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Effect of NO synthase inhibition on cardiovascular and pulmonary disfunction in a porcine short-term model of endotoxic shock (Articolo in rivista)
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- Effect of NO synthase inhibition on cardiovascular and pulmonary disfunction in a porcine short-term model of endotoxic shock (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
Albertini M., Lafortuna C.L., Clement M.G., Radice S., Hussain S.N.A. (2002)
Effect of NO synthase inhibition on cardiovascular and pulmonary disfunction in a porcine short-term model of endotoxic shock
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Albertini M., Lafortuna C.L., Clement M.G., Radice S., Hussain S.N.A. (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Note
- ISI Web of Science (WOS) (literal)
- Titolo
- Effect of NO synthase inhibition on cardiovascular and pulmonary disfunction in a porcine short-term model of endotoxic shock (literal)
- Abstract
- In a porcine model of endotoxic shock, we evaluated the
circulatoryand respiratoryeffects of NO synthase (NOS)
blockade.Twenty anaesthetised pigs were divided into three groups
and studied for 240min after induction of endotoxic shock with
lipopolysaccharides of Escherichia coli (LPS). After180min of
endotoxic shock, one group (n = 6) received aminoguanidine, another
group (n=6) received NG-nitro-L-argininemethyl ester (L-NAME) and a
third group (n = 8) received onlyL PS. A sham group (n = 3) was also
studied. LPS decreased systemic arterial pressure and cardiac
output (CO) and increased mean pulmonary arterial pressure
(MPAP), pulmonary vascular resistance (PVR) and heart
rate.Significant changes were also observed in compliance (-18.4%)
and resistance (+33.6%) of the respiratory system. Aminoguanidine
did not modify LPS-dependent effects,
while, after L-NAME, a significant increase in MPAP,PVR and SVR
and a decrease in CO were observed. In conclusion,
aminoguanidine does not play a significant cardiocirculatory and
pulmonary role in the short-term dysfunction of endotoxic shock,
while L-NAME has a detrimental effect on haemodynamics,
suggesting a protective role of constitutive NOproduction at vascular
level during the early stages of endotoxaemia. 2002 Elsevier Science
Ltd.All rights reserved. (literal)
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