Critically ill patients are susceptible to reductions in cardiac output caused by positive pressure breathing in addition to pathologic factors, e.g. hemorrhage. There is much information regarding vascular responses to hemorrhage but less is known about venoconstrictive responses to positive pressure breathing. This study compared venous and arterial reflex responses to changes in transmural atrial pressure (Ptm) induced by PEEP (8, 12, 16, and 20 mmHg) and simulated hemorrhage (lower body negative pressure [LBNP] -10,-15, -20, -25 mmHg) in 5 healthy young adults. Changes in venous pressure in the hemodynamically isolated forearm, forearm blood flow (venous occlusion plethysmography) and arterial blood pressure were measured to quantify venous and arterial responses. Ptm was calculated from direct measurements of central venous and esophageal pressures. Cardiac output (CO) was measured by impedance cardiography. All data are shown as mean (s.e.). PEEP/LBNP, respectively, induced a progressive reduction in Ptm from 6.1 (.5)/6.5 (.6) → 3.0(.9)/2.0 (.2) mmHg (baseline → minimum). In response CO decreased from 6.5 (.5)/6.0 (.5) → 5.0 (.5)/3.9 (.5) L/min and forearm vascular resistance (FVR) increased from 21.5 (3.8)/22.2 (2.7) → 36.7 (8.0)/52.5(7.2) RU. The change in CO and FVR with PEEP and LBNP were comparable for the same Ptm. With each decrease in Ptm, venous pressure showed a mild but graded increase from 9.5 (1.3)/10.4 (1.7) → 12.9 (1.3)/13.5 (1.9) mm Hg, indicating an increase in venomotor tone. However, this response was transient, usually < 1 min. These data indicate that mechanisms affecting peripheral blood volume mobilization from skeletal muscle and skin are similar in PEEP and simulated hemorrhage, with arteriolar rather than venomotor reflexes appearing more important. Thus, we speculate that factors affecting peripheral blood volume distribution in pathologic states are likely related to disturbances in reflex control of arteriolar rather than venous tone.Support: HL-39818