Cugno M, Nussberger J, Biglioli P, Alamanni F, Coppola R, Agostoni A
Department of Internal Medicine, IRCCS Maggiore Hospital, University of Milan, Italy.
Chest. 2001 Dec;120(6):1776-82. doi: 10.1378/chest.120.6.1776.
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.
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 (TNF).
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, C(3)a, 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.
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.
包括低血压发作在内的血流动力学并发症常与体外循环（CPB）相关，且可归因于一种全身性炎症反应，其中缓激肽可能是一种介质。本研究的目的是测定CPB期间患者血浆中缓激肽 -（1 - 9）九肽的水平以及肺对缓激肽的生理性清除情况。
前瞻性观察研究。
大学医院心脏外科病房。
监测27例接受心脏手术CPB患者的动脉内血压，并采集系列血样。我们测定了血浆缓激肽以及凝血、纤维蛋白溶解、补体、接触系统和细胞因子肿瘤坏死因子（TNF）的参数。
平均动脉压在CPB结束前逐渐下降（-18 mmHg，p = 0.001），但在手术结束时恢复到基线水平。静脉缓激肽水平在基础状态下正常（中位数为1.90 fmol/mL），从CPB开始后15分钟（5.71 fmol/mL）到手术结束时升高（p = 0.001），至（7.07 fmol/mL），在CPB结束时达到峰值（9.81 fmol/mL；p = 0.0001）；24小时后恢复时正常（2.81 fmol/mL）。当肺循环完全恢复且患者仍在接受CPB时，缓激肽血浆水平在肺内下降60%。手术开始后，活化因子XII、凝血酶 - 抗凝血酶复合物、凝血酶原片段F1 + 2、纤溶酶 - 抗纤溶酶复合物、C(3)a和TNF显著升高，在CPB期间进一步上升，并持续升高至手术结束，但它们在24小时内均恢复正常。血浆缓激肽水平的变化与其他任何变量均无相关性。
在CPB期间，血浆缓激肽逐渐升高，这至少部分是由于肺分流导致分解代谢减少所致。缓激肽的升高可能导致血压下降。
