Hsu Shu-Fen, Chao Chien-Ming, Chang Ching-Ping, Lin Mao-Tsun, Cheng Bor-Chih
Department of Nursing, Shu-Zen Junior College of Medicine and Management, Kaohsiung City 821, Taiwan.
Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan 736, Taiwan.
Int J Cardiol. 2016 Sep 15;219:63-9. doi: 10.1016/j.ijcard.2016.05.004. Epub 2016 May 3.
We attempted to test the hypothesis that preinduction of heat shock protein (HSP) 72 in the heart would improve left ventricular performance in rat heatstroke.
Cardiac expression of HSP 72 was quantitatively evaluated by western blot analysis in rats 0h, 12h, or 72h after mild heat preconditioning (MHP; 43°C for 30min). They were subjected to severe heat stress (SHS; 43°C for 70min) to induce heatstroke. A 1.2F catheter-tip pressure transducer was inserted into the left ventricle of these group rats under general anesthesia to record hemodynamic in the closed chest with a pressure-volume loop module data recording and analysis system.
At the time point of heatstroke onset, compared with normothermic controls, group rats with 12h post-MHP had significantly increased cardiac HSP 72, decreased hyperthermia, decreased hypotension, decreased bradycardia, increased end-systolic pressure, increased end-diastolic pressure, increased stroke volume, decreased end-systolic volume, decreased end-diastolic pressure, increased cardiac output, increased ejection fraction, increased stroke work, increased arterial elastance, and decreased time constant of fall in ventricular pressure by Glantz-methods. With the loss of cardiac HSP 72 expression observed at 72h in post-MHP group rats, an insignificant protection against left ventricular performance was observed.
Preinduction of cardiac HSP 72 may improve hypotension in heatstroke rats by increasing both cardiac mechanical efficiency and arterial elastance.
我们试图验证心脏中热休克蛋白（HSP）72预诱导可改善大鼠中暑时左心室功能的假说。
通过蛋白质免疫印迹分析对轻度热预处理（MHP；43°C，30分钟）后0小时、12小时或72小时的大鼠心脏中HSP 72的表达进行定量评估。对这些大鼠施加严重热应激（SHS；43°C，70分钟）以诱导中暑。在全身麻醉下将一根1.2F导管尖端压力传感器插入这些组大鼠的左心室，使用压力-容积环模块数据记录和分析系统在闭胸状态下记录血流动力学。
在中暑发作时间点，与正常体温对照组相比，MHP后12小时的组大鼠心脏HSP 72显著增加，体温过高减轻，低血压减轻，心动过缓减轻，收缩末期压力增加，舒张末期压力增加，每搏量增加，收缩末期容积减少，舒张末期压力降低，心输出量增加，射血分数增加, 每搏功增加，动脉弹性增加，并且根据格兰茨方法心室压力下降的时间常数减小。在MHP后组大鼠72小时观察到心脏HSP 72表达丧失，对左心室功能的保护作用不显著。
心脏HSP 72的预诱导可能通过提高心脏机械效率和动脉弹性来改善中暑大鼠的低血压。
