Deterioration of donor lung function contributes to the shortage of donor organs and early postoperative failure after transplantation. A decrease in donor pulmonary function is associated with opacification of lung fields on radiographs, rendering the lungs unsuitable for transplantation, which may be related to the effects of brain death (BD) on pulmonary hemodynamics. Twenty mongrel canines (25.5 +/- 0.7 kg) underwent 20 BD experiments using a previously validated BD organ donor model. An ultrasonic flowmeter was applied on the pulmonary artery and micromanometers were inserted into the right ventricle, pulmonary artery, and left atrium to measure, which allowed the hemodynamic assessment and impedance profile analysis of the pulmonary vasculature by Fourier transformation. Characteristic impedance (Zo) was compared with input resistance (RIN) and with calculated pulmonary vascular resistance (PVR), the conventional index. Right ventricular hydraulic power was analyzed and divided in its components oscillatory and steady power. The results are expressed as means and SEM (analysis of variance, paired two-tailed t tests). Cushing reflex, hemodynamic response, and diabetes insipidus were consistent findings following BD. PVR, Zo, and RIN decreased significantly (p < 0.05) from 367 +/- 40 dyne.s.cm-5, 226 +/- 13 dyne.s.cm-5, and 771 +/- 52 dyne.s.cm-5 to 261 +/- 25 dyne.s.cm-5, 159 +/- 10 dyne.s.cm-5, and 651 +/- 69 dyne.s.cm-5 6 h after BD. Pulmonary artery blood flow increased significantly from 1,499 +/- 107 mL/min to 2,064 +/- 209 mL/min (p < 0.05) after BD. Hydraulic power increased from 69 +/- 6 mW to 104 +/- 13 mW (p < 0.05) and the oscillatory power to steady power ratio of 33%/67% changed to 23%/77% following BD. Extravascular pulmonary water content increased significantly by 10% after BD. BD causes a significant change in pulmonary vascular hemodynamics. The decrease in impedance and right ventricular afterload may lead to significant pulmonary overflow injury and edema. The increase in steady power represents an important reserve of the right ventricle to sustain pulmonary blood flow following BD.