Effect of beta-receptor stimulation on Kupffer cell complement receptor clearance function.

Abstract

The clearance function of complement receptors on Kupffer cells is depressed after several forms of experimental injury. In vitro studies have shown that stimulation of beta-receptors on macrophages causes a depression of several aspects of macrophage function. The present study evaluated the possibility that the increase in sympathetic activity associated with injury contributes to the depression of Kupffer cell complement receptor function. Complement receptor function was assessed in rats from the hepatic uptake of rat erythrocytes coated with IgM. Isoproterenol caused a depression of receptor function when infused at a rate of 5.0 and 0.5 micrograms/kg/min for 15 min but not after infusion of 0.05 micrograms/kg/min. Infusion of isoproterenol, norepinephrine, and epinephrine at 0.5 micrograms/kg/min depressed receptor function by 41%, 38%, and 29%, respectively. Beta-receptor blockade with propranolol prevented the depression of receptor function caused by isoproterenol and norepinephrine. Thermal injury depressed receptor function by 65%, and this depression was reduced to 35% by beta-receptor blockade. Therefore, stimulation of beta-receptors on macrophages by increased circulating levels of catecholamines after injury could contribute to the depression of Kupffer cell function caused by injury.