Nitric oxide and fever: immune-to-brain signaling vs. thermogenesis in chicks
Nitric oxide and fever: immune-to-brain signaling vs. thermogenesis in chicks
复制标题
DOI：
10.1152/ajpregu.00453.2015
复制
发表时间：
2016-05-15
影响因子：
2.8
通讯作者：
Bicego, Kenia C.
中科院分区：
文献类型：
--
作者：
Dantonio, Valter;Batalhao, Marcelo E.;Bicego, Kenia C.
一氧化氮（NO）在大鼠的生热作用中起作用，但不介导免疫到脑的发热信号。有人认为鸟类的情况不同，但潜在的证据并不令人信服。本研究旨在通过低剂量或高剂量的细菌LPS对5日龄雏鸡进行攻击，以澄清这一问题。低剂量LPS （2 μ g/kg）在注射后3-5小时引起发烧，而100 μ g/kg注射后1小时降低核心体温（T-c），随后4或5小时发烧。注射LPS后4 h血浆硝酸盐水平升高，但与发热程度无关。NO合成酶抑制剂（ng -硝基- l -精氨酸甲酯，L-NAME; 50 mg/kg）在31-32℃条件下可减轻两种剂量LPS诱导的发热，并增强高剂量LPS诱导的Tc降低幅度。这些作用与代谢率的抑制有关，至少在高剂量LPS的情况下是这样。相反，在35-36℃的温度下，L-NAME对Tc的影响消失了，这表明发热信号基本上没有受到影响。因此，lps诱导的脑PGE(2)水平升高不受L-NAME的影响。此外，L-NAME增强了lps诱导的抱团，这表明在产热减弱的情况下，存在发热的代偿机制。因此，与大鼠一样，全身抑制NO合成通过影响热效应活性而不是通过干扰免疫-脑信号传导来减弱lps诱导的雏鸡发热。这可能构成了一氧化氮在恒温动物中的保守作用。
Nitric oxide (NO) plays a role in thermogenesis but does not mediate immune-to-brain febrigenic signaling in rats. There are suggestions of a different situation in birds, but the underlying evidence is not compelling. The present study was designed to clarify this matter in 5-day-old chicks challenged with a low or high dose of bacterial LPS. The lower LPS dose (2 mu g/kg im) induced fever at 3-5 h postinjection, whereas 100 mu g/kg im decreased core body temperature (T-c) (at 1 h) followed by fever (at 4 or 5 h). Plasma nitrate levels increased 4 h after LPS injection, but they were not correlated with the magnitude of fever. The NO synthase inhibitor (NG-nitro-L-arginine methyl ester, L-NAME; 50 mg/kg im) attenuated the fever induced by either dose of LPS and enhanced the magnitude of the Tc reduction induced by the high dose in chicks at 31-32 degrees C. These effects were associated with suppression of metabolic rate, at least in the case of the high LPS dose. Conversely, the effects of L-NAME on Tc disappeared in chicks maintained at 35-36 degrees C, suggesting that febrigenic signaling was essentially unaffected. Accordingly, the LPS-induced rise in the brain level of PGE(2) was not affected by L-NAME. Moreover, L-NAME augmented LPS-induced huddling, which is indicative of compensatory mechanisms to run fever in the face of attenuated thermogenesis. Therefore, as in rats, systemic inhibition of NO synthesis attenuates LPS-induced fever in chicks by affecting thermoeffector activity and not by interfering with immune-to-brain signaling. This may constitute a conserved effect of NO in endotherms.