THERMOREGULATORY EFFECTS OF CYANIDE AND AZIDE IN THE TOAD, BUFO-MARINUS

An important adaptation to hypoxia is a regulated reduction in body te mperature (T-b; anapyrexia), presumably because it lowers metabolic ra te when oxygen supply is limited. Although this beneficial response oc curs in organisms ranging from protozoans to mammals, little is known of the cellular mechanisms involved. We showed previously that inhibit ion of oxidative phosphorylation mediates hypoxia-induced anapyrexia i n the paramecium. In this study, we tested the hypothesis that inhibit ion of oxidative phosphorylation also causes anapyrexia in a vertebrat e, Bufo marinus. T-b in toads was measured in a thermal gradient 24 h before and 24 h after administration of either NaCN or NaN3, both inhi bitors of oxidative phosphorylation. Subcutaneous NaCN (0.6 mmol/kg) r educed T-b from 29.1 +/- 0.8 to 19.6 +/- 0.6 degrees C (P = 0.002). In fusion of NaCN (0.6 mu mol/kg) into the fourth ventricle of the brain reduced T-b from 30.0 +/- 0.9 to 24.8 +/- 1.2 degrees C (P = 0.01). Re sponses to NaN3 were similar to the NaCN responses. Control injections and subcutaneous injections of 0.6 mu mol/kg NaCN and NaN3 had no sig nificant effect on T-b (P > 0.32). Neither NaCN nor NaN3 had significa nt effects on arterial PO2, PCO2, or pH at 26 degrees C. These results indicate that inhibition of oxidative phosphorylation in the central nervous system leads to the selection of cooler temperatures. Thus red uced oxidative phosphorylation within the brain may be an important fa ctor eliciting hypoxia-induced anapyrexia.