The purpose of this study was to investigate the mechanisms of the leukemic glaucoma. We established a cell culture from leukemic cells collected from the aqueous humor of a living patient with chronic lymphocytic leukemia (CLL) and glaucoma secondary to the leukemia. We then perfused 16 pairs of fresh cadaver normal human eyes at a constant pressure of 10 mmHg at 37 degrees C. We delivered as a bolus either cultured CLL cells or cultured normal lymphocytes, using 3 x 10(2), 3 x 10(3), 3 x 10(4) or 3 x 10(5) cells in Bárány's solution, into one eye of each pair. The other eye of the pair served as a control, receiving a sham bolus of Bárány's solution alone. In addition, CLL and normal lymphocytes were perfused through 0.2, 0.6, 2, and 3 microns millipore filters. Following perfusion, the tissue and the filters were examined histopathologically by light, transmission and scanning electron microscopy. Cultured leukemic lymphocytes perfused into normal cadaver eyes caused a significantly more profound reduction in outflow facility than normal lymphocytes (P < 0.05); however, there was no significant difference in the effect on outflow facility between leukemic and normal lymphocytes when they were perfused through the millipore filters. Histopathology confirmed the presence of lymphocytes in the trabecular meshwork and Schlemm's canal, deforming on passage through the inner wall. Our results suggest that leukemic lymphocytes in CLL may reduce outflow facility by means of a biological interaction with the tissues of the outflow pathways, rather than by mechanical obstruction due to a lack of distensibility. Questions remain as to the nature of this biological interaction.