ArticleLung2012
Surfactant protein A (SP-A) and angiotensin converting enzyme (ACE) as early biomarkers for pulmonary edema formation in ventilated human lung lobes.
Article in Lung, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Research advances in consistency and variability inJournal of thoracic disease · 2026Review
- Human Pulmonary 3D Models For Translational Research.Biotechnology journal · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEx vivo perfused and ventilated lung lobes frequently develop pulmonary edema. We were looking for a suitable and early detectable biomarker in the perfusion fluid indicating lung cell damage and loss of tissue integrity in ventilated human lung lobes. Therefore, we elucidated whether surfactant protein A (SP-A) and angiotensin-converting enzyme (ACE) were measurable in the perfusion fluid and whether they were suitable indicators for edema formation occurring within the experimental time frame of 1-2 h.
methodsPatients (n = 39) undergoing a lobectomy, bilobectomy or pneumonectomy due to primary bronchial cell carcinoma were included in the studies. Lung lobes were extracorporally ventilated and perfused for up to 2 h. Two different perfusion fluids were used, plain perfusion buffer and perfusion buffer containing packed erythrocytes or buffy coats. Perfusion fluid samples were analyzed for SP-A and ACE using immunoassays served as perfusion fluids.
resultsSP-A and ACE concentrations were analyzed in fluid sample sets of 39 and 33 perfusion experiments, respectively. Degrees of edema formation were arbitrarily classified into three groups (≤ 29, 30-59, ≥ 60 % weight gain). The maximum increase of SP-A and ACE concentrations in the perfusate was significantly higher for more pronounced edemas in case of perfusions using a mixture of blood components and buffer. Interestingly, the time courses of ACE and SP-A were highly similar.
conclusionWe suggest that SP-A and ACE are promising early biochemical markers for the development for pulmonary edema formation in the ex vivo lung lobe perfusion.
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Registered trials
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