Yellon D M, Iliodromitis E, Latchman D S, Van Winkle D M, Downey J M, Williams F M, Williams T J
Hatter Department of Academic Cardiology, University College Hospital, London, United Kingdom.
Cardiovasc Res. 1992 Apr;26(4):342-6. doi: 10.1093/cvr/26.4.342.
It has recently been shown that induction of heat stress proteins by whole body heat stress confers myocardial protection in the isolated in vitro rat and rabbit heart. This study extends the above studies by examining the effects of stress protein synthesis on the limitation of infarct size in the in vivo rabbit heart model.
30 male New Zealand white rabbits were used. Six rabbits were used for measurement of heat stress protein; 10 were used for infarct size determination in a heat stress group (HS); 14 were used for infarct size determination in a control group. There were 10 exclusions. Under anaesthesia, body temperature was raised to 42 degrees C for 15 min in the HS group. Following 24 hours of recovery rabbits were reanaesthetised and the hearts subjected to a 45 min period of regional ischaemia followed by 3 h reperfusion. The risk zone was defined with fluorescent particles and the infarct area determined by tetrazolium staining. Western blotting showed an increase in the 72 KD heat stress protein in hearts in the HS group.
Infarct size as a percent of risk area was 61.4 (SEM 6.4)% (n = 14) in control hearts and 71.8(7.3)% (n = 10) in the HS hearts. These results were not statistically significant.
No protective effect of heat stress could be seen when infarct size was used as the end point. Either the protection seen in earlier studies using the Krebs perfused isolated heart model does not accurately reflect protection against myocardial infarction, or heat stress itself may induce injurious factors in the blood which will negate any direct protective effect to the myocardium in this model.
最近有研究表明，全身热应激诱导热应激蛋白可在离体大鼠和兔心脏中发挥心肌保护作用。本研究通过检测应激蛋白合成对兔体内心脏梗死面积限制的影响，扩展了上述研究。
使用30只雄性新西兰白兔。6只用于测量热应激蛋白；10只用于热应激组（HS）梗死面积测定；14只用于对照组梗死面积测定。有10只被排除。在麻醉状态下，HS组体温升至42℃持续15分钟。恢复24小时后，兔子再次麻醉，心脏经历45分钟的局部缺血期，随后再灌注3小时。用荧光颗粒界定危险区，用四氮唑染色确定梗死面积。蛋白质印迹法显示HS组心脏中72KD热应激蛋白增加。
对照组心脏梗死面积占危险区的百分比为61.4（标准误6.4）%（n = 14），HS组心脏为71.8（7.3）%（n = 10）。这些结果无统计学意义。
以梗死面积为终点时，未观察到热应激的保护作用。要么早期使用克雷布斯灌注离体心脏模型观察到的保护作用不能准确反映对心肌梗死的保护，要么热应激本身可能在血液中诱导有害因素，从而抵消该模型中对心肌的任何直接保护作用。
