{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T11:46:00Z","timestamp":1767008760146},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1997,2]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            Near-infrared spectroscopy (NIRS) derives information about the concentrations of oxyhemoglobin (HbO\n            <jats:sub>2<\/jats:sub>\n            ) and deoxyhemoglobin (Hb) from measurements of light attenuation caused by these chromophores. The aim of this study was to assess NIRS as a tool for testing CO\n            <jats:sub>2<\/jats:sub>\n            reactivity in patients with carotid artery disease.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            One hundred patients with symptomatic carotid occlusive disease were examined (age range, 44 to 83 years). The severity of stenosis ranged from 30% to 100% (median, 80%) on the ipsilateral side and 0% to 100% (median, 30%) on the contralateral side. Monitored parameters included transcranial Doppler flow velocity, changes in concentration of HbO\n            <jats:sub>2<\/jats:sub>\n            and Hb, cutaneous laser-Doppler blood flow, end-tidal CO\n            <jats:sub>2<\/jats:sub>\n            , arterial blood pressure, and arterial oxygen saturation. Hypercapnia was induced with the use of a 5% CO\n            <jats:sub>2<\/jats:sub>\n            \/air mixture for inhalation. To estimate the contribution of skin flow to NIRS during reactivity testing, the superficial temporal artery was compressed, and the NIRS changes in response to the fall in laser-Doppler blood flow were recorded. Finally, reproducibility of reactivity testing was assessed in 10 patients who were subjected to repeated examinations over 3 days.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            Flow velocity\u2013 and HbO\n            <jats:sub>2<\/jats:sub>\n            -derived reactivity values were related to the severity of the stenosis (\n            <jats:italic>P<\/jats:italic>\n            =.0001 and\n            <jats:italic>P<\/jats:italic>\n            =.017, respectively). The correlation between the two reactivity modalities was significant (\n            <jats:italic>r<\/jats:italic>\n            =.49,\n            <jats:italic>P<\/jats:italic>\n            &lt;.000001). The median estimated contribution of skin flow to NIRS changes was 15.8%. Another variable affecting HbO\n            <jats:sub>2<\/jats:sub>\n            signal changes during the CO\n            <jats:sub>2<\/jats:sub>\n            challenge was arterial blood pressure (\n            <jats:italic>P<\/jats:italic>\n            =.025). Reproducibility of HbO\n            <jats:sub>2<\/jats:sub>\n            reactivity was similar to flow velocity reactivity (14.3% and 18.6% variation, respectively).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            NIRS shows potential as an alternative technique for testing CO\n            <jats:sub>2<\/jats:sub>\n            reactivity in patients with carotid disease provided that conditions are carefully controlled. Marked changes in arterial blood pressure may render the NIRS reactivity indices unreliable, and the contribution from extracranial tissue must be taken into account when significant.\n          <\/jats:p>","DOI":"10.1161\/01.str.28.2.331","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"331-338","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":72,"title":["Clinical Evaluation of Near-Infrared Spectroscopy for Testing Cerebrovascular Reactivity in Patients With Carotid Artery Disease"],"prefix":"10.1161","volume":"28","author":[{"given":"Peter","family":"Smielewski","sequence":"first","affiliation":[{"name":"the Medical Research Council Cambridge Center for Brain Repair and Academic Neurosurgical Unit, Addenbrooke's Hospital, University of Cambridge (UK)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marek","family":"Czosnyka","sequence":"additional","affiliation":[{"name":"the Medical Research Council Cambridge Center for Brain Repair and Academic Neurosurgical Unit, Addenbrooke's Hospital, University of Cambridge (UK)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John D.","family":"Pickard","sequence":"additional","affiliation":[{"name":"the Medical Research Council Cambridge Center for Brain Repair and Academic Neurosurgical Unit, Addenbrooke's Hospital, University of Cambridge (UK)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Kirkpatrick","sequence":"additional","affiliation":[{"name":"the Medical Research Council Cambridge Center for Brain Repair and Academic Neurosurgical Unit, Addenbrooke's Hospital, University of Cambridge (UK)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"74","volume":"59","year":"1993","unstructured":"Elwell CE, Owen-Reece H, Cope M, Wyatt JS, Edwards AD, Delpy DT, Reynolds EO. 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