Cornelussen R N, Garnier A V, van der Vusse G J, Reneman R S
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
J Mol Cell Cardiol. 1998 Feb;30(2):365-72. doi: 10.1006/jmcc.1997.0606.
Improvement of post-ischemic cardiac function 24 h after heat stress has been attributed to the increased cardiac tissue content of the inducible heat stress protein hsp70. Previous studies indicated that hsp70 is already significantly upregulated a few hours after heat stress. To delineate the relationship between hsp70 tissue content and heat stress-induced cardioprotection in the early time frame after heat stress, if any, post-ischemic functional recovery of isolated, ejecting rat hearts and the actual cardiac hsp70 content were investigated 0.5, 3, 6 and 24 h after heat stress (42 degrees C for 15 min). Recovery (% of pre-ischemic value) of cardiac output, left ventricular developed pressure, and positive and negative left ventricular dP/dtmax was studied during reperfusion after 45 min of global ischemia. Anesthetized non heat-stressed rats served as controls. The recovery of all hemodynamic variables was significantly worse in hearts isolated 30 min after heat stress than in control hearts. When the time interval between heat treatment and the ischemic episode was prolonged, a gradual improvement of post-ischemic functional recovery was observed. Only 24 h after heat treatment functional recovery was significantly better in the heat-stressed than in the control group. Compared to control hearts (0.27+/-0.10 mg/g total protein) cardiac hsp70 content was already significantly increased 0.5 h after heat stress (0.51+/-0.03 mg/g total protein). The cardiac hsp70 content further increased to 0. 70+/-0.11, 0.89+/-0.35 and 1.01+/-0.25 mg/g total protein, at 3, 6 and 24 h after heat stress, respectively. The present findings clearly show that heat stress is associated with a fast rise in the myocardial hsp70 content which, however, is not uniquely correlated with improved ischemia tolerance of the treated hearts, which only occurs 24 h later.
热应激后24小时缺血后心脏功能的改善归因于诱导型热应激蛋白hsp70的心脏组织含量增加。先前的研究表明，热应激后数小时hsp70就已显著上调。为了阐明热应激后早期hsp70组织含量与热应激诱导的心脏保护之间的关系（若存在这种关系），研究了热应激（42℃，15分钟）后0.5、3、6和24小时离体、有射血功能的大鼠心脏的缺血后功能恢复情况以及心脏实际的hsp70含量。在45分钟全心缺血后的再灌注期间，研究了心输出量、左心室舒张末压以及左心室dp/dtmax的正负值的恢复情况（相对于缺血前值的百分比）。麻醉的非热应激大鼠作为对照。热应激后30分钟分离的心脏中，所有血流动力学变量的恢复情况均显著差于对照心脏。当热应激与缺血发作之间的时间间隔延长时，观察到缺血后功能恢复逐渐改善。仅在热应激后24小时，热应激组的功能恢复明显优于对照组。与对照心脏（0.27±0.10毫克/克总蛋白）相比，热应激后0.5小时心脏hsp70含量已显著增加（0.51±0.03毫克/克总蛋白）。热应激后3、6和24小时，心脏hsp70含量分别进一步增加至0.70±0.11、0.89±0.35和1.01±0.25毫克/克总蛋白。目前的研究结果清楚地表明，热应激与心肌hsp70含量的快速升高有关，然而，这与治疗后心脏缺血耐受性的改善并非唯一相关，缺血耐受性改善仅在24小时后出现。
