Almeida M C, Carnio E C, Branco L G
Faculdade de Odontologia and Escola de Enfermagem de Ribeirão Preto, Universidade de São Paulo, 14040-904 Ribeirão Preto, Brazil.
J Appl Physiol (1985). 1999 Dec;87(6):2186-90. doi: 10.1152/jappl.1999.87.6.2186.
Hypoxia causes a regulated decrease in body temperature (T(b)), and nitric oxide (NO) is now known to participate in hypoxia-induced hypothermia. Hypoxia also inhibits lipopolysaccharide (LPS)-induced fever. We tested the hypothesis that NO may participate in the hypoxia inhibition of fever. The rectal temperature of awake, unrestrained rats was measured before and after injection of LPS, with or without concomitant exposure to hypoxia, in an experimental group treated with N(omega)-nitro-L-arginine (L-NNA) for 4 consecutive days before the experiment and in a saline-treated group (control). L-NNA is a nonspecific NO synthase inhibitor that blocks NO production. LPS caused a dose-dependent typical biphasic rise in T(b) that was completely prevented by hypoxia (7% inspired oxygen). L-NNA caused a significant drop in T(b) during days 2-4 of treatment. When LPS was injected into L-NNA-treated rats, inhibition of fever was observed. Moreover, the effect of hypoxia during fever was significantly reduced. The data indicate that the NO pathway plays a role in hypoxia inhibition of fever.
缺氧会导致体温（Tb）有规律地下降，并且现在已知一氧化氮（NO）参与缺氧诱导的体温过低。缺氧还会抑制脂多糖（LPS）诱导的发热。我们检验了NO可能参与缺氧对发热的抑制作用这一假说。在实验前连续4天用N（ω）-硝基-L-精氨酸（L-NNA）处理的实验组以及生理盐水处理组（对照组）中，测量清醒、未受束缚大鼠在注射LPS前后的直肠温度，注射LPS时伴有或不伴有缺氧暴露。L-NNA是一种阻断NO生成的非特异性一氧化氮合酶抑制剂。LPS导致Tb出现剂量依赖性的典型双相升高，而缺氧（吸入氧浓度为7%）可完全阻止这种升高。L-NNA在治疗的第2至4天导致Tb显著下降。当向用L-NNA处理的大鼠注射LPS时，观察到发热受到抑制。此外，发热期间缺氧的作用显著降低。数据表明NO途径在缺氧对发热的抑制中起作用。
