Effect of ethanol on hemoperfusion and O2 sufficiency in livers in vivo.

Hemoperfusion and rate of O2 uptake in the livers in vivo following ethanol ingestion were measured by reflectance spectrophotometry. Pressurization on the liver in situ above the sinusoidal blood pressure caused complete blocking of blood flow, followed by spectral changes due to transition from hepatic normoxia to anoxia. Analyses of such spectra provided informations as to the rate of O2 consumption in situ and the redox level of cytochrome c (+cl)) in the mitochondrial respiratory chain. The rate of O2 consumption thus calculated remained constant until the apparent O2-saturation of hemoglobin in situ decreased to less than 10% of the total of hemoglobin. In parallel with the decrease of the rate of O2 consumption, the apparent reduction level of cytochrome c (+Cl) increased. It was shown in fed rats that the ethanol ingestion (1 g/kg) stimulated O2 uptake in the liver by 29% which initially caused a decrease in O2-saturation of hemoglobin, followed by an increase in blood supply to the liver. Thus, the ethanol consumption resulted in an increase in hepatic oxidative metabolism, possibly leading to hepatic hypoxia and liver damage.