2021
DOI: 10.1161/strokeaha.121.033849
|View full text |Cite
|
Sign up to set email alerts
|

Combatting Secondary Injury From Intracerebral Hemorrhage With Supplemental Antioxidant Therapy

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

0
1
0

Year Published

2022
2022
2024
2024

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(1 citation statement)
references
References 12 publications
(10 reference statements)
0
1
0
Order By: Relevance
“…1–3 The hyperacute phase of ICH encompasses primary injury caused by the hematoma and its expansion, and secondary injury that results from the activation of inflammation and coagulation cascades. 4–7 The pathophysiologic hallmark of early brain inflammation after ICH is neutrophil extravasation, which occurs within 4 to 5 hours of ICH onset and peaks at 3 days. 8 Neutrophils damage the brain by producing reactive oxygen species, releasing proinflammatory proteases, affecting blood–brain barrier permeability, and promoting neuronal death.…”
mentioning
confidence: 99%
“…1–3 The hyperacute phase of ICH encompasses primary injury caused by the hematoma and its expansion, and secondary injury that results from the activation of inflammation and coagulation cascades. 4–7 The pathophysiologic hallmark of early brain inflammation after ICH is neutrophil extravasation, which occurs within 4 to 5 hours of ICH onset and peaks at 3 days. 8 Neutrophils damage the brain by producing reactive oxygen species, releasing proinflammatory proteases, affecting blood–brain barrier permeability, and promoting neuronal death.…”
mentioning
confidence: 99%