To evaluate possible physiologic mechanisms in hemorrhagic shock, sequential hemodynamics, O2 transport, conjunctival O2 (PcjO2), transcutaneous blood gases (PtcO2, PtcCO2), and core and conjunctival temperature (Tcore, Tcj) were measured during a control period, after hemorrhage, after reinfusion of the shed blood, and subsequently during terminal normovolemic shock in eight anesthetized dogs. The PtcO2 sensor requires surface heating to 44 degrees or 45 degrees C, whereas the PcjO2 sensor measures surface temperature but does not heat the tissue, thus avoiding heat-induced artifacts. Shortly after onset of hemorrhage, hemodynamic variables, bulk O2 transport, and tissue O2 tensions decreased abruptly. Prolongation of hemorrhage further deteriorated these variables. Reinfusion of the shed blood returned all values except PcjO2 to the normal range. In the terminal stage, all variables except PaO2 again deteriorated; decreased O2 transport impaired oxygen consumption, which in turn reduced both central and peripheral heat production. Lowered oxygen consumption, Tcore and Tcj reflect decreases in total-body and local tissue metabolism. These data are consistent with the concept that tissue O2 tension represents the balance between O2 supply and O2 demand and thus reflects overall O2 metabolism, which may be rate-limited by circulatory deficiencies.