In anesthetized and vagotomized rats, an intense cerebral compression (CC) by intracra-nial placement of a space-occupying mass evoked systemic arterial hypertension (SAH), pulmonary venous hypertension (PVH), and pulmonary hemorrhagic edema (PHE) in 2-3 minutes. Observation of the regional weight changes revealed an acute increase in pulmonary blood volume with a decrease in the volume of the systemic vascular beds. With chronically instrumented flow probes, we demonstrated that the overall pattern of imbalance in right and left cardiac outputs was characterized by an immediate fall in aortic flow by 52% accompanying a slower decline pulmonary arterial flow. In 10 rats with a right heart bypass (venous return to reservoir and constant pulmonary inflow), CC produced severe PVH and PHE associated with SAH, reservoir volume reduction, and no significant change in pulmonary vascular resistance. The increases in left atrial pressure and lung index (lung: body weight x 100) were much greater than those obtained with natural circulation. In 20 left heart-bypassed rats (constant aortic flow either with or without a reservoir between the left atrium and roller pump), CC induced SAH, whereas no significant changes occurred in the lungs. The lung index was not different from the normal value. The results indicate that neurogenic constriction of the systemic capacitance vessels to favor venous return is not an important hemodynamic event in the centrogenic pulmonary pathology. Pulmonary volume loading leading to pulmonary hypertension and PHE is evoked princi-pally by a dramatic pulmonary hypertension decrease in left ventricular output due to ventricular strain in the face of an intense arteriolar constriction.Circ Res 47: 366-373, 1980