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Sökning: WFRF:(Hambraeus Jonzon Kristina) > (2000-2004) > Pulmonary Vasoconst...

  • Hambraeus-Jonzon, Kristina (författare)

Pulmonary Vasoconstriction during Regional Nitric Oxide Inhalation : Evidence of a Blood-borne Regulator of Nitric Oxide Synthase Activity

  • Artikel/kapitelEngelska2001

Förlag, utgivningsår, omfång ...

  • Ovid Technologies (Wolters Kluwer Health),2001
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-54872
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-54872URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:1945354URI
  • https://doi.org/10.1097/00000542-200107000-00020DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • BACKGROUND: Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect. METHODS: Nitric oxide concentration was measured in exhaled air (NO(E)), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [FIO2] = 0.05), with and without INO to HL (FIO2 = 0.8), and during cross-circulation of blood from pigs with and without INO. RESULTS: Left lower lobar hypoxia increased exhaled NO from the LLL (NO(E)LLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P < 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86] vs. 162 [96] pmol x g(-1) x min(-1), P < 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol x g(-1) x min(-1) (P < 0.01), and NO(E)LLL to 2.0 [0.8] ppb (P < 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NO(E)LLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P < 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol x g(-1) x min(-1) (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P < 0.05), but more so in hypoxic (P < 0.01) than in hyperoxic (P < 0.05) lung regions, resulting in a further redistribution (P < 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions. CONCLUSIONS: Inhaled nitric oxide downregulates endogenous NO production in other, predominantly hypoxic, lung regions. This distant effect is blood-mediated and causes vasoconstriction in lung regions that do not receive INO.

Ämnesord och genrebeteckningar

  • MEDICINE
  • MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Chen, LuniUppsala universitet,Institutionen för medicinska vetenskaper,Clinical Physiology (författare)
  • Freden, FilipUppsala universitet,Institutionen för kirurgiska vetenskaper,Anaesthesiology and Intensive Care (författare)
  • Wiklund, PeterKarolinska Institutet (författare)
  • Hedenstierna, GöranUppsala universitet,Institutionen för medicinska vetenskaper,Clinical Physiology (författare)
  • Uppsala universitetInstitutionen för medicinska vetenskaper (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Anesthesiology: Ovid Technologies (Wolters Kluwer Health)95:1, s. 102-1120003-30221528-1175

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