Using position emission tomography (PET) and equilibrium imaging with oxygen-15 labelled gases, the cerebral blood flow (CBF), blood volume (CBV), oxygen extraction fraction (OEF) and oxygen consumption rate (CMRO2) were measured in multiple regions of interest over the cerebral cortex of 5 control subjects, 4 patients with strictly unilateral longstanding carotid artery occlusion, 1 patient with middle cerebral artery embolic stroke in the acute stage, and 4 patients with subcortical stroke and no cervical arterial disease. In each control subject, the regional CBV was linearly and positively correlated with both CBF and CMRO2, while the local mean transit time (t = CBV/CBF) was uniformly distributed, reflecting the local adaptation of both the vascular tone and the capillary density to the metabolic demand at constant cerebral perfusion pressure that characterizes the normal brain. In patients with subcortical stroke, cortical blood volume was reduced in proportion to the matched reduction in CBF and CMRO2, suggesting that the metabolic depression resulting from cortical deafferentation increases the resting tone of pial vessels. Unilateral carotid occlusion induced larger CBV and t, and steeper slopes of the CBV-CBF relationship, particularly on the occluded but also on the patent side. The assessment of the local cerebral perfusion pressure (CPP) as judged by the ratio CBF/CBV in 3 patients with focally raised OEF and preserved or reduced CMRO2, allowed the demonstration in multiple cerebral regions of single patients of two well-known physiological phenomena: the autoregulation of CBF, followed by the rise of the OEF as local CPP falls further. In addition, the depression of CMRO2 in the ischaemic cortex was associated with a trend for CBV to return towards normal values, compared with the maximally elevated CBV found in oligaemic but metabolically normal areas. This suggests that a process of metabolic vasoconstriction may participate, among other factors, in the vascular collapse that occurs, and would serve to regenerate some haemodynamic reserve, at very low CPP levels.