Mickley G A, Cobb B L, Farrell S T
Radiofrequency Radiation Division (AL/OER), Armstrong Laboratory, Brooks AFB, TX 78235-5324, USA.
Int J Hyperthermia. 1997 Jan-Feb;13(1):99-114. doi: 10.3109/02656739709056434.
Microwaves have been proposed to alter neural functioning through both thermal and non-thermal mechanisms. We attempted to determine if local cerebral glucose utilization (LCGU) depends on the type of hyperthermic agent employed. We exposed the heads of rats to two different hyperthermic agents (5.6 GHz microwave exposure or exposure to hot/moist air) to create a 2 degree C rise in midbrain temperature. Other rats were sham exposed and remained normothermic. The 2-Deoxy-D-glucose (2DG) autoradiographic method was then used to determine LCGU during a 45-min period of stable hyperthermia. Hyperthermia (created by either hyperthermic agent) caused a general rise in brain glucose utilization. Hot-air exposed rats showed significantly higher LCGUs than microwaved rats in portions of the motor cortex, hypothalamus, lateral lemniscus and the substantia nigra (reticulata). Microwave exposure did not produce significantly higher levels of LCGU (compared to hot-air exposed hyperthermic controls) in any of the 47 brain areas sampled. A time analysis of lateral hypothalamic (LH) temperature during these different heating procedures revealed that microwave exposure produced a more-rapid rise in temperature than did not/moist air. Thus, we wondered if the nuclei-specific differences in LCGU could be explained by localized differences in rate of brain heating during the two hyperthermic treatments. In a second study we carefully matched both the rate of lateral hypothalamic temperature rise and the peak temperatures achieved by our two hyperthermic methods and again measured LH LCGUs. We found that this precise matching eliminated the difference in hypothalamic LCGU previously observed following microwave or hot-air exposure. These data suggest that hyperthermia causes a general rise in brain metabolism and that (as long as steady state and rate of local brain temperature increase are well matched) microwave and hot-air induced hyperthermia produce similar changes in LCGU.
有人提出，微波可通过热机制和非热机制改变神经功能。我们试图确定局部脑葡萄糖利用（LCGU）是否取决于所使用的热疗剂类型。我们将大鼠头部暴露于两种不同的热疗剂（5.6 GHz微波照射或热/湿空气暴露）下，使中脑温度升高2摄氏度。其他大鼠进行假暴露，保持正常体温。然后使用2-脱氧-D-葡萄糖（2DG）放射自显影法在45分钟的稳定热疗期间测定LCGU。热疗（由任何一种热疗剂引起）导致脑葡萄糖利用普遍增加。在运动皮层、下丘脑、外侧丘系和黑质（网状部）的部分区域，热空气暴露的大鼠显示出比微波照射的大鼠显著更高的LCGU。在47个采样脑区中的任何一个区域，微波照射均未产生比热空气暴露的热疗对照更高的LCGU水平。对这些不同加热程序期间下丘脑外侧（LH）温度的时间分析表明，微波照射比热/湿空气使温度升高得更快。因此，我们想知道，两种热疗治疗期间脑加热速率的局部差异是否可以解释LCGU在核特异性上的差异。在第二项研究中，我们仔细匹配了下丘脑外侧温度升高的速率以及我们两种热疗方法所达到的峰值温度，并再次测量了LH的LCGU。我们发现，这种精确匹配消除了先前在微波或热空气暴露后观察到的下丘脑LCGU差异。这些数据表明，热疗会导致脑代谢普遍增加，并且（只要稳态和局部脑温度升高速率匹配良好）微波和热空气诱导的热疗在LCGU方面产生相似的变化。
