Pang L M, Stalcup S A, Lipset J S, Hayes C J, Bowman F O, Mellins R B
Circulation. 1979 Dec;60(7):1503-7. doi: 10.1161/01.cir.60.7.1503.
To determine whether cold could activate the kallikrein-kinin system in vivo as it does in vitro, the circulating systemic concentrations of bradykinin were serially measured in 10 cyildren with congenital diseases of the heart undergoing corrective cardiac surgery. Bradykinin was measured by radioimmunoassay in blood samples obtained before, during and after profound hypothermia (to 18 degrees C) and cardiopulmonary bypass. The circulating concentrations of bradykinin increased significantly as body temperature decreased during surface cooling. The increase in circulating bradykinin was associated with a decrease in the circulating level of bradykininogen, the precursor of bradykinin. With the onset of cardiopulmonary bypass and hence, removal of the lung and pulmonary converting enzyme from the circulation, there was a further rise in the already elevated concentrations of bradykinin. This is the first in vivo demonstration that hypothermia leads to an increase in the circulating concentrations of bradykinin.
为了确定寒冷是否能像在体外那样在体内激活激肽释放酶-激肽系统，对10名接受心脏矫正手术的先天性心脏病患儿的循环系统中缓激肽的浓度进行了连续测量。在深度低温（降至18摄氏度）和体外循环之前、期间和之后采集血样，通过放射免疫分析法测定缓激肽。在体表降温过程中，随着体温下降，循环中的缓激肽浓度显著增加。循环中缓激肽的增加与缓激肽原（缓激肽的前体）循环水平的降低有关。随着体外循环的开始，从而使肺和肺转换酶从循环中去除，已经升高的缓激肽浓度进一步上升。这是首次在体内证明低温会导致循环中缓激肽浓度增加。
