Hepatic resection promotes such a high degree of surgical stress that
it induces deterioration of various vital functions, which may involve
the breakdown of signal transduction systems. To investigate the infl
uence of surgical stress on signal transduction, we studied ligand-rec
eptor specific binding activity after hepatic resection, focusing on l
ymphocyte beta(2)-adrenoceptors. The maximum binding capacity (B-max)
and the dissociation constant (K-D) were determined by radioligand bin
ding assay using (-)H-3-CGP12177 as a ligand. In the hepatectomy group
, B-max significantly decreased from 1380 +/- 109 to 799 +/- 49 recept
ors/cell on postoperative day (POD) 3 and to 802 +/- 93 receptors/cell
on POD 7 (P < 0.05). In the control group, however, it did not signif
icantly change after the operation. No significant changes in K-D were
found in either of these groups. The B-max alteration was not due to
the redistribution of lymphocyte subsets or receptor down regulation,
but to the decrease in the B-max of the individual subset. The hepatec
tomy group was divided into two groups according to the postoperative
arterial ketone body ratio (AKBR): Group A, AKBR maintained at 0.7 or
more; and Group B, AKBR decreased to below 0.7. The B-max decrease, a
percentage of the preoperative value, of Group B was significantly sma
ller than that of Group A (48.4 +/- 3.9 and 72.3 +/- 7.3%, respectivel
y, P < 0.05). These results suggest that intense surgical stress, prod
uced by hepatic resection, may influence even ligand-receptor binding
parameters, and the decrease in AKBR can indicate the magnitude of sur
gical stress. (C) 1995 Academic Press, Inc.