Background: Patients with aneurysmal subarachnoid haemorrhage (SAH) might have impaired cerebral autoregulation, that is, CBF – and thereby oxygen delivery – passively increase with an increase in CPP. This physiological study aimed to investigate the cerebral haemodynamic effects of controlled blood pressure increase in the early phase after SAH before any signs of delayed cerebral ischaemia (DCI) occurred. Methods: The study was carried out within 5 days after ictus. Data were recorded at baseline and after 20 min of noradrenaline infusion to increase mean arterial blood pressure (MAP) by a maximum of 30 mmHg and to an absolute level of no more than 130 mmHg. The primary outcome was the difference in middle cerebral artery blood flow velocity (MCAv) measured by transcranial Doppler (TCD), while differences in intracranial pressure (ICP), brain tissue oxygen tension (PbtO₂), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction. Results: Thirty-six participants underwent the intervention 4 (median, IQR: 3–4.75) days after ictus. MAP was increased from 82 (IQR: 76–85) to 95 (IQR: 88–98) mmHg (p-value: <.001). MCAv remained stable (baseline, median 57, IQR: 46–70 cm/s; controlled blood pressure increase, median: 55, IQR: 48–71 cm/s; p-value:.054), whereas PbtO₂ increased significantly (baseline, median: 24, 95%CI: 19–31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24–33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged. Conclusion: In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO₂ increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD. Trial registration: clinicaltrials.gov (NCT03987139; 14 June 2019).