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Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs

F Grimminger1, R Spriestersbach, N Weissmann

  • 1Department of Internal Medicine, Justus-Liebig University, Giessen, Germany.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 1, 1995
PubMed
Summary

Hypoxic pulmonary vasoconstriction in rabbit lungs involves nitric oxide (NO). Alveolar hypoxia reduces exhaled NO but not intravascular NO release, suggesting a complex regulatory role for NO.

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Area of Science:

  • Pulmonary Physiology
  • Cardiovascular Research
  • Nitric Oxide Biology

Background:

  • Pulmonary vasoconstriction is a critical response to hypoxia.
  • Nitric oxide (NO) is a key regulator of vascular tone.
  • The precise role of NO in hypoxic pulmonary vasoconstriction (HPV) remains incompletely understood.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) generation in hypoxic pulmonary vasoconstriction (HPV) in buffer-perfused rabbit lungs.
  • To differentiate between exhaled NO and intravascular NO release during HPV.

Main Methods:

  • Buffer-perfused rabbit lungs were used to measure exhaled NO via chemiluminescence.
  • Intravascular NO release was quantified by perfusate accumulation of nitrite, peroxynitrite, and nitrate (NOx).

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  • Alveolar hypoxia was induced, and pressor responses were measured. The effects of NG-monomethyl-L-arginine (L-NMMA) were assessed.

    • Main Results:

    • Baseline exhaled NO was 45.3 ± 4.1 ppb (1.8 ± 0.2 nmol/min); lung NOx release was 4.1 ± 0.4 nmol/min.
    • Alveolar hypoxia induced pressor responses and a sharp drop in exhaled NO, while perfusate NOx accumulation remained unchanged.
    • L-NMMA dose-dependently suppressed NO exhalation and amplified pressor responses to hypoxia, U-46619, and angiotensin II.

    Conclusions:

    • Baseline NO generation from sites accessible to the gaseous space decreases during alveolar hypoxia.
    • Intravascular NO release is unaffected by alveolar hypoxia.
    • Differential regulation of lung NO synthesis during hypoxia suggests a complex role in modulating HPV.