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document
Contribution of endogenous bradykinin to fibrinolysis , inflammation , and blood product transfusion following cardiac surgery : a randomized clinical trial . 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 .
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Outcome_Physical
fibrinolysis
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Outcome_Physical
inflammation
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Outcome_Physical
blood product transfusion
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Outcome_Physical
release of nitric oxide , inflammatory cytokines , and tissue-type plasminogen activator ( t-PA )
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Outcome_Physical
fibrinolytic and inflammatory response to CPB and that bradykinin B2 receptor antagonism reduces fibrinolysis , inflammation , and subsequent transfusion requirements .
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Participant_Condition
following cardiac surgery :
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Participant_Condition
cardiopulmonary bypass ( CPB )
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Participant_Sample-size
Patients ( N = 115 )