Trial reportClinical pharmacology and therapeutics2013
Contribution of endogenous bradykinin to fibrinolysis, inflammation, and blood product transfusion following cardiac surgery: a randomized clinical trial.
Trial report in Clinical pharmacology and therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00223704 (Bradykinin Receptor Antagonism During Cardiopulmonary Bypass), which is not on this map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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.
Bradykinin Receptor Antagonism During Cardiopulmonary Bypass
Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Effects of interventions targeting the systemic inflammatory response to cardiac surgery on clinical outcomes in adults.The Cochrane database of systematic reviews · 2023Pooled it
- Trial
- A comprehensive review on current understanding of bradykinin in COVID-19 and inflammatory diseases.Molecular biology reports · 2022Review
- Crosstalk between the renin-angiotensin, complement and kallikrein-kinin systems in inflammation.Nature reviews. Immunology · 2022Review
- The Predictive Role of Intraoperative Blood Transfusion Components in the Prognosis of Heart Transplantation.Frontiers in cardiovascular medicine · 2022Article
- A Systematic Review of Molecular Imaging Agents Targeting Bradykinin B1 and B2 Receptors.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Mechanisms involved in kinin-induced glioma cells proliferation: the role of ERK1/2 and PI3K/Akt pathways.Journal of neuro-oncology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bradykinin increases during cardiopulmonary bypass (CPB) and stimulates the release of nitric oxide, inflammatory cytokines, and tissue-type plasminogen activator (t-PA), acting through its B2 receptor. This study tested the hypothesis that endogenous bradykinin contributes to the fibrinolytic and inflammatory response to CPB and that bradykinin B2 receptor antagonism reduces fibrinolysis, inflammation, and subsequent transfusion requirements. Patients (N = 115) were prospectively randomized to placebo, ε-aminocaproic acid (EACA), or HOE 140, a bradykinin B2 receptor antagonist. Bradykinin B2 receptor antagonism decreased intraoperative fibrinolytic capacity as much as EACA, but only EACA decreased D-dimer formation and tended to decrease postoperative bleeding. Although EACA and HOE 140 decreased fibrinolysis and EACA attenuated blood loss, these treatments did not reduce the proportion of patients transfused. These data suggest that endogenous bradykinin contributes to t-PA generation in patients undergoing CPB, but that additional effects on plasmin generation contribute to decreased D-dimer concentrations during EACA treatment.
Indexed as
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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.