Non-technical summary Two mechanisms control brain blood flow by changing blood vessel diameter: autoregulation maintains flow in the face of perfusion pressure changes, and brain metabolism adjusts flow to meet metabolic requirements. Brain blood vessel reactivity to CO 2 and O 2 is an important component of the latter. We used a specialised rebreathing technique to change CO 2 over a wide range at constant O 2 , estimating brain blood flow responses from measurements of middle cerebral artery flow velocity. We found that below a threshold CO 2 , blood pressure was unchanged, but blood flow increased in response to CO 2 . This response had a sigmoidal shape, centred at a CO 2 close to resting. Above the threshold, both blood flow and pressure increased with CO 2 . We concluded that this method measures the brain blood flow reactivity to CO 2 without the confounding influence of blood pressure changes. The results obtained contribute to our understanding of brain blood flow regulation.Abstract Carbon dioxide (CO 2 ) increases cerebral blood flow and arterial blood pressure. Cerebral blood flow increases not only due to the vasodilating effect of CO 2 but also because of the increased perfusion pressure after autoregulation is exhausted. Our objective was to measure the responses of both middle cerebral artery velocity (MCAv) and mean arterial blood pressure (MAP) to CO 2 in human subjects using Duffin-type isoxic rebreathing tests. Comparisons of isoxic hyperoxic with isoxic hypoxic tests enabled the effect of oxygen tension to be determined. During rebreathing the MCAv response to CO 2 was sigmoidal below a discernible threshold CO 2 tension, increasing from a hypocapnic minimum to a hypercapnic maximum. In most subjects this threshold corresponded with the CO 2 tension at which MAP began to increase. Above this threshold both MCAv and MAP increased linearly with CO 2 tension. The sigmoidal MCAv response was centred at a CO 2 tension close to normal resting values (overall mean 36 mmHg). While hypoxia increased the hypercapnic maximum percentage increase in MCAv with CO 2 (overall means from 76.5 to 108%) it did not affect other sigmoid parameters. Hypoxia also did not alter the supra-threshold MCAv and MAP responses to CO 2 (overall mean slopes 5.5% mmHg −1 and 2.1 mmHg mmHg −1 , respectively), but did reduce the threshold (overall means from 51.5 to 46.8 mmHg). We concluded that in the MCAv response range below the threshold for the increase of MAP with CO 2 , the MCAv measurement reflects vascular reactivity to CO 2 alone at a constant MAP.

BACKGROUND AND PURPOSE: BOLD MR imaging combined with a technique for precision control of end-tidal pCO 2 was used to produce quantitative maps of CVR in patients with Moyamoya disease. The technique was validated against measures of disease severity by using conventional angiography; it then was used to study the relationship between CVR, vascular steal, and disease severity.

Present methods for measuring red cell volume are based on the dilution of radioactively labelled cells. This precludes the investigation in neonates and pregnant women. We present a simple method for labelling red cells with biotin. These cells may be injected intravenously and subsequently detected using streptavidin-FITC and flow-cytometry. A comparison of the red cell volume estimated using both 51Cr and biotin labelled cells in 19 patients showed no consistent clinically significant difference between the two. This novel label appears to allow red volume to be reliably estimated without using radioactivity.

Accounting for normal test-to-test differences in cerebrovascular reactivity enables the assessment of significant changes in disease status (stability, progression, or regression) in patients with time.