Document Detail


Endotoxemic pulmonary hypertension is largely mediated by endothelin-induced venous constriction.
MedLine Citation:
PMID:  18214440     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To analyze the effect of endothelin-1 on pulmonary arterial and venous contractile force in vitro and on up- and downstream pulmonary vascular resistance in vivo under sham and endotoxemic conditions in pigs. MATERIALS AND METHODS: In vitro: paired preparations of pulmonary arteries and veins were mounted in a myograph (n=13) for measurements of contractile responses to increasing concentrations of phenylephrine, endothelin-1, and sarafotoxin (endothelin receptor type B agonist). In vivo: 20 pigs were anesthetized, mechanically ventilated, and subjected to phenylephrine (reference substance), endothelin-1, sarafotoxin, endotoxin, and tezosentan (dual endothelin receptor antagonist). Hemodynamic and gas-exchange variables were monitored. Pulmonary capillary pressure, used for calculation of upstream and downstream vascular resistance, was assessed by the pulmonary vascular occlusion technique. MEASUREMENTS AND RESULTS: Pulmonary veins were more sensitive than arteries to endothelin-1 both in vitro and in vivo. This difference was more pronounced with sarafotoxin, where almost no arterial effects were noted. In vivo and in vitro exposure to phenylephrine resulted in selective arterial constriction. Endotoxin infusion resulted in pulmonary hypertension with a clear downstream dominance. The latter changes including the increase in capillary pressure were totally abolished by intervention with the dual endothelin receptor antagonist tezosentan. CONCLUSIONS: The endothelin system is extensively involved in endotoxemic pulmonary venous hypertension, an effect possibly mediated by the endothelin B receptor.
Authors:
Patrik Rossi; Björn Persson; Piet J M Boels; Anders Arner; Eddie Weitzberg; Anders Oldner
Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-24
Journal Detail:
Title:  Intensive care medicine     Volume:  34     ISSN:  0342-4642     ISO Abbreviation:  Intensive Care Med     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-04-18     Completed Date:  2008-10-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7704851     Medline TA:  Intensive Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  873-80     Citation Subset:  IM    
Affiliation:
Section of Anesthesiology and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet Solna, 17176 Stockholm, Sweden. patrik.rossi@ki.se
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MeSH Terms
Descriptor/Qualifier:
Animals
Ciprofloxacin / analogs & derivatives
Endothelin-1 / metabolism*
Female
Hypertension, Pulmonary / metabolism,  physiopathology*
Lipopolysaccharides
Lung / blood supply*
Male
Pyridines / pharmacology
Respiratory Distress Syndrome, Adult / metabolism,  physiopathology*
Sepsis / metabolism,  physiopathology*
Swine
Tetrazoles / pharmacology
Vascular Resistance / drug effects
Vasoconstriction / drug effects
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Lipopolysaccharides; 0/Pyridines; 0/Tetrazoles; 0/Vasodilator Agents; 0/tezosentan; 85721-33-1/Ciprofloxacin; 98105-99-8/sarafloxacin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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