Previous reports have indicated a significant degree of hindlimb skeletal muscle vasodilation coincident with the decompensatory phase of shock induced by prolonged hemorrhagic hypotension. The first objective of the present investigation was to examine the relationship between this apparent vascular decompensation and the arterial and venous skeletal muscle PO2, PCO2, VO2, VCO2, pH, Na+ and K+. The second objective was to examine the possibility that a stable blood-borne, remotely or locally released, vasodilator substance caused the vascular decompensation. Anesthetized dogs were bled in 5 ml/kg steps into a suspended reservoir until mean arterial pressure (MAP) was 35-40 mm Hg; this pressure was maintained until signs of decompensation were apparent. The blood remaining in the reservoir was returned and the animals were followed until MAP fell below 50 mm Hg. MAP, central venous pressure (CVP), lead II of ECG, heart rate (HR), and skeletal muscle venous flow were monitored and correlated with arterial and venous CO2, O2, and electrolytes. The results suggest that the skeletal muscle vascular decompensation was not caused by a stable blood-borne substance but may at least in part be due to the increased H+ and K+ in skeletal muscle blood and to mild skeletal muscle hypoxia.