ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Attenuation of experimental hepatopulmonary syndrome in endothelin B receptor-deficient rats.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Sorafenib in Hepatopulmonary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2019Trial
- The Role of Nitric Oxide in Chronic Liver Disease: A Review.Journal of clinical and translational hepatology · 2026Review
- Quercetin ameliorates acute lung injury in a rat model of hepatopulmonary syndrome.BMC complementary medicine and therapies · 2022Article
- Hepatopulmonary syndrome: An update.World journal of hepatology · 2021Review
- Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats.BMC cardiovascular disorders · 2020Article
- Potential Clinical Targets in Hepatopulmonary Syndrome: Lessons From Experimental Models.Hepatology (Baltimore, Md.) · 2018Review
- Hepatopulmonary syndrome: What we know and what we would like to know.World journal of gastroenterology · 2016Review
- Hepatopulmonary Syndrome and Liver Transplantation: A Recent Review of the Literature.Journal of clinical and translational hepatology · 2016Review
- Hepatopulmonary Syndrome.Digestive diseases and sciences · 2015Review
- Aggravation of hepatopulmonary syndrome after sildenafil treatment in a patient with coexisting portopulmonary hypertension.Korean circulation journal · 2015Article
- HPS: Diagnosis, clinical features, and medical therapy.Clinical liver disease · 2014Article
- [Pulmonary complications in liver diseases].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2014Review
- Pulmonary vascular complications of liver disease.American journal of respiratory and critical care medicine · 2013Review
- Transition from hepatopulmonary syndrome to portopulmonary hypertension: a case series of 3 patients.Case reports in pulmonology · 2013Article
- The lung in liver disease: old problem, new concepts.Transactions of the American Clinical and Climatological Association · 2013Article
- Hepatopulmonary syndrome: update on pathogenesis and clinical features.Nature reviews. Gastroenterology & hepatology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL) in rat is accompanied by increased lung vascular endothelial endothelin B (ETB) receptor expression and increased circulating levels of endothelin-1 (ET-1). The onset of HPS is hypothesized to be triggered by ET-1/ETB receptor activation of endothelial nitric oxide synthase (eNOS)-derived NO production in the pulmonary endothelium. However, whether functional pulmonary vascular ETB receptors are required for the development of experimental HPS is not defined. We evaluated the effects of vascular ETB receptor deficiency on the development of experimental HPS. The molecular and physiological alterations of HPS were compared in 2-wk CBDL wild-type and ETB receptor-deficient (transgenic sl/sl) rats. Relative to wild-type rats, basal hepatic and plasma ET-1 levels were elevated in sl/sl controls although, unlike wild-type animals circulating ET-1 levels, did not increase further after CBDL in sl/sl animals. In contrast to wild-type animals, ETB receptor-deficient rats did not develop increased Akt and eNOS expression and activation and did not develop gas exchange abnormalities of HPS after CBDL. There was a similar degree of pulmonary intravascular monocyte accumulation in both 2-wk CBDL sl/sl and wild-type animals. In conclusion, ETB receptor deficiency inhibits lung Akt/eNOS activation and prevents the onset of experimental HPS after CBDL. This effect is independent of inhibition of pulmonary intravascular monocyte accumulation. These results demonstrate that ET-1/ETB receptor signaling plays a key role in the initiation of experimental HPS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.