Background: High pO2 responses in cerebral circulation can be altered in disease(1,2,3,4). This study aimed to determine the effects of acute hyperoxia on cerebrovascular reactivity (CVR), thromboxane B2 (TXB2, a stable metabolit of TXA2) plasma levels and systemic haemodynamic parameters in acute stroke patients(SP) and healthy volunteers(HV). Methods: The study protocol and procedures were approved by the Ethical Committee of the Faculty of Medicine Osijek, and conformed to the standards set by the latest revision of the Declaration of Helsinki. 52 SP (age 68±6.7 yrs) with acute ischemic stroke (within 72 hours) and 52 HV (64.5±8.3 yrs) were included. Mean blood flow velocity (MBFV) in middle cerebral artery (MCA), pulsality index (IP) and resistance index (IR) were determined by transcranial Doppler before (basal), during 15 minutes (hyperoxia), and 15 minutes after the acute hyperoxia (inhalation of 100% O2 over facial mask). Systolic and diastolic blood pressure (SBP, DBP), heart rate (HR) and pO2 (measured by pulse oxymeter) were assessed at the same time points. Tromboxane B2 (TXB2) levels in venous blood samples were measured by ELISA before and immediately after hyperoxia. Mixed factorial ANOVA with repeated measures and Games-Howell post hoc test were used with logarithmic transformation; p<0.05 was considered significant. Data are expressed as mean±SD. Results: Basal MBFV was significantly lower in SP(53±14) compared to HV(61±17). During hyperoxia MBFV significantly increased in SP(58±15; by 10%), while it decreased in HV(57±16; by 7%) compared to respective basal values. IP (basal=1±0.36; hyperoxia=1± 0.35; after=1± 0,40) and IR (basal=0.67±0.08; hyperoxia=0.67±0.10; after=0.66±0.08) were significantly higher in SP compared to HV (PI: basal=1±0.30; hyperoxia=1±0.35; after= 1±0.28); RI: basal=0.61±0.09; hyperoxia=0.61±0.09; after=0.60±0.08) in all 3 time points. Hyperoxia did not affect IP and IR in both groups, nor HR in SP, while HR decreased in HV (7%, p<0.01). SP had significantly higher SBP/DBP (basal=144±18/91±12; hyperoxia=145±18/92±12; after=142±17/89±11) at all 3 points compared to HV (SBP/DBP: basal=129±17/83±11; hyperoxia=130±15/87±11; after=126±19/82±10). SBP/DPB significantly increased in both groups during hyperoxia compared to basal values. pO2 during hyperoxia increased in SP only (4%, p< 0.001). There was 8% decrease in TXB2 levels in SP and 4% increase in TXB2 in HV in hyperoxia, however, did not reach significance (p>0,05). TXB2 showed weak negative correlation with MBFV in both studied groups. Conclusion:This study demonstrated paradoxical vasodilation of MCA, with decreased TXB2 in SP, and vasoconstriction with increased TXB2 in HV, suggesting the role of cyclooxygenases’ metabolites mediating these changes in both, SP and HV. Hyperoxia affected haemodynamic parameters also.