Although hypothermia and ischaemic preconditioning (IP) are independently recognised mechanisms of cardioprotection, interactions between myocardial temperature and preconditioning have not been investigated. Therefore, this study explored the possibility of inducing IP during hypothermia and quantifying its effects at two temperature regimens commonly used in clinical practice. One hundred and four patients undergoing coronary artery bypass grafting (CABG) with intermittent cross-clamping and ventricular fibrillation were randomised to four groups: N=normothermia (36.5+/-0.5 degrees C); NP=normothermia+preconditioning, H=hypothermia (31.5+/-0.5 degrees C), HP=hypothermia+preconditioning. The primary outcome measure was release of cardiac Troponin I (cTnI), measured at 6 time points from pre- to 72 h after the end of CPB. There were no hospital deaths and no significant differences in pre- and intra-operative variables (P>or=0.05). There were significant differences in cTnI release between all groups, as follows: N: 117+/-12 microg/l (P<or=0.05 vs. all groups), NP: 87+/-8 microg/l (P<or=0.05 vs. groups N and HP), H: 76+/-6 microg/l (P<or=0.05 vs. groups N and HP), HP: 44+/-6 microg/l (P<or=0.05 vs. all groups). In conclusion, IP can be induced at both normothermia and moderate hypothermia, where it significantly reduces myocardial damage. Further studies are warranted to investigate the effects of the addition of hypothermia to pharmacological myocardial preconditioning.
尽管低温和缺血预处理(IP)是被独立认可的心脏保护机制,但心肌温度和预处理之间的相互作用尚未得到研究。因此,本研究探讨了在低温期间诱导IP以及在临床实践中常用的两种温度方案下量化其效果的可能性。104例接受冠状动脉旁路移植术(CABG)且采用间歇性阻断和心室颤动的患者被随机分为四组:N = 常温(36.5±0.5℃);NP = 常温 + 预处理,H = 低温(31.5±0.5℃),HP = 低温 + 预处理。主要结局指标是心脏肌钙蛋白I(cTnI)的释放,在体外循环(CPB)结束前至结束后72小时的6个时间点进行测量。无住院死亡病例,术前和术中变量无显著差异(P≥0.05)。所有组之间cTnI释放存在显著差异,如下:N:117±12微克/升(与所有组相比P≤0.05),NP:87±8微克/升(与N组和HP组相比P≤0.05),H:76±6微克/升(与N组和HP组相比P≤0.05),HP:44±6微克/升(与所有组相比P≤0.05)。总之,IP可在常温及中度低温下诱导,且能显著减少心肌损伤。有必要进一步研究在药物性心肌预处理基础上增加低温的效果。