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Ventilation-induced pulmonary vasodilatation in lambs with congenital diaphragmatic hernia is modulated by nitric oxide.

Authors
Publication Date
Volume
34
Issue
7
Identifiers
DOI: 10.1080/01902140802221896
Keywords
  • Animals
  • Disease Models
  • Animal
  • Electric Stimulation
  • Enzyme Inhibitors/Pharmacology
  • Gestational Age
  • Hemodynamics
  • Hernia
  • Diaphragmatic/Congenital
  • Hernia
  • Diaphragmatic/Physiopathology
  • Lung/Blood Supply
  • Nitric Oxide/Metabolism
  • Nitric Oxide Synthase/Antagonists & Inhibitors
  • Nitric Oxide Synthase/Metabolism
  • Nitroarginine/Pharmacology
  • Pulmonary Circulation/Drug Effects
  • Respiration
  • Artificial
  • Sheep
  • Vascular Resistance
  • Vasodilation/Drug Effects
Disciplines
  • Design
  • Medicine

Abstract

Endogenous nitric oxide (NO) mediates pulmonary vasodilatation at birth, but inhaled NO fails to reduce pulmonary vascular resistance (PVR) in newborns with congenital diaphragmatic hernia (CDH). This study was designed to investigate the effects of ventilation, and the nature of its endogenous mediator, in fetal lambs with experimental CDH. Investigations at 138 days of gestation showed that ventilation markedly decreased PVR. Inhibition of NO synthesis reduced ventilation-induced pulmonary vasodilatation in vivo and increased in vitro isometric tension of vascular rings. Ventilation therefore reduces PVR at birth in lambs with CDH, and endogenous NO seems to contribute to this reduction.

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