Study objectives: Hemodynamic complications
including hypotensive episodes are frequently associated with
cardiopulmonary bypass (CPB) and can be attributed to a generalized
inflammatory response in which bradykinin may be a mediator. The
purpose of this study was to determine the plasma levels of
bradykinin-(1–9)nonapeptide in patients during CPB and the physiologic
elimination of bradykinin by the lungs.
Prospective, observational study.
University hospital, cardiac surgery unit.
methods: Intra-arterial BP was monitored and serial blood samples
were obtained from 27 patients undergoing CPB for cardiac surgery. We
measured plasma bradykinin and parameters of coagulation, fibrinolysis,
complement, contact system, and the cytokine tumor necrosis factor
Results: Mean arterial pressure fell
progressively until the end of CPB (− 18 mm Hg, p = 0.001) but
returned to baseline by the end of surgery. The venous bradykinin
level, normal in basal conditions (median, 1.90 fmol/mL), was increased
(p = 0.001) from 15 min after the beginning of CPB (5.71 fmol/mL) to
the end of the operation (7.07 fmol/mL), with a peak at the end of CPB
(9.81 fmol/mL; p = 0.0001); it was normal at recovery 24 h later
(2.81 fmol/mL). Bradykinin plasma levels fell 60% across the lung when
the pulmonary circulation was fully restored while the patients were
still receiving CPB. Activated-factor XII, thrombin-antithrombin
complexes, prothrombin fragment F1 + 2, plasmin-antiplasmin
complexes, C3a, and TNF increased significantly after the
beginning of the surgical procedure, rising further during CPB, and
remained elevated until the end of surgery, but they all returned to
normal within 24 h. Changes in plasma bradykinin levels were not
correlated with any of the other variables.
Conclusions: During CPB, there is a progressive increase of
plasma bradykinin that is at least partially due to reduced catabolism
as a consequence of shunting the lungs. The increase in bradykinin may
contribute to the fall in BP.