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(Stroke. 1999;30:1616-1620.)
© 1999 American Heart Association, Inc.

Original Contributions

Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans

A PET Study

Hiroshi Ito, MD, PhD; Toshibumi Kinoshita, MD, PhD; Yoshikazu Tamura, MD, PhD; Ikuo Yokoyama, MD, PhD Hidehiro Iida, DSc, PhD

From the Departments of Radiology and Nuclear Medicine (H. Ito, T.K., H. Iida) and Internal Medicine (Y.T.), Akita Research Institute of Brain and Blood Vessels, Akita, Japan, and the Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine (I.Y.), Tokyo, Japan.

Correspondence and reprint requests to Hiroshi Ito, MD, Department of Radiology and Nuclear Medicine, Akita Research Institute of Brain and Blood Vessels, 6-10 Senshu-kubota-machi, Akita City, Akita 010-0874, Japan. E-mail hito{at}akita-noken.go.jp

Background and Purpose—Dipyridamole increases the concentration of circulating adenosine, which is a potent vasodilator, by inhibition of uptake of adenosine into the erythrocytes, and hence produces coronary vasodilation. However, the effects of dipyridamole on cerebral circulation is not pronounced. This study investigates the effects of intravenous dipyridamole on cerebral blood flow (CBF) in humans with use of positron emission tomography (PET).

Methods—In each of 13 healthy subjects, CBF was measured using ¹⁵O-labeled water and PET at rest and during hypercapnia, hypocapnia, and dipyridamole stress; corresponding CBF values were then compared.

Results—CBF values during dipyridamole stress were significantly lower than those measured at rest. The dipyridamole stress PaCO₂ was also significantly lower than the resting PaCO₂. The change in CBF during dipyridamole stress relative to PaCO₂ closely followed the relationship between CBF and PaCO₂ during hypocapnia.

Conclusions—These results indicate that the observed decrease in CBF during dipyridamole stress was caused by a decrease in PaCO₂ rather than by any direct action of dipyridamole on CBF. The decrease in PaCO₂ during dipyridamole stress was most likely due to hyperventilation, which was a side effect of adenosine. These results support the hypothesis that circulating adenosine is largely prevented from binding to adenosine receptors of cerebral vessels by the blood-brain barrier.

Key Words: carbon dioxide • cerebral blood flow • dipyridamole • tomography, emission computed