{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T05:46:33Z","timestamp":1772171193016,"version":"3.50.1"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1999,8]]},"abstract":"<jats:p><jats:italic>Background and Purpose<\/jats:italic>\u2014Dipyridamole 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).<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>\u2014In each of 13 healthy subjects, CBF was measured using<jats:sup>15<\/jats:sup>O-labeled water and PET at rest and during hypercapnia, hypocapnia, and dipyridamole stress; corresponding CBF values were then compared.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>\u2014CBF values during dipyridamole stress were significantly lower than those measured at rest. The dipyridamole stress Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>was also significantly lower than the resting Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>. The change in CBF during dipyridamole stress relative to Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>closely followed the relationship between CBF and Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>during hypocapnia.<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>\u2014These results indicate that the observed decrease in CBF during dipyridamole stress was caused by a decrease in Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>rather than by any direct action of dipyridamole on CBF. The decrease in Pa<jats:sc>co<\/jats:sc><jats:sub>2<\/jats:sub>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.<\/jats:p>","DOI":"10.1161\/01.str.30.8.1616","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:10:52Z","timestamp":1308341452000},"page":"1616-1620","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans"],"prefix":"10.1161","volume":"30","author":[{"given":"Hiroshi","family":"Ito","sequence":"first","affiliation":[{"name":"From the Departments of Radiology and Nuclear Medicine (H. Ito, T.K., H. 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