ArticleIntensive care medicine1998
The role of endothelin-1 as a mediator of the pressure response after air embolism in blood perfused lungs.
Article in Intensive care medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 31 citations in OpenAlex.
- Endothelin ETA receptors predominate in chronic thromboembolic pulmonary hypertension.Life sciences · 2016Article
- Gas exchange and pulmonary hypertension following acute pulmonary thromboembolism: has the emperor got some new clothes yet?Pulmonary circulation · 2014Review
- Effects of aspirin on the expression of nuclear factor-κB in a rat model of acute pulmonary embolism.World journal of emergency medicine · 2014Article
- Increase in exhaled nitric oxide and protective role of the nitric oxide system in experimental pulmonary embolism.British journal of pharmacology · 2007Article
- Estimation of endothelin-mediated vasoconstriction in acute pulmonary thromboembolism.Pulmonary circulationArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIt is well known that lung embolism is associated with an increase in pulmonary vascular resistance. Since the mechanisms of pulmonary vascular reactions during embolism are still unclear, the aim of this study was to investigate the potential involvement of endothelin-1 (ET-1) and thromboxane A2 (TXA2) as mediators of the pulmonary artery pressure (PAP) increase after embolism using the selective ETA receptor antagonist LU135252 [1], the ETB receptor antagonist BQ788 [2], and the cyclooxygenase inhibitor diclofenac.
designProspective experimental study in rabbits.
settingExperimental laboratory in a university teaching hospital. SUBJECTS: 36 adult rabbits of either sex.
interventionsThe experiments were performed in 36 isolated and ventilated rabbit lungs which were perfused with a buffer solution containing 10% of autologous blood. Embolism was induced by the injection of 0.75 ml air into the pulmonary artery. MEASUREMENTS AND
resultsPAP and lung weight, reflecting edema formation, were continuously recorded. Perfusate samples were drawn intermittently to determine TXA2 and ET-1 concentrations. Air injection resulted in an immediate increase in PAP up to 22.8 +/- 1.4 mm Hg at 2.5 min (control, n = 6), which was parallelled by an enhanced generation of TXA2. No relevant edema formation occurred during the observation period. Pretreatment with the ETA receptor antagonist LU135252 significantly reduced the pressure reaction after air embolism (p < 0.001) whereas the ETB receptor antagonist BQ788 (n = 6) was without marked effects. The administration of diclofenac (n = 6) did not alter the PAP increase 2.5 min after embolism, but significantly reduced the pressure reaction during the further observation period (p < 0.001). The application of LU135252 and diclofenac together (n = 6) also significantly reduced the PAP increase from 2.5 min during the total observation period (p < 0.001).
conclusionsThe acute pressure reaction after air embolism is mainly mediated via ET-1 by an ETA receptor related mechanism. TXA2 seems to maintain this reaction for a longer time.
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