Normobaric Hyperoxia in Patients With Acute Stroke: Enhancing Neuroprotection Through Inhibition of Inflammation

Inflammatory response is an important pathological and physiological mechanism in the occurrence and development of acute ischemic stroke. This study investigated the effects of normobaric hyperoxia on the inflammatory response in acute ischemic stroke and explored the role of inflammation in stroke-induced brain injury.

This secondary analysis of the OPENS (Normobaric Hyperoxia Combined With Reperfusion for Acute Ischemic Stroke) trial, included 86 acute ischemic stroke patients with anterior circulation large vessel occlusion: 43 received normobaric hyperoxia (10 L/min, 100% oxygen for 4 hours) with endovascular thrombectomy, and 43 received endovascular thrombectomy alone. Inflammatory markers were measured at different time points (admission, 24 hours, 7 days), and National Institutes of Health Stroke Scale score and cerebral infarction volume were also recorded. The main outcome measures were serum CRP (C-reactive protein) levels, peripheral blood leukocyte count, neutrophil count, and neutrophil-to-lymphocyte ratio. Correlation analysis was used to analyze the relationship between inflammatory markers and stroke.

The results showed that the normobaric hyperoxia group had significantly lower levels of inflammatory markers compared with the control group at 24 hours (P<0.05). Early correlation analysis (within 24 hours) showed a significant positive association between 24-hour inflammatory marker levels and early neurological function scores (National Institutes of Health Stroke Scale) as well as early infarct volume (assessed at 24-48 hours).

Normobaric hyperoxia attenuates early postthrombectomy inflammation, as evidenced by reduced CRP, neutrophil counts, and neutrophil-to-lymphocyte ratio. These inflammation markers were significantly associated with acute stroke severity and infarct volume.

URL: https://www.clinicaltrials.gov; Unique Identifier: NCT03620370.