Bicego Kenia C, Steiner Alexandre A, Gargaglioni Luciane H, Branco Luiz G S
Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Pflugers Arch. 2002 Sep;444(6):810-5. doi: 10.1007/s00424-002-0886-x. Epub 2002 Jul 16.
Hypoxia causes a regulated decrease in body core temperature ( T(c)), termed anapyrexia, which seems to be a very effective way of preventing hypoxia-associated cell damage. Since during several pathological states the supply of O(2) is a limiting factor, the clinical importance of anapyrexia is evident. However, the mechanisms involved in this response remain unclear. We tested the hypothesis that lactate, a classic companion of hypoxia, is a mediator of hypoxia-induced anapyrexia, using the inhibitor of acid lactic production dichloroacetate (DCA). Each of 28 rats was placed in a chamber ventilated with humidified air at an ambient temperature of 24-26 degrees C. After a control period of 30 min the animals were given saline or 100 mg/kg DCA i.p. Then, 30 min later, the chamber was flushed with a 7% O(2) gas mixture for 2 h. At the end of the experiment, the animals were decapitated and blood samples collected for measurements of plasma lactate. T(c) was measured by biotelemetry. DCA did not affect the T(c) or basal lactate levels of normoxic rats. Hypoxia elicited a significant decrease in T(c) and an increase in plasma lactate levels. Although DCA decreased plasma lactate levels during hypoxia, it caused no change in the course of hypoxia-induced anapyrexia. Correspondingly, no correlation was found between the drop in T(c) and the rise in plasma lactate during hypoxic conditions. These results do not support the hypothesis that lactate is a mediator of hypoxia-induced anapyrexia in rats.
缺氧会导致机体核心温度（T(c)）出现一种有调节的下降，即所谓的低体温，这似乎是预防缺氧相关细胞损伤的一种非常有效的方式。由于在几种病理状态下，氧气供应是一个限制因素，所以低体温的临床重要性是显而易见的。然而，这种反应所涉及的机制仍不清楚。我们使用乳酸生成抑制剂二氯乙酸（DCA）来检验这样一个假设：乳酸作为缺氧的经典伴随物，是缺氧诱导低体温的介质。将28只大鼠每只置于一个在24 - 26摄氏度环境温度下用湿化空气通风的实验箱中。在30分钟的对照期后，给动物腹腔注射生理盐水或100mg/kg的DCA。然后，30分钟后，用7%的氧气混合气体冲洗实验箱2小时。实验结束时，将动物断头并采集血样以测定血浆乳酸水平。通过生物遥测法测量T(c)。DCA对常氧大鼠的T(c)或基础乳酸水平没有影响。缺氧导致T(c)显著下降以及血浆乳酸水平升高。尽管DCA在缺氧期间降低了血浆乳酸水平，但它并未改变缺氧诱导低体温的进程。相应地，在缺氧条件下，未发现T(c)下降与血浆乳酸升高之间存在相关性。这些结果不支持乳酸是大鼠缺氧诱导低体温介质这一假设。
