArticleInternational journal of molecular sciences2024
Secondary Brain Injury After Parenchymal Cerebral Hemorrhage in Humans: The Role of NOX2-Mediated Oxidative Stress and Endothelin-1.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Advances in Stereotactic Hematoma Evacuation for Hypertensive Intracerebral Hemorrhage and the Value of Multimodal Monitoring.Cerebrovascular diseases (Basel, Switzerland) · 2026Review
- Hematoma Coagulation is Associated with Perihematoma Edema Volume in Patients with Acute Intracerebral Hemorrhage.Neurocritical care · 2026Article
- Focusing on perihematomal hypoperfusion following intracerebral hemorrhage: from oxidative stress to prospective therapeutic approaches.Frontiers in physiology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Perihematomal hypoperfusion may lead to ischemic damage during intraparenchymal cerebral hemorrhage (ICH), resulting in worse prognosis. We aimed to (1) investigate the relationship between serum biomarkers related to oxidative stress and vasoactive substances and the occurrence of hypoperfusion and ischemic perihematomal lesions in ICH and (2) evaluate their correlation with the volumetric evolution of the hematoma and perihematomal edema. We enrolled 28 patients affected by ICH. Blood samples were collected at three different time points from symptom onset: T0, T1, and T2 (admission, 12-24 h, and 48-72 h, respectively), to measure endothelin-1 (ET-1), nitrites/nitrates (NO), soluble nicotinamide adenine dinucleotide 2 (NOX2)-derived peptide (sNOX2-dp), and asymmetric dimethylarginine (ADMA). Patients underwent brain MRI with perfusion study at T1 and MRI without perfusion at T2. 12 patients had ischemic perihematomal lesions at T1. A higher sNOX2-dp concentration at T0 was observed in patients with ischemic perihematomal lesions compared to those without (
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