{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T21:31:23Z","timestamp":1776893483449,"version":"3.51.2"},"reference-count":22,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1995,11]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            Neuropsychological deficits after cardiac surgery are attributed to the side effects of cardiopulmonary bypass (CPB). To protect the brain from ischemic damage, the influences of temperature, blood pressure, blood gases, acid-base status, and hemodilution on cerebral oxygenation have to be elucidated and quantified.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            Forty-one consecutive patients were investigated during cardiac surgery while on CPB. Operative management included moderate hypothermia of 26\u00b0C and the alpha-stat pH management. With near-infrared spectrophotometry, changes in oxygenated hemoglobin (Hb\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            , representing oxygen delivery) and oxidized cytochrome a,a3 (Ct\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            , cellular oxygenation) in brain tissue were obtained noninvasively. In addition, venous saturation of the brain was measured via a catheter in the jugular bulb (S\n            <jats:sub>BJ<\/jats:sub>\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            ). The influence of operative management parameters on cerebral oxygenation was calculated by univariate and multiple regression analyses.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            Before and after CPB there was no significant multivariate determinant of cerebral oxygenation. During CPB, Hb\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            depended solely on P\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01;\n            <jats:italic>r<\/jats:italic>\n            =.89). Ct\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            was determined by pH (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), esophageal temperature (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), P\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), and Hb (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01). These parameters explained nearly all changes of the cytochrome measurements during CPB (\n            <jats:italic>r<\/jats:italic>\n            =.99). Arterial P\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) and pH (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) influenced brain venous oxygen saturation (S\n            <jats:sub>BJ<\/jats:sub>\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            ;\n            <jats:italic>r<\/jats:italic>\n            =.98).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            Cerebral oxygenation is autoregulated during cardiac surgery before and after CPB. During CPB, Hb, temperature, pH, and P\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            determine at least 85% of all changes in cerebral oxygenation. The main causes of impaired cerebral oxygenation are the decrease in Hb with hemodilution, vasoconstriction due to hypocapnia, and the leftward shift of the Hb binding curve in alkalosis and hypothermia.\n          <\/jats:p>","DOI":"10.1161\/01.cir.92.9.327","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"327-333","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":68,"title":["Determinants of Cerebral Oxygenation During Cardiac Surgery"],"prefix":"10.1161","volume":"92","author":[{"given":"Georg","family":"Nollert","sequence":"first","affiliation":[{"name":"From the Department of Cardiac Surgery and Institute for Anesthesiology (P.T.-P.), Klinikum Gro\u00dfhadern, University of Munich, Munich, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrick","family":"Mo\u0308hnle","sequence":"additional","affiliation":[{"name":"From the Department of Cardiac Surgery and Institute for Anesthesiology (P.T.-P.), Klinikum Gro\u00dfhadern, University of Munich, Munich, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Tassani-Prell","sequence":"additional","affiliation":[{"name":"From the Department of Cardiac Surgery and Institute for Anesthesiology (P.T.-P.), Klinikum Gro\u00dfhadern, University of Munich, Munich, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruno","family":"Reichart","sequence":"additional","affiliation":[{"name":"From the Department of Cardiac Surgery and Institute for Anesthesiology (P.T.-P.), Klinikum Gro\u00dfhadern, University of Munich, Munich, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.18.4.3496690"},{"key":"e_1_3_1_2_2","first-page":"816","volume":"1","year":"1984","unstructured":"Henriksen L. 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Cerebral perfusion and metabolism during profound hypothermia in children. 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