• H Ito, T Kinoshita, Y Tamura, I Yokoyama, and H Iida.
• Department of Radiology, Akita Research Institute of Brain and Blood Vessels, Akita, Japan. hito@akita-noken.go.jp
• Stroke. 1999 Aug 1; 30 (8): 1616-20.

Background And PurposeDipyridamole 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).MethodsIn each of 13 healthy subjects, CBF was measured using (15)O-labeled water and PET at rest and during hypercapnia, hypocapnia, and dipyridamole stress; corresponding CBF values were then compared.ResultsCBF values during dipyridamole stress were significantly lower than those measured at rest. The dipyridamole stress PaCO(2) was also significantly lower than the resting PaCO(2). The change in CBF during dipyridamole stress relative to PaCO(2) closely followed the relationship between CBF and PaCO(2) during hypocapnia.ConclusionsThese results indicate that the observed decrease in CBF during dipyridamole stress was caused by a decrease in PaCO(2) rather than by any direct action of dipyridamole on CBF. The decrease in PaCO(2) 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.

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