Am. J. Respir. Crit. Care Med., Vol 149, No. 3, Mar 1994, 744-750.
Vagal stimulation induces increased pulmonary vascular permeability in guinea pig
S Liu, HP Kuo, MN Sheppard, PJ Barnes and TW Evans
Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.
The effects of vagal stimulation on pulmonary vascular permeability were
studied in guinea pigs in vivo using 125I-labeled albumin as a marker of
plasma extravasation. Bilateral vagus nerve stimulation (NS) significantly
increased the plasma leakage index in both parenchyma and tracheobronchial
tissues. The NS-induced plasma leakage in the parenchyma was unaffected by
the alpha-adrenoceptor antagonist phentolamine, the muscarinic receptor
antagonist atropine, the ganglionic blocker hexamethonium, or pretreatment
with 6- hydroxydopamine or capsaicin, but it was significantly potentiated
by the beta-adrenoceptor antagonist propranolol. NS-induced
tracheobronchial vascular leakage was markedly inhibited by pretreatment
with atropine, hexamethonium, or capsaicin, although it was unaffected by
pretreatment with phentolamine, propranolol, or 6- hydroxydopamine. By
itself, NG-nitro L-arginine methyl ester (L-NAME), an inhibitor of nitric
oxide (NO) synthase, had no effect on pulmonary vascular leakage, but it
significantly enhanced the NS-induced plasma leakage to parenchyma in a
dose-related and L-arginine-reversible manner. Elevation of blood pressure
to a similar extent as that induced by L-NAME by a phenylephrine infusion
had no significant effect on the increased plasma leakage induced by NS.
These results suggest that vagal stimulation increases plasma extravasation
in lung parenchyma through the release of unidentified transmitter(s) in a
process that is modulated by endogenous NO and catecholamines (via
activation of beta- adrenoceptors), and that different mechanisms are
involved in the vagally induced plasma extravasation in the pulmonary and
tracheobronchial vascular beds.
