1. ¹Department of Radiology and Nuclear Medicine, Akita Research Institute of Brain and Blood Vessels, Akita, Japan
2. ²Department of Nuclear Medicine and Radiology, Division of Brain Sciences, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan

Correspondence: Dr H Ito, Department of Nuclear Medicine and Radiology, Division of Brain Sciences, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-Machi, Aoba-Ku, Sendai 980-8575, Japan. E-mail: hito@idac.tohoku.ac.jp

Received 31 August 2004; Revised 8 October 2004; Accepted 19 October 2004; Published online 16 February 2005.

Abstract

Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume (V_a) and CBV during hypercapnia and hypocapnia were investigated in humans using PET with H₂¹⁵O and ¹¹CO. Arterial blood volume was determined from H₂¹⁵O PET data by means of a two-compartment model that takes V_a into account. Baseline CBV and values during hypercapnia and hypocapnia in the cerebral cortex were 0.0340.003, 0.0380.003, and 0.0310.003 mL/mL (means.d.), respectively. Baseline V_a and values during hypercapnia and hypocapnia were 0.0150.003, 0.0250.011, and 0.0070.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO₂, and V_a changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (=CBV-V_a). This indicates that changes in CBV during hypercapnia and hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.