Chello M, Mastroroberto P, Patti G, D'Ambrosio A, Di Sciascio G, Covino E
Interdisciplinary Center for Biomedical Research (CIR), Department of Cardiovascular Sciences, University Campus Bio-Medico of Rome, Italy.
Cardiovasc Surg. 2003 Oct;11(5):367-74. doi: 10.1016/S0967-2109(03)00078-4.
Recent studies have demonstrated that the induction of heat shock protein-72 (HSP72) by different stimuli preserves the heart function after cardioplegic arrest. Based on these findings, we investigated whether intermittent warm blood cardioplegia would induce changes in the myocardial expression of HSP72.
Forty patients scheduled for aortocoronary bypass were randomly assigned to receive either cold or warm intermittent blood cardioplegia. In all patients HSP72 and HSP72 mRNA were assayed in biopsies from the right atrium at baseline, and during the reperfusion period. Plasma CK-MB and troponin-T, and myocardial oxygen extraction and lactate release were also measured.
In both groups, myocardial expression of HSP72 increased throughout the reperfusion period, but the values of HSP72 band lengths were significantly higher in the warm group. Correspondingly, HSP72 mRNA levels increased progressively in both groups, with significant difference between groups observed in biopsies at the reperfusion. Warm blood cardioplegia was associated with lower levels of CK-MB and troponin-T. Myocardial oxygen extraction and lactate release were higher during intermittent warm cardioplegia, indicating a more profound ischemic anaerobic metabolism in the warm group.
Intermittent warm blood cardioplegia induces an increased expression of HSP72 and it is associated with a better myocardial protection, by a mechanism involving a variant of the classical ischemic preconditioning model.
近期研究表明，不同刺激诱导热休克蛋白-72（HSP72）可在心脏停搏后保护心脏功能。基于这些发现，我们研究了间歇性温血心脏停搏液是否会引起心肌HSP72表达的变化。
40例计划行主动脉冠状动脉搭桥术的患者被随机分配接受冷或温间歇性血液心脏停搏液。所有患者在基线时以及再灌注期间，均取右心房活检组织检测HSP72和HSP72 mRNA。同时还测量了血浆肌酸激酶同工酶（CK-MB）和肌钙蛋白-T，以及心肌氧摄取和乳酸释放。
两组患者在整个再灌注期间，心肌HSP72表达均增加，但温血组HSP72条带长度值显著更高。相应地，两组患者HSP72 mRNA水平均逐渐升高，在再灌注时的活检组织中观察到组间存在显著差异。温血心脏停搏液与较低的CK-MB和肌钙蛋白-T水平相关。间歇性温血心脏停搏期间心肌氧摄取和乳酸释放更高，表明温血组存在更严重的缺血无氧代谢。
间歇性温血心脏停搏液可诱导HSP72表达增加，并且通过涉及经典缺血预处理模型变体的机制，与更好的心肌保护相关。
