{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:13:14Z","timestamp":1761707594714,"version":"3.40.4"},"reference-count":11,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2003,1,1]],"date-time":"2003-01-01T00:00:00Z","timestamp":1041379200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2003,1,1]],"date-time":"2003-01-01T00:00:00Z","timestamp":1041379200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Vasc Res"],"published-print":{"date-parts":[[2003]]},"abstract":"The ability of an arteriole to conduct vasomotor responses along its length contributes to the control of organ perfusion. Sepsis, a systemic inflammatory response to infection, may compromise this control. We aimed to determine whether sepsis, induced by cecal ligation and perforation (CLP), reduces conducted vasoconstriction 24 h post-CLP. We locally stimulated mouse cremaster arterioles with KCl, measured the resulting local and the conducted constriction (500 \u00b5m upstream) and, based on these measurements, determined the communication ratio (CR<sub>500<\/sub>) as an index of the conducted response. Sepsis significantly reduced the CR<sub>500<\/sub> from 0.75 to 0.20. Based on a mathematical model, this reduction was predicted to have a significant impact on blood flow control. In septic mice, either a 1-hour washout of the cremaster muscle with physiological saline or a treatment of this muscle with the tyrosine kinase inhibitor PP-2 (100 n<i>M<\/i>) restored the CR<sub>500<\/sub> to the control level. Treatment of septic arterioles with the nitric oxide synthase inhibitor N<sup>\u03c9<\/sup>-nitro-<i>L<\/i>-arginine methyl ester (100 \u00b5<i>M<\/i>) partially restored the CR<sub>500<\/sub> from 0.2 to 0.4. In control mice, lipopolysaccharide (LPS; 10 \u00b5g\/ml) superfused over the cremaster muscle for 1 h reduced the CR<sub>500<\/sub>; the nitric oxide (NO) donor S-nitroso-N-acetyl-penicillamine (50 \u00b5<i>M<\/i>) also reduced the CR<sub>500<\/sub>. Thus, LPS and NO could be two factors mediating reduced conduction of vasoconstriction in sepsis. We conclude that sepsis reduces the KCl-induced conducted vasoconstriction in the mouse cremaster muscle by a tyrosine kinase- and nitric oxide- dependent mechanism.<\/jats:p>","DOI":"10.1159\/000070712","type":"journal-article","created":{"date-parts":[[2003,6,13]],"date-time":"2003-06-13T14:21:30Z","timestamp":1055514090000},"page":"149-158","source":"Crossref","is-referenced-by-count":28,"title":["Conducted Vasoconstriction Is Reduced in a Mouse Model of Sepsis"],"prefix":"10.1159","volume":"40","author":[{"given":"Darcy","family":"Lidington","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yves","family":"Ouellette","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fuyan","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karel","family":"Tyml","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2003,6,19]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1002\/1097-4652(200010)185:1<117::AID-JCP11>3.0.CO;2-7"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1159\/000064519"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-200201000-00010"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1999.2198"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0721843.x"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.8.4193"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1996.0001q.x"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1007\/s007950100008"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1161\/hq0102.104125"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1002\/1526-968X(200101)29:1<1::AID-GENE1000>3.0.CO;2-0"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1006\/cyto.1997.0287"}],"container-title":["Journal of Vascular Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/70712","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/70712","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T03:23:20Z","timestamp":1745465000000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000070712"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003]]},"references-count":11,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2003,4,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000070712","archive":["Portico"],"relation":{},"ISSN":["1018-1172","1423-0135"],"issn-type":[{"type":"print","value":"1018-1172"},{"type":"electronic","value":"1423-0135"}],"subject":[],"published":{"date-parts":[[2003]]}}}