Vogt Sebastian, Troitzsch Dirk, Abdul-Khaliq Hashim, Moosdorf Rainer
Biomedical Research Center, Cardiovascular Research Lab and Heart Surgery, University Hospital, Philipps-University Marburg, Marburg, Germany.
J Surg Res. 2007 May 15;139(2):176-81. doi: 10.1016/j.jss.2006.07.041. Epub 2007 Mar 2.
The capacity of heat stress induction to improve myocardial tolerance against ischemia is well known. We investigated cardiac energy metabolism after hsp 72(+)/73(+) induction in isolated perfused neonatal rabbit hearts subjected to prolonged cold cardioplegic ischemia.
Hearts from neonatal rabbits were excised, isolated perfused and arrested by 2-h cold cardioplegic ischemia. Rectal temperature of eight neonatal rabbits was raised to 42.0 to 42.5 degrees C for heat shock protein expression in a whole body water bath for 15 min before the onset of arrest. Another set of eight rabbits without hyperthermia pretreatment served as control. Recovery of left ventricle function was assessed by aortic flow, cardiac output, and max dP/dt. Status of high-energy phosphates was measured by (31)phosphorus nuclear magnetic resonance-spectroscopy.
Immunoblot analysis revealed clear hsp 72+/73+ induction after a brief period of systemic hyperthermia. Heat stress pretreatment resulted in a better recovery of left ventricular function (aortic flow and cardiac output improvement P < 0.05, max dP/dt P < 0.01) than in controls at 60 min after reperfusion. During ischemia and reperfusion, myocardial energy metabolism was better preserved in hearts after hsp induction as a consequence of increased gamma-, alpha-, and beta-ATP as well as phosphocreatine-values over controls. The ischemia-induced pH-decrease was attenuated.
These data contribute to the evidence of heat stress mediated beneficial effects on functional myocardial recovery and improved cardiac energy metabolism after prolonged cold cardioplegic ischemia. More importantly, the attenuation of ischemic pH reduction and better restoration suggest an involvement of mitochondrial membrane potential alterations.
热应激诱导改善心肌对缺血耐受性的能力已广为人知。我们研究了在长时间冷停搏缺血的离体灌注新生兔心脏中，热休克蛋白72（+）/73（+）诱导后的心脏能量代谢情况。
切除新生兔心脏，进行离体灌注，并通过2小时冷停搏缺血使其停跳。在停跳开始前，将8只新生兔的直肠温度在全身水浴中升至42.0至42.5摄氏度，持续15分钟以诱导热休克蛋白表达。另一组8只未经热预处理的兔子作为对照。通过主动脉流量、心输出量和最大dP/dt评估左心室功能的恢复情况。通过磷-31核磁共振波谱法测量高能磷酸盐的状态。
免疫印迹分析显示，短暂的全身热疗后可明显诱导热休克蛋白72+/73+表达。热应激预处理导致再灌注60分钟时左心室功能的恢复情况（主动脉流量和心输出量改善，P<0.05；最大dP/dt，P<0.01）优于对照组。在缺血和再灌注期间，热休克蛋白诱导后的心脏中，由于γ-、α-和β-ATP以及磷酸肌酸的值高于对照组，心肌能量代谢得到更好的保存。缺血诱导的pH值下降得到缓解。
这些数据为热应激介导的对长时间冷停搏缺血后心肌功能恢复和心脏能量代谢改善的有益作用提供了证据。更重要的是，缺血pH值降低的减轻和更好的恢复表明线粒体膜电位改变参与其中。
