Inhaled Nitric Oxide Reverses Vascular and Respiratory Effects of ET-1 and PAF in Pigs
In anaesthetized paralysed, mechanically ventilated pigs, the vascular and respiratory effects of 80 ppm nitric oxide (NO) inhaled for 6 min were evaluated. To evoke different levels of smooth muscle contraction ET-1 or PAF, mediators involved in pulmonary disorders, were used. In control conditions...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000621 |
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| Summary: | In anaesthetized paralysed, mechanically ventilated pigs, the
vascular and respiratory effects of 80 ppm nitric oxide (NO) inhaled
for 6 min were evaluated. To evoke different levels of smooth
muscle contraction ET-1 or PAF, mediators involved in pulmonary
disorders, were used. In control conditions, inhaled NO caused
selective pulmonary vasodilatation without affecting respiratory
resistances. This pulmonary vascular activity influenced the
distensibility of the respiratory system and decreased inspiratory
work. ET-1 administration significantly increased pulmonary arterial
pressure and modestly changed mechanical properties of the
respiratory system, while PAF caused potent vasoconstriction and
bronchoconstriction associated with a marked change in
volume-pressure relationship. In both cases, the changes in vascular
and mechanical properties of the respiratory system increased
inspiratory work. The vascular and respiratory activities of inhaled
NO were correlated with preconstriction levels. The data show that
the combination of vascular and respiratory effects improves
pulmonary function, suggesting that inhalation of NO is a possible
therapeutic approach for obstructive and inflammatory pulmonary
diseases. |
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| ISSN: | 0962-9351 1466-1861 |