Contribution of Endogenous Bradykinin to Fibrinolysis, Inflammation, and Blood Product Transfusion Following Cardiac Surgery: A Randomized Clinical Trial. Issue 4 (24th December 2012)
- Record Type:
- Journal Article
- Title:
- Contribution of Endogenous Bradykinin to Fibrinolysis, Inflammation, and Blood Product Transfusion Following Cardiac Surgery: A Randomized Clinical Trial. Issue 4 (24th December 2012)
- Main Title:
- Contribution of Endogenous Bradykinin to Fibrinolysis, Inflammation, and Blood Product Transfusion Following Cardiac Surgery: A Randomized Clinical Trial
- Authors:
- Balaguer, J M
Yu, C
Byrne, J G
Ball, S K
Petracek, M R
Brown, N J
Pretorius, M - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>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 B<sub>2</sub> receptor. This study tested the hypothesis that endogenous bradykinin contributes to the fibrinolytic and inflammatory response to CPB and that bradykinin B<sub>2</sub> receptor antagonism reduces fibrinolysis, inflammation, and subsequent transfusion requirements. Patients (<italic>N</italic> = 115) were prospectively randomized to placebo, ε‐aminocaproic acid (EACA), or HOE 140, a bradykinin B<sub>2</sub> receptor antagonist. Bradykinin B<sub>2</sub> 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.</p> <p> <italic>Clinical Pharmacology &amp; Therapeutics</italic> (2013); <bold>93</bold> 4, 326–334. doi:<ext-link ext-link-type="doi" xlink:type="simple"<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>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 B<sub>2</sub> receptor. This study tested the hypothesis that endogenous bradykinin contributes to the fibrinolytic and inflammatory response to CPB and that bradykinin B<sub>2</sub> receptor antagonism reduces fibrinolysis, inflammation, and subsequent transfusion requirements. Patients (<italic>N</italic> = 115) were prospectively randomized to placebo, ε‐aminocaproic acid (EACA), or HOE 140, a bradykinin B<sub>2</sub> receptor antagonist. Bradykinin B<sub>2</sub> 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.</p> <p> <italic>Clinical Pharmacology &amp; Therapeutics</italic> (2013); <bold>93</bold> 4, 326–334. doi:<ext-link ext-link-type="doi" xlink:type="simple" xmlns:xlink="http://www.w3.org/1999/xlink">10.1038/clpt.2012.249</ext-link></p> </abstract> … (more)
- Is Part Of:
- Clinical pharmacology & therapeutics. Volume 93:Issue 4(2013)
- Journal:
- Clinical pharmacology & therapeutics
- Issue:
- Volume 93:Issue 4(2013)
- Issue Display:
- Volume 93, Issue 4 (2013)
- Year:
- 2013
- Volume:
- 93
- Issue:
- 4
- Issue Sort Value:
- 2013-0093-0004-0000
- Page Start:
- 326
- Page End:
- 334
- Publication Date:
- 2012-12-24
- Subjects:
- Pharmacology -- Periodicals
Therapeutics -- Periodicals
615.5 - Journal URLs:
- http://www.nature.com/clpt/index.html ↗
http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1532-6535 ↗
http://www.nature.com/ ↗
http://firstsearch.oclc.org ↗
http://www.mosby.com/cpt ↗
http://www.sciencedirect.com/science/journal/00099236 ↗
http://www2.us.elsevierhealth.com/scripts/om.dll/serve?action=searchDB&searchdbfor=home&id=cp ↗ - DOI:
- 10.1038/clpt.2012.249 ↗
- Languages:
- English
- ISSNs:
- 0009-9236
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3286.330000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 3317.xml