Objectives To explore the effect and the underlying mechanisms of rapid hemodialysis on cardiac and pulmonary function. Methods Water content in the lung tissue, indexes of pulmonary vascular pressure, and pathological changes of lung tissue were evaluated after hemodialysis in animals with experimental acute renal failure. Results Plasma levels of urea nitrogen, creatinine and osmotic pressure were decreased rapidly and significantly after rapid hemodialysis, and consequently an increase of water content in lung lead to pulmonary congestion and edema.There were also statistically significant changes (P<0.05) among pre and posthemodialysis as for RAP (10.80±3.08)mmHg vs (17.90±4.89)mmHg, PCWP(-1.30±1.95)mmHg vs (17.90±4.46)mmHg, RVP(7.10±2.85) mmHg vs (18.32±3.95)mmHg, PAP (10.80±3.08)mmHg vs (17.90±4.89)mmHg, CVP(0.50±1.65)cmH2O vs (1.3 0±2.00) cmH2O), TPRI (2.25±0.37)u·m2 vs (2.83±0.63)u·m2) and CI(5.21±0. 92)L/min vs (3.89±0.93)L/min, SI(0.041±0.009)L/min vs (0.025±0.007)L/min). Pu lmonary congestion was evidenced with chest X-ray photography, determination of water content of the lung tissue, index of pulmonary edema and pathological examination of the lung. Conclusions The result of the study suggest that, the rapid he modialysis can induce pulmonary congestion and edema and acute heart failure in ARF patients. Its underlying mechanism might be associated with reverse urea effect which is due to the formation of lung/plasma osmotic gradient, and ultimately water in plasma permeating into lung tissue. 