Loegering D J, Commins L M
Department of Physiology, Albany Medical College, NY 12208.
Circ Shock. 1988 Aug;25(4):325-32.
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.
在几种形式的实验性损伤后，库普弗细胞上补体受体的清除功能会受到抑制。体外研究表明，刺激巨噬细胞上的β受体可导致巨噬细胞功能多个方面的抑制。本研究评估了与损伤相关的交感神经活动增加是否会导致库普弗细胞补体受体功能抑制的可能性。通过肝脏对包被有IgM的大鼠红细胞的摄取来评估大鼠的补体受体功能。当以5.0和0.5微克/千克/分钟的速率输注异丙肾上腺素15分钟时，会导致受体功能抑制，但以0.05微克/千克/分钟的速率输注后则不会。以0.5微克/千克/分钟的速率输注异丙肾上腺素、去甲肾上腺素和肾上腺素，分别使受体功能抑制41%、38%和29%。用普萘洛尔进行β受体阻断可防止异丙肾上腺素和去甲肾上腺素引起的受体功能抑制。热损伤使受体功能抑制65%，而通过β受体阻断可将这种抑制降低至35%。因此，损伤后循环中儿茶酚胺水平升高对巨噬细胞β受体的刺激可能导致损伤引起的库普弗细胞功能抑制。
