Mariak Z, Jadeszko M, Lewko J, Lebkowski W, Lyson T
Department of Neurosurgery, University Medical School, Bialystok, Poland.
Acta Neurochir (Wien). 1998;140(6):585-90. doi: 10.1007/s007010050144.
Knowledge about human brain temperature is still very limited, despite evidence demonstrating the critical influence of mild increases in temperature on the ischaemic brain. It has been suggested that in passive and exercise hyperthermia the brain may be protected against thermal damage by a mechanism of selective brain cooling (SBC). It is said to bring about suppression of the temperature of the brain, rendering it significantly lower than trunk and arterial blood temperature. Yet very little is known about the possible role of this mechanism in fever, a condition fundamentally different from "physiological" hyperthermia, especially when it occurs in brain-damaged patients. In our investigation we retrospectively analysed the results of direct recordings of cerebral temperature within the subdural space (Tsd) and within the brain parenchyma (Tbr-16 cases) in 63 unanaesthetized patients following neurosurgical procedures, including 23 with fever > 38 degrees C. The difference between trunk temperature, measured in the rectum (Tre) or in the oesophagus (Tes), and the intracranial temperature, were calculated in all subjects. A statistically significant reduction of these differences, in step with increasing fever, would be compatible with demonstrating a process of selective brain cooling. The offsets Tre-Tsd, Tre-Tbr, and Tes-Tsd were plotted against Tre over a wide range of body temperature and near zero correlation was found. This finding suggests that brain temperature in fever was not selectively suppressed by any specific thermolytic mechanism and that dissipation of the main bulk of cerebral metabolic heat both in normothermia and in fever depends on heat uptake by arterial blood. The results suggest that the brain in fever can be seriously jeopardized by heat stress and no specific cooling mechanism exists, to reduce it below body temperature in feverish neurosurgical patients. Tbr and/or Tsd remained the highest body temperature in 14 out of the 23 patients during fever.
尽管有证据表明体温轻度升高对缺血性脑具有关键影响，但目前关于人脑温度的知识仍然非常有限。有人提出，在被动性和运动性体温过高状态下，大脑可能通过选择性脑冷却（SBC）机制来抵御热损伤。据说这种机制能抑制大脑温度，使其显著低于躯干和动脉血温度。然而，对于该机制在发热（一种与“生理性”体温过高根本不同的情况，尤其是在脑损伤患者中出现时）中可能发挥的作用，人们知之甚少。在我们的研究中，我们回顾性分析了63例接受神经外科手术后未麻醉患者硬膜下间隙（Tsd）和脑实质内（Tbr - 16例）脑温直接记录的结果，其中包括23例体温超过38摄氏度的发热患者。计算了所有受试者直肠（Tre）或食管（Tes）测量的躯干温度与颅内温度之间的差异。随着发热程度增加，这些差异出现统计学上的显著降低，这将与证明选择性脑冷却过程相符。在广泛的体温范围内，绘制了Tre - Tsd、Tre - Tbr和Tes - Tsd与Tre的差值，发现相关性接近零。这一发现表明，发热时脑温并未被任何特定的散热机制选择性抑制，并且在正常体温和发热状态下，大脑主要代谢热的消散均依赖于动脉血的热摄取。结果表明，发热时大脑可能会因热应激而受到严重损害，且不存在将发热的神经外科患者的脑温降低至体温以下的特定冷却机制。在23例发热患者中，有14例的Tbr和/或Tsd在发热期间始终是最高体温。
