Nitric oxide synthase inhibition restores hypoxic pulmonary vasoconstriction in sepsis

Stefanie R. Fischer, Donald J. Deyo, Hans C. Bone, Roy Mcguire, Lillian D. Traber, Daniel L. Traber

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

Hypoxic pulmonary vasoconstriction (HPV) is inhibited by inhaled nitric oxide (NO) in healthy animals and is blunted in endotoxemia. We investigated whether the loss of HPV during sepsis could be reversed by NO synthase (NOS) inhibition. Hypoxic challeges were induced in intubated, awake sheep breathing 100% nitrogen to the left lung and 100% oxygen to the right lung. HPV was assessed as the decrease in left pulmonary blood flow during hypoxia, measured with an ultrasonic flow probe around the left pulmonary artery. Group I (n = 5) received carrier solutions and Groups II (n = 6) and III (n = 8) received an infusion containing Pseudomonas aeruginosa. After 24 h, Group III also received an infusion of 6.6mg kg h1 Nω-monomethyl-L-arginine (L- NMMA). After 24 h of sepsis, HPV decreased from 60 ± 9% in Group III to 27 ± 2% and 26 ± 4%, respectively. Group I showed no change in HPV. During infusion of L-NMMA, HPV increased to 38 ± 4%. Pulmonary shunt during hypoxia increased in Group III to 161 ± 10% of its baseline value, and decreased to 121 ± 11% during infusion of L-NMMA. We conclude that L-NMMA improves but does not restore HPV, indicating that other vasodilatatory mediators besides NO also influence HPV in pepsis.

Original languageEnglish (US)
Pages (from-to)833-839
Number of pages7
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume156
Issue number3 I
DOIs
StatePublished - Jan 1 1997

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

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