Ambient temperature modulates the differentiated cardiorespiratory pattern generated by the central noradrenergic...

In conscious rabbits with indwelling intracisternal (i.c.) catheters i.c. injections of 600 micrograms kg-1 6-hydroxydopamine (6-OHDA) elicited with short latencies an increase in metabolic rate followed by cutaneous vasoconstriction and a reduction in renal sympathetic nerve activity; in addition there was depression of respiratory rate, bradycardia and a fall of blood pressure. This differentiated cardiorespiratory activity pattern was fully established about 1 h after i.c. 6-OHDA, when injected at thermoneutrality. At warm ambient temperatures the metabolic and cardiorespiratory responses to i.c. 6-OHDA were considerably diminished and there was tachycardia. Intravenous (i.v.) injection of 4 micrograms kg-1 bacterial endotoxin (LPS) in intact rabbits evoked with short latency an increase in metabolic rate and the typical cardiorespiratory activity pattern normally seen in cold defense, consisting of cutaneous vasoconstriction, a depression of respiratory rate and, as shown in a previous study, a decrease in renal sympathetic nerve activity while heart rate and arterial blood pressure is little altered. When LPS was i.v. injected 2-3 days after i.c. 6-OHDA, the febrile response was attenuated with lesser cutaneous vasoconstriction and respiratory rate depression. There was no early inhibition in renal sympathetic nerve activity but rather marked excitation, with increases in heart rate and arterial blood pressure. The results indicate that the effects on autonomic system activities being produced by transmitter release at noradrenergic terminals acutely following i.c. 6-OHDA are considerably modulated by ambient temperature. Comparison of autonomic system reactions in fever obtained in the intact animal and after i.c. 6-OHDA reveals the important role of central noradrenergic pathways in preserving blood pressure homeostasis and heat conservation. The appearance of cardiorespiratory responses similar to those obtained after i.c. noradrenaline or i.c. 6-OHDA, when non-thermal activation of thyrotropin-releasing hormone (TRH) neurons occurs (as demonstrated in a previous study), suggests the hypothesis that TRH neurons known to be specifically influenced by changes in body temperature, converge onto the central noradrenergic system producing the typical cardiorespiratory pattern of cold defense.