Evidence map›Paper›PMID 31955320›Full record

ArticleGeneral thoracic and cardiovascular surgery2020

The N-terminal lectin-like domain of thrombomodulin reduces acute lung injury without anticoagulant effects in a rat cardiopulmonary bypass model.

Tatsuya Itonaga, Shingo Hirao, Kazuhiro Yamazaki, Tadashi Ikeda, Kenji Minatoya, Hidetoshi Masumoto

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Article in General thoracic and cardiovascular surgery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Tatsuya ItonagaDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Shingo HiraoDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Kazuhiro YamazakiDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Tadashi IkedaDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Kenji MinatoyaDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Hidetoshi MasumotoDepartment of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan. masumoto@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-4059-2827
Kyoto University · JP

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan 16H05424
6 · The paper itself

Abstract

objectivesSystemic inflammation evoked by cardiopulmonary bypass (CPB) leads to acute lung injury (ALI) and respiratory failure. Although recombinant human soluble thrombomodulin (rTM) consists of three domains (D1-3), is reported to attenuate systemic inflammation through the N-terminal lectin-like domain (D1), anticoagulant domain (D2) may exacerbate coagulopathy after CPB. We investigated the potential of selective D1 against CPB-mediated ALI free from anticoagulant effects using a rat CPB model.

methodsRats were divided into three groups: control (CPB alone, n = 5), D1 (CPB + D1, n = 4), and D123 (CPB + D123, n = 6). D1 or D123 was administrated to the rats of each group before CPB establishment. Blood samples are collected before, during and after CPB. Blood coagulability was assessed by a coagulation analyzer. Lung samples are collected at 1 h after the termination of CPB for histological analyses.

resultsD123 group exhibited significantly prolonged glass beads-activated clotting time with heparinase after CPB compared to that in control group, whereas no significant prolongation in control and D1 group (control vs. D1 vs. D123: 65.4 ± 9.2 vs. 65.3 ± 10.9 vs. 83.5 ± 4.6 s, p = 0.036 [control vs. D123], 0.99 [control vs. D1]) indicating the absence of anticoagulant activities of D1. Histological studies revealed less congestion, edema, inflammation, and hemorrhage in both D1 and D123 groups compared to those in control group indicating protective effects of both D1 and D123 against ALI mediated by CPB.

conclusionsN-terminal lectin-like domain of rTM may reduce the risk of ALI without anticoagulant effects.

Indexed as

Acute Lung InjuryAnimalsAnticoagulantsCardiopulmonary BypassDisease Models, AnimalMaleRandom AllocationRatsRats, Sprague-DawleyThrombomodulinAnticoagulantsThrombomodulinAcute lung injuryAnimal modelCardiopulmonary bypassCoagulopathyThrombomodulin

Identifiers

PMID31955320
OpenAlexW2999726906

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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.