Maintenance of corneal hydration is dependent on the active transport properties of the corneal endothelium. We tested the hypothesis that lactate efflux, facilitated by buffering, is a component of endothelial transport. Rabbit corneas were perfused with Bicarbonate-Rich (BR) or Bicarbonate-Free (BF) ringer of varying buffering power, while corneal thickness was measured. Perfusate was collected and analyzed for lactate efflux. In BF with no added HEPES, the maximal corneal swelling rate was 30.0±4.1µm/hr, compared to 5.2±0.9 µm/hr in BR. Corneal swelling decreased directly with [HEPES], such that with 60 mM HEPES corneas swelled at 7.5±1.6µm/hr. Perfusate [lactate] increased directly with [HEPES]. Similarly, reducing the [HCO₃^-] increased corneal swelling and decreased lactate efflux. Corneal swelling was inversely related to ringer buffering power (β), while lactate efflux was directly related to β. Ouabain (100 μM) produced maximal swelling and reduction in lactate efflux, whereas carbonic anhydrase inhibition and an MCT1 inhibitor produced intermediate swelling and decreases in lactate efflux. Conversely, 10μM adenosine reduced the swelling rate to 4.2±0.8 μm/hr and increased lactate efflux by 25%. We found a strong inverse relation between corneal swelling and lactate efflux (r=0.98, p<0.0001). Introducing lactate in the ringer transiently increased corneal thickness, reaching a steady-state (0±0.6 μm/hr) within 90 minutes. We conclude that corneal endothelial function does not have an absolute requirement for bicarbonate; rather it requires a perfusate with high buffering power. This facilitates lactic acid efflux, which is directly linked to water efflux, indicating that lactate flux is a component of the corneal endothelial pump.