The effects of respiratory alkalosis on pulmonary and systemic hemodynamics in the intact anesthetized dog were measured and compared to a control period with normal pH and pCO2. Pulmonary artery, pulmonary vein, and systemic artery pressures were measured through fluoroscopically placed cardiac catheters. Transmural pressures were determined by subtraction of intrapleural from vascular pressures. Cardiac output was determined in duplicate by the indicator-dilution technique using Cardio-green. Respiratory alkalosis in passively hyperventilated intact anesthetized dogs did not significantly alter cardiac output, or systemic or pulmonary vascular resistance in 13 experiments. The possibility that increased intratracheal pressure during hyperventilation may have mechanically masked a decrease in pulmonary vascular resistance was ruled out in a second series of 17 experiments in which intratracheal pressure was maintained constant. An inverse relationship between pulmonary vascular resistance and pH was not found in this study. Note: (With the Technical Assistance of Robert Powell) pulmonary vascular resistance; pulmonary circulation; respiratory alkalosis; acid-base effects; cardiac output Submitted on December 19, 1963