{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T09:36:13Z","timestamp":1781602573016,"version":"3.54.5"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1996,11]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            The aim of this study was to compare the effect of vasodilative stimuli for the measurement of cerebrovascular reactivity obtained by acetazolamide and hypercapnia in patients with chronic occlusive major cerebral artery disease.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            We examined 24 patients with unilateral occlusive lesions of a major cerebral artery using the\n            <jats:sup>133<\/jats:sup>\n            Xe inhalation technique and single-photon emission CT. Regional cerebral blood flow (CBF) was measured during a resting state, during inhalation of 5% CO\n            <jats:sub>2<\/jats:sub>\n            , and 15 minutes after the administration of acetazolamide consecutively in the same patients. Normative values of resting CBF and acetazolamide reactivity were obtained in 21 normal subjects.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            All patients with the exception of 1 showed an increase in CBF during hypercapnia ipsilateral to the occlusive lesion. Ipsilateral acetazolamide reactivity was preserved in 13 patients. Conversely, 11 patients showed an absent response or paradoxical CBF reduction. Ipsilateral CO\n            <jats:sub>2<\/jats:sub>\n            reactivity did not correlate with acetazolamide reactivity when all 24 patients were considered. However, there was a significant correlation between acetazolamide and CO\n            <jats:sub>2<\/jats:sub>\n            in the 13 patients who showed preserved acetazolamide reactivity (\n            <jats:italic>r<\/jats:italic>\n            =.60,\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). No significant correlation was present in the remaining 11 patients with reduced acetazolamide reactivity. Although significant blood pressure augmentation was observed in hypercapnia, we could not find a correlation between change of blood pressure and CO\n            <jats:sub>2<\/jats:sub>\n            reactivity.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            Acetazolamide identified patients with reduced vasomotor reactivity who appeared to have preserved CO\n            <jats:sub>2<\/jats:sub>\n            reactivity. Acetazolamide testing may be useful in the assessment of cerebral hemodynamics. However, further investigations are necessary to assess the clinical utility of these tests.\n          <\/jats:p>","DOI":"10.1161\/01.str.27.11.2052","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:10:52Z","timestamp":1308341452000},"page":"2052-2058","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":34,"title":["Dissociation of Vasoreactivity to Acetazolamide and Hypercapnia"],"prefix":"10.1161","volume":"27","author":[{"given":"Ken","family":"Kazumata","sequence":"first","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naruhiko","family":"Tanaka","sequence":"additional","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuya","family":"Ishikawa","sequence":"additional","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoshi","family":"Kuroda","sequence":"additional","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyohiro","family":"Houkin","sequence":"additional","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenji","family":"Mitsumori","sequence":"additional","affiliation":[{"name":"the Department of Neurosurgery, Hokkaido University School of Medicine, and Hokkaido Neurosurgical Memorial Hospital (K.M.), Sapporo, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1002\/bjs.1800720506"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.3171\/jns.1988.69.1.0024"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.20.11.1127"},{"key":"e_1_3_2_4_2","first-page":"310","volume":"11","year":"1984","unstructured":"Gibbs JM, Wise RJS, Leenders KL, Jones T. 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