Abstract
Mice reduce ventilation and metabolism under hyperthermia, which indicates a reduction of thermogenesis. In order to examine the contribution of histamine (HA) H1 receptors to this process, we examined ventilation, aerobic metabolism and arterial blood gasses at normothermia and hyperthermia in HA H1 receptor knock out (HIRKO) and wild type (WT) mice. Measurements were performed in the unrestrained and conscious state. At hyperthermia, VE decreased in proportion to the decrease of O2 consumption (VO2) and CO2 excretion (VCO2) in WT mice. The VE/VO2 ratio remained constant and blood gas showed normocapnia at both body temperatures (BTs) in WT mice. H1RKO mice increased VE and decreased VO2 and VCO2 compared to WT mice at both BTs. The VE/VO2 ratios were constant at both BTs, whereas the ratio was higher and PaCO2 was lower in H1RKO mice than in WT mice at both BTs, suggesting hyperventilation. That hyperthermia reduces VE and VO2 in H1RKO and WT mice suggests that the HA H1 receptor does not contribute to the thermal control of respiration in mice. However, H1RKO mice showed hyperventilation induced by a decrease of VO2 and an increase of VE, indicating that the HA H1 receptor contributes to the maintenance of metabolism. It is known that central HA reduces feeding and increases energy consumption through sympathetic pathway via H1 receptors. Therefore, the hypometabolism in H1RKO mice is reasonable, but relatively high VE with respect to the decreased VO2 in H1RKO mice warrants further study. [Jpn J Physiol 54 Suppl:S110 (2004)]
