Acute hypoxia in newborns of various species including humans is associated with decreased thermogenesis and a fall in body temperature. We have investigated the cardiorespiratory consequences of correcting the fall in colonic temperature (Tc) during acute hypoxia in newborn cats. Experiments were conducted on 21 unanesthetized kittens (12 +/- 1 d SEM, 244 +/- 8 g) instrumented with catheters in the left common carotid artery and superior vena cava for measurements of systemic arterial pressure, central venous pressure, heart rate, arterial blood gases, arterial O2 saturation (SaO2) and mixed venous O2 saturation. Oxygen consumption (VO2) and CO2 production (VCO2) were also measured. Alveolar ventilation (VA), cardiac index (CI), and systemic vascular resistance index (SVRI) were calculated. These determinations were made in 21% O2 at an ambient temperature (Tamb) of 25 degrees C, and after 80 min of exposure to Fio2 = 0.10. In one group Tamb was maintained at 25 degrees C (n = 8) during hypoxia and Tc fell by 2.7 +/- 0.4 degrees C whereas in a second group Tamb was increased to 35 degrees C for the second 40 min of hypoxia to raise Tc the prehypoxic level (n = 13). VO2, VCO2, VA, SaO2, and systemic arterial pressure during hypoxia did not differ between the animals which were warmed and those which were not. However, CI and heart rate were greater (452 +/- 23 versus 346 +/- 30 mL.min-1.kg-1 p < 0.05, 279 +/- 8 versus 228 +/- 12 beats.min-1 p < 0.05) and SVRI lower (0.115 +/- 0.022 versus 0.153 +/- 0.014 mm Hg.mL-1.min.kg, p < 0.05) during hypoxia in the warmed animals compared with the unwarmed group. Thus, artificially raising Tc during hypoxia resulted in peripheral vasodilation, whereas systemic arterial pressure was maintained by the increase in cardiac output. We conclude that, in the hypoxic kitten, raising Tc to normoxic values elicits a response that may reflect a condition of relative hyperthermia.