Taylor R P, Harris M B, Starnes J W
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas 78712, USA.
Am J Physiol. 1999 Mar;276(3):H1098-102. doi: 10.1152/ajpheart.1999.276.3.H1098.
The aim of this study was to determine the effects of acute bouts of exercise on myocardial recovery after ischemia and heat shock protein expression. Adult female Sprague-Dawley rats were divided into five groups: 1) 1-day run (1DR; n = 6) and 2) 3-day run (3DR; n = 7), in which rats ran for 100 min at a speed of 20 m/min up a 6 degrees grade for 1 or 3 consecutive days; 3) 1-day cold run (1CR), in which rats ran the same as 1DR but with wet fur at 8 degrees C, which prevented an elevation of core temperature (n = 8); 4) heat shock sedentary (HS), in which rats had their core temperatures raised to 42 degrees C one time for 15 min (n = 5); and 5) sedentary control (n=15). Cardiac function was analyzed 24 h after the last treatment using an isolated, working heart model. Nonpaced hearts were initially perfused under normoxic conditions, then underwent 17 min of global, normothermic (37 degrees C) ischemia, and, finally, were allowed to recover for 30 min under normoxic conditions. The concentration of the 72-kDa heat shock protein (HSP 72) was measured in each left ventricle. Compared with that in the sedentary group, recovery of cardiac output x systolic pressure (CO x SP) was enhanced (P < 0.05) in all treatment groups when the postischemic value was covaried with the preischemic value. No differences in CO x SP were found (P > 0.05) between the following groups: 1DR vs. 3DR, 1DR vs. HS, and 1DR vs. 1CR. Heat shock protein concentration was significantly greater (P < 0.05) than that in the sedentary controls in HS, 1DR, and 3DR groups, but not for 1CR. The concentration of HSP 72 was not significantly correlated with postischemic CO x SP (R2 = 0.197, P > 0.05). We conclude that acute bouts of exercise can produce cardioprotective effects without an elevation of HSP 72.
本研究的目的是确定急性运动发作对缺血后心肌恢复和热休克蛋白表达的影响。成年雌性Sprague-Dawley大鼠分为五组：1）1天跑步组（1DR；n = 6）和2）3天跑步组（3DR；n = 7），其中大鼠以20米/分钟的速度在6度坡度上连续跑100分钟，持续1天或3天；3）1天冷跑步组（1CR），其中大鼠跑步方式与1DR相同，但在8摄氏度下毛发潮湿，这可防止核心体温升高（n = 8）；4）热休克静息组（HS），其中大鼠的核心体温一次性升高到42摄氏度，持续15分钟（n = 5）；5）静息对照组（n = 15）。在最后一次处理24小时后，使用离体工作心脏模型分析心脏功能。未起搏的心脏最初在常氧条件下灌注，然后经历17分钟的全心、常温（37摄氏度）缺血，最后在常氧条件下恢复30分钟。测量每个左心室中72 kDa热休克蛋白（HSP 72）的浓度。当缺血后值与缺血前值进行协变量分析时，与静息组相比，所有处理组的心输出量×收缩压（CO×SP）恢复均增强（P < 0.05）。以下各组之间未发现CO×SP有差异（P > 0.05）：1DR与3DR、1DR与HS以及1DR与1CR。热休克蛋白浓度在HS、1DR和3DR组中显著高于静息对照组（P < 0.05），但1CR组无此现象。HSP 72的浓度与缺血后CO×SP无显著相关性（R2 = 0.197，P > 0.05）。我们得出结论，急性运动发作可产生心脏保护作用，而无需HSP 72升高。
