{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T06:02:18Z","timestamp":1789365738989,"version":"build-2803163510"},"reference-count":27,"publisher":"Springer Science and Business Media LLC","issue":"6","license":[{"start":{"date-parts":[[2007,11,28]],"date-time":"2007-11-28T00:00:00Z","timestamp":1196208000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"},{"start":{"date-parts":[[2007,11,28]],"date-time":"2007-11-28T00:00:00Z","timestamp":1196208000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Crit Care"],"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                        <jats:title>Background<\/jats:title>\n                        <jats:p>Most patients with sepsis develop potentially irreversible cerebral dysfunctions. It is yet not clear whether cerebral haemodynamics are altered in these sepsis patients at all, and to what extent. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>After approval of the institutional ethics committee, 10 mechanically ventilated patients with sepsis syndrome and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure by 0.93 \u00b1 0.7 kPa iu by ypervent ilation. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A <jats:italic>t<\/jats:italic> test for matched pairs was used for statistical analysis (<jats:italic>P<\/jats:italic> &lt; 0.05).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>During stable mean arterial pressure and cardiac index, reduction of the arterial carbon dioxide partial pressure led to a significant increase of the capillary closing pressure from 25 \u00b1 11 mmHg to 39 \u00b1 15 mmHg (<jats:italic>P<\/jats:italic> &lt; 0.001), with a consecutive decrease of blood flow velocity in the middle cerebral artery of 21.8 \u00b1 4.8%\/kPa (<jats:italic>P<\/jats:italic> &lt; 0.001), of cerebral blood flow from 64 \u00b1 29 ml\/100 g\/min to 39 \u00b1 15 ml\/100 g\/min (<jats:italic>P<\/jats:italic> &lt; 0.001) and of jugular venous oxygen saturation from 75 \u00b1 8% to 67 \u00b1 14% (<jats:italic>P<\/jats:italic> &lt; 0.01).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusion<\/jats:title>\n                        <jats:p>In contrast to other experimental and clinical data, we observed no pathological findings in the investigated parameters of cerebral perfusion and oxygenation.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/cc6185","type":"journal-article","created":{"date-parts":[[2007,11,29]],"date-time":"2007-11-29T07:13:20Z","timestamp":1196320400000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome"],"prefix":"10.1186","volume":"11","author":[{"given":"Christof","family":"Thees","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Kaiser","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Scholz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Semmler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael T","family":"Heneka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georg","family":"Baumgarten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Hoeft","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Putensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2007,11,28]]},"reference":[{"key":"5609_CR1","first-page":"297","volume":"13","author":"GB Young","year":"1990","unstructured":"Young GB, Bolton CF, Austin TW, Archibald YM, Gonder J, Wells GA: The encephalopathy associated with septic illness.\n                           Clin Invest Med 1990, 13: 297-304.","journal-title":"Clin Invest Med"},{"key":"5609_CR2","doi-asserted-by":"publisher","first-page":"294","DOI":"10.1007\/s00101-003-0496-9","volume":"52","author":"V Eggers","year":"2003","unstructured":"Eggers V, Schilling A, Kox WJ, Spies C: Septic encephalopathy. 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