{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T11:32:59Z","timestamp":1790854379763,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2002,10,3]],"date-time":"2002-10-03T00:00:00Z","timestamp":1033603200000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Anaesthesiol Scand"],"published-print":{"date-parts":[[2002,10]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Endotoxin (lipopolysaccharide, LPS) up\u2010regulates inducible nitric oxide synthase (iNOS) in blood vessels during septic shock. This promotes the production of nitric oxide (NO), leading to dilation of the vessels. The aim of the study was to investigate the effects of the LPS\u2010binding endogenous antibiotic bactericidal\/permeability\u2010increasing protein (BPI) on the action of LPS on the blood vessels wall and to identify possible influence on underlying NO\u2010related mechanisms.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> Isolated segments of rat thoracic aorta and cultured primary smooth muscle cells were incubated for 5\u201348\u2003h in the presence of the following combinations of compounds: (a) LPS; (b) interleukin\u20101\u03b2 (IL\u20101\u03b2); (c) BPI; (d) BPI\u2003+\u2003LPS; (e) BPI\u2003+\u2003IL\u20101\u03b2 or (f) neither BPI, LPS nor IL\u20101\u03b2 (control). After incubation of intact segments, we measured smooth muscle contraction in response to phenylephrine and accumulation of the NO end products nitrate and nitrite in surrounding medium. Western blot was used to assess the levels of inducible nitric oxide synthase (iNOS) in cultured cells.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> Both LPS and IL\u20101\u03b2 decreased contractility and increased NO production, as well as iNOS. Co\u2010incubation with BPI attenuated all the effects of LPS but only the effects of prolonged exposure to IL\u20101\u03b2 in cultured cells.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold> We conclude that BPI attenuates the LPS\u2010induced changes in vascular reactivity by inhibiting the expression of iNOS resulting in decreased NO formation and restored responsiveness to vasoconstrictors. The data suggest that BPI can prevent circulatory disturbances during Gram\u2010negative sepsis.<\/jats:p>","DOI":"10.1034\/j.1399-6576.2002.460909.x","type":"journal-article","created":{"date-parts":[[2003,3,10]],"date-time":"2003-03-10T09:50:52Z","timestamp":1047289852000},"page":"1111-1118","source":"Crossref","is-referenced-by-count":20,"title":["Bactericidal\/permeability\u2010increasing protein inhibits endotoxin\u2010induced vascular nitric oxide synthesis"],"prefix":"10.1111","volume":"46","author":[{"given":"C. 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