z-logo
open-access-imgOpen Access
Inhaled Nitric Oxide Counterbalances ET‐1 Dependent Pulmonary Hypertension and Bronchoconstriction in the Pig
Author(s) -
M.G. Clement,
Milena Dimori
Publication year - 1994
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/s0962935194000165
Subject(s) - bronchoconstriction , nitric oxide , airway resistance , respiratory system , anesthesia , medicine , inhalation , vascular resistance , exhaled nitric oxide , pulmonary hypertension , bronchodilator , endothelin 1 , hemodynamics , pharmacology , cardiology , airway , asthma , receptor
In anaesthetized, paralysed, ventilated pigs the ability of inhaled nitric oxide (80 ppm in 0(2)) to reduce the haemodynamic and respiratory effects of endothelin-1 administration (200 pmol/kg, i.v.) was evaluated. The mechanical properties of the respiratory system were evaluated by the rapid airway occlusion technique. The overall respiratory resistance, the interrupter resistance and the additional resistance that reflects the viscoelastic properties of tissues and the inequality of the time constant within the system were also evaluated. The results show that inhaled nitric oxide can act as a selective pulmonary vasodilator and as a bronchodilator to counteract the vasoconstrictor and bronchoconstrictor activity of endothelin-1. In the pig, nitric oxide inhaled at 80 ppm for 6 mitt reduced the changes in respiratory-, interrupter- and additional resistance due to endothelin-1 administration without significantly changing the static and dynamic elastance of the respiratory system.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom