LaManna J C, McCracken K A, Patil M, Prohaska O J
Department of Neurology, University Hospitals of Cleveland, Ohio 44106.
Metab Brain Dis. 1989 Dec;4(4):225-37. doi: 10.1007/BF00999769.
A new thin-film, multisensor probe was used to determine tissue oxygen tension, tissue temperature, and electrical activity at two depths below the brain surface in chloral hydrate- or nitrous oxide/halothane-anesthetized rats. Brain tissue temperature at both depths was found to be lower than core temperature by 1-2 degrees C. Electrical activation, spreading depression, and pentylenetetrazol seizures all resulted in transient increases of brain tissue temperature of a few tenths degree centigrade. Vasodilation, induced by hypercapnia or hypoxia, caused a warming of brain tissue. Near-maximum oxygen metabolism, reached upon reoxygenation after severe hypoxia, was accompanied by tissue temperature rises of greater than 1 degree C. It was concluded that brain tissue temperature in the anesthetized rat is lower than core temperature due to extensive radiative and conductive heat loss to the environment through the head. Transient increases in tissue temperature during activation are caused by vasodilation and increased metabolism.
使用一种新型薄膜多传感器探头,测定水合氯醛或氧化亚氮/氟烷麻醉大鼠脑表面以下两个深度的组织氧张力、组织温度和电活动。发现两个深度的脑组织温度均比核心温度低1-2摄氏度。电激活、扩散性抑制和戊四氮惊厥均导致脑组织温度短暂升高十分之几度。高碳酸血症或低氧血症诱导的血管舒张导致脑组织升温。严重低氧后再给氧时达到的接近最大氧代谢伴随着组织温度升高超过1摄氏度。得出的结论是,麻醉大鼠的脑组织温度低于核心温度,这是由于通过头部向环境大量散热,包括辐射散热和传导散热。激活过程中组织温度的短暂升高是由血管舒张和代谢增加引起的。