Effect of Ethanol on Hemoperfusion and O₂ Sufficiency in Livers in Vivo

Abstract

Hemoperfusion and rate of 0₂ 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 0₂ consumption in situ and the redox level of cytochrome c (+c_l) in the mitochondrial respiratory chain. The rate of 0₂ consumption thus calculated remained constant until the apparent 0₂-saturation of hemoglobin in situ decreased to less than 10% of the total of hemoglobin. In parallel with the decrease of the rate of 0₂ consumption, the apparent reduction level of cytochrome c (+c_l) increased. It was shown in fed rats that the ethanol ingestion (1 g/kg) stimulated 0₂ uptake in the liver by 29% which initially caused a decrease in 0₂-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.