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Background: Induced hypertension is used clinically to increase cerebral blood flow (CBF) in conditions such as vasospasm after subarachnoid hemorrhage. However, increased blood pressure also raises pulsatile force. Cerebrovascular compliance plays a key role in buffering flow dynamics and protecting the microcirculation, but whether it adapts to elevated pressure remains unclear. This study assessed the response of compliant cerebral arteries to induced hypertension in healthy adults using phase-contrast magnetic resonance imaging (PCMRI) and two compliance models: a two-element Windkessel (CWK) and a simplified model (CVP), representing the extremes of pulsatility transmission at the capillary level.

Methods: Eighteen healthy adults (median age: 34 years; 9 females) underwent PCMRI at baseline and after increasing mean arterial pressure by 20% using norepinephrine (NE) infusion. PCMRI quantified CBF and cardiac output, while cerebrovascular resistance and systemic vascular resistance were derived. Flow waveforms were combined with blood pressure to assess CWK and CVP in CBF, ascending/descending aorta, and external carotid arteries, while corresponding regions of interest were used to calculate cross-sectional flow areas. Data are reported as median (interquartile range).

Results: NE increased cerebrovascular compliance significantly; CWK by 110% (56% to 163%; P=0.001) and CVP by 11% (−2% to 26%; P=0.018). CWK increased in the external carotid artery by 12% (1% to 32%; P=0.037) but did not change in the ascending or descending aorta. CVP decreased in the descending aorta by 5% (-11% to 2%; P=0.028), with no changes in the ascending aorta or external carotid artery. Cross-sectional area of cerebral arteries contributing to CBF decreased by 5% (-17% to -3%; P=0.033), while the ascending and descending aorta areas increased by 7% (4% to 11%; P=0.012) and 8% (6% to 11%; P<0.001), respectively.

Conclusion: Cerebral arteries enhanced their compliance during NE-induced hypertension, unlike systemic arteries, regardless of the assumed degree of pulsatility transmission.

Background: Maintaining cerebral perfusion during anesthesia and intensive care is critical, yet the relationship between mean arterial pressure (MAP) and cerebral blood flow (CBF) remains poorly defined. In patients with aneurysmal subarachnoid hemorrhage (aSAH), pharmacologically induced hypertension is commonly applied to support cerebral perfusion, but its effects are uncertain.

Methods: This protocol describes two parallel clinical studies using identical methodology. The first study population includes adults undergoing elective general anesthesia (MAP-ANE), and the second comprises sedated intensive care patients with aSAH (MAP-SAH). In both study populations, MAP will be increased stepwise with norepinephrine (NE) infusion under continuous invasive blood pressure monitoring, and CBF measured with phase-contrast MRI (PCMRI) and arterial spin labeling (ASL), while near-infrared spectroscopy (NIRS) will be performed in parallel to evaluate its validity as a surrogate marker. The primary outcome is the change in total CBF between baseline and elevated MAP, directly testing whether induced hypertension increases CBF. Secondary outcomes include ASL perfusion changes, the slope of the MAP–CBF relationship, systemic–cerebral hemodynamic correlations, and NIRS responses.

Expected impact: These studies test the hypothesis that pharmacological MAP augmentation does not predictably increase CBF. By combining quantitative MRI with invasive monitoring, it aims to clarify MAP–CBF interactions, define the physiological basis of induced hypertension, and assess whether NIRS can serve as a clinically useful proxy. Findings are expected to inform safer and more individualized blood pressure management in perioperative and neurocritical care.