Aminopyrine demethylation was investigated in rats after a 70%
hepatectomy to assess possible parallelism between the recovery of mass and function. Tests were performed by analyzing 14CO2 exhalation from 0.1 microCi per 100 gm of
body weight of [
dimethylamine-14C]
aminopyrine given intraperitoneally with incremental doses of unlabeled
drug. Early after 70%
hepatectomy, Vmax was reduced by 52%. This discordance between mass and function was not due to extrahepatic
aminopyrine demethylation, since liver exclusion reduced demethylation of
aminopyrine to nearly nil. Whether it results from increased liver blood flow in the remnant liver is less clear:
portacaval anastomosis provoked an identical fall in Vmax and liver blood flow, but aortal-portal
fistula which increased liver blood flow by 70% did not modify Vmax. The early increase in Vmax could be related to a "hepatotrophic" factor of splanchnic origin which increased after partial
hepatectomy and decreased after
portacaval shunt. After the early period, Vmax, expressed per gram of actual liver weight, returned to control range. Throughout regeneration (4 to 144 hr), no modification was observed in Km nor in
cytochrome P-450 concentration. Enzymatic induction with
phenobarbital increased the demethylation capacity more than liver weight in intact and regenerating liver. Except for the first hours after partial
hepatectomy or after enzymatic induction, the
aminopyrine demethylation capacity directly correlated with liver mass and may be useful in evaluating liver regeneration in vivo.