Protective effect of CO2-induced hyperventilation on the hepatotoxicity elicited by carbon tetrachloride.

Following oral intake or inhalation, halogenated hydrocarbons are metabolized to hepatotoxic intermediates in the liver to only a small extent, the major part being eliminated via the lungs without biochemical transformation. Following intoxication, increased pulmonary elimination of hydrocarbons can be achieved in patients by treatment with CO2-induced hyperventilation. To investigate the efficacy of this new therapy under exact experimental conditions, female Wistar rats received 2.5 ml CCl4/kg BW by gastric intubation and were then treated with CO2-induced hyperventilation. In comparison to untreated animals, hyperventilated rats showed only a few signs of hepatic injury by histological evaluation, whereas massive centrolobular necroses and fatty infiltrations were observed in non-hyperventilated animals. By biochemical assessment, significant decreases of GOT, GPT and GDH activity were observed in the serum, when hyperventilated rats were compared to untreated animals. Moreover, the LD50 for CCl4 was almost trebled after hyperventilation compared to the non-hyperventilated animals. The increased LD50, and the biochemical and histological results therefore substantiate the usefulness of CO2-induced hyperventilation therapy in the treatment of intoxications by hydrocarbons under standardized experimental conditions.