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 influence of surgical stress on signal transduction, we studied ligand-receptor specific binding activity after hepatic resection, focusing on lymphocyte beta 2-adrenoceptors. The maximum binding capacity (Bmax) and the dissociation constant (KD) were determined by radioligand binding assay using (-)3H-CGP12177 as a ligand. In the hepatectomy group, Bmax significantly decreased from 1380 +/- 109 to 799 +/- 49 receptors/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 significantly change after the operation. No significant changes in KD were found in either of these groups. The Bmax alteration was not due to the redistribution of lymphocyte subsets or receptor down regulation, but to the decrease in the Bmax of the individual subset. The hepatectomy 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 Bmax decrease, a percentage of the preoperative value, of Group B was significantly smaller than that of Group A (48.4 +/- 3.9 and 72.3 +/- 7.3%, respectively, P < 0.05). These results suggest that intense surgical stress, produced by hepatic resection, may influence even ligand-receptor binding parameters, and the decrease in AKBR can indicate the magnitude of surgical stress.