To examine the opposing vascular reflexes that regulate blood pressure and heat dissipation 8 healthy young adults were exposed to different levels of lower body negative pressure (LBNP, -10 to -90 mm Hg) to reduce cardiac output in normothermia (N) and during passive heating (H). We measured central venous pressure (CVP), blood pressure, heart rate, cardiac stroke volume (impedance), forearm blood flow (plethysmography) and venomotor tone (occluded limb technique). H raised esophageal temperature by ±0.5 degrees C. All data are mean ± sem. CVP was lower during H than during N (6.1±0.6vs. 8.0±0.6 mm Hg) but dropped to similar levels during LBNP(e.g. -60 mm Hg: H: -0.4±0.6. N: -0.1±0.7 mm Hg). Mean arterial pressure was also lower during H (78±3 vs 91±3 mm Hg), but was not altered during LBNP. H did not change the pressure-volume relationship of the heart. Compared to N. H reduced systemic vascular resistance from 13.9±1.5 to 10.5±1.2 resistance units (RU) which increased to 18.3±2.1 vs. 15.1±1.5 RU in response to LBNP -60, respectively. Forearm vascular resistance representing skin blood flow decreased from 16.7±2.9 to 5.7±1.7 RU and increased with LBNP to 39.1±0.4 vs. 12.6±1.5 RU. Venomotor responses were attenuated during H. Conclusions: The major compensation to a reduction in cardiac preload is an increase in vascular resistance and redistribution of blood flow which may be compromised by mechanisms evoked for heat dissipation. Thus, reduction of thermal stress is import during restoration of cardiac output in critically ill children.