Scammell T E, Elmquist J K, Saper C B
Department of Neurology, Beth Israel Hospital, Boston, Massachusetts 02115, USA.
Am J Physiol. 1996 Aug;271(2 Pt 2):R333-8. doi: 10.1152/ajpregu.1996.271.2.R333.
The labile gas nitric oxide (NO) mediates a wide variety of thermoregulatory processes including vasomotor control, brown fat thermogenesis, and neuroendocrine regulation. Additionally, during endotoxemia, NO modulates the release of cytokines and hypothalamic peptides. To determine the role of NO in thermoregulation and fever, we intravenously injected the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and measured its effects on body temperature during normal thermoregulation and endotoxemia in awake, unrestrained rats. L-NAME produced a stereoselective, dose-dependent hypothermia that lasted up to 4 h after bolus intravenous injection. Intravenous lipopolysaccharide (LPS) produced fever in a dose-dependent manner, which was preceded by hypothermia at higher doses alpha-LPS. NOS inhibition reduced the febrile response to LPS and produced marked hypothermia with a low dose of LPS. These findings indicate that NO may play an important role in thermoregulation and suggest that NO is required for the production of fever.
不稳定气体一氧化氮（NO）介导多种体温调节过程，包括血管舒缩控制、棕色脂肪产热和神经内分泌调节。此外，在内毒素血症期间，NO调节细胞因子和下丘脑肽的释放。为了确定NO在体温调节和发热中的作用，我们给清醒、不受约束的大鼠静脉注射一氧化氮合酶（NOS）抑制剂NG-硝基-L-精氨酸甲酯（L-NAME），并在正常体温调节和内毒素血症期间测量其对体温的影响。静脉注射L-NAME后产生了立体选择性、剂量依赖性的体温过低，推注后持续长达4小时。静脉注射脂多糖（LPS）以剂量依赖性方式引起发热，在较高剂量的α-LPS时先出现体温过低。抑制NOS可降低对LPS的发热反应，并在低剂量LPS时产生明显的体温过低。这些发现表明NO可能在体温调节中起重要作用，并提示发热的产生需要NO。
