| dc.description.abstract | Low and high LPS doses (endotoxin) have been used as models to study fever and endotoxic shock, respectively. In rats, systemic nitric oxide (NO) directly affects thermogenesis, but does not mediate those responses. Even though few studies in birds suggest NO as a pyrogenic signalling to brain, there is not enough evidence for confirming this suggestion. We hypothesise that, compared to mammals, systemic NO presents similar thermogenic action during endotoxin challenge in birds, even in early life. As precocial birds, chickens have a developed thermoregulatory capacity immediately after hatching, which constitutes an interesting model to study thermoregulation in early life. Thus, we investigated the role of NO in LPS-induced fever and endotoxic shock in 5-day-old chicks. The doses of 2 (LPS2) and 10 g kg-1 of LPS induced fever 3-5 hours after intramuscular (IM) injection, while 50 and 100 (LPS100) g kg-1 decreased Tc within the first hour followed by fever at 4-5 hours postinjection. Plasma nitrate levels increased 4 hours, but not 1 hour, after treatment with LPS2 and LPS100 (higher increase). There was no correlation between plasma nitrate concentrations and Tc at both LPS doses. L-NAME (non-selective NOS inhibitor; 50 mg kg-1; IM) inhibited LPS2- and LPS100-induced fever and increased the magnitude of the fall in Tc caused by LPS100. In contrast, no effect of L-NAME was observed in LPS-treated chicks in warm conditions. L-NAME decreased oxygen consumption in LPS2- and LPS100-treated chicks, but the response was more pronounced with LPS100. Moreover, LPS-induced huddling (heat conservation behaviour) was accentuated by LNAME. Our results seem to indicate that, like in rats, systemic NO is not a mediator of fever and endotoxic shock in chicks, but does affect thermogenesis in these animals, which may constitute a common effect of NO in the endothermic vertebr. | |
