In the present study our aim was to determine whether or not neurogenic pulmonary edema would develop from a brief pulse of intracranial pressure (ICP) in the absence of any obvious pulmonary hypertension. There were three groups of cats: sham-operated controls, ICP only, and ICP plus variable occlusion of the pulmonary artery. Partial occlusion of the pulmonary artery was carried out by placing a ligature around the pulmonary trunk and mechanically constricting the artery to maintain pulmonary arterial pressure (PAP) and left atrial pressure (LAP) at pre-ICP levels. In sham-operated animals the extravascular lung water/blood free dry weight ratio (EVLW/BFDW) was 3.26 k 0.07 and broncho-alveolar lavage (BAL) protein, 6.49 2 0.62 mg/g lung. ICP-only caused a rise in PAP, left atrial pressure, and EVLW/BFDW to 3.67 t-0.08 (P < 0.05). ICP with partial occlusion of the pulmonary artery prevented any rise in PAP or LAP while EVLW/BFDW rose to 3.67 +_ 0.10 (P < 0.05) and BAL protein was 8.37 f 1.27 mg/g lung. Our results show that EVLW/BFDW can increase with neurogenic pulmonary edema in cats in the absence of an obvious increase in pulmonary arterial or left atrial pressure. o 1987 Society for Experimental Biology and Medicine.