Simms H H, D'Amico R, Burchard K W
Department of Surgery, Rhode Island Hospital, Providence 02903.
J Surg Res. 1990 Jul;49(1):49-54. doi: 10.1016/0022-4804(90)90110-n.
In vitro studies have shown that phagocytic cells are capable of undergoing activation in response to inflammatory signals and that the activation process is quite complex. A relationship between polymorphonuclear leukocyte (PMN) Fc receptor-mediated phagocytosis and oxidative metabolism has been seen in humans. We have sequentially examined circulating polymorphonuclear leukocytes (PMNs) from a total of 13 postoperative swine with either no sepsis, untreated intraabdominal sepsis, or treated intraabdominal sepsis to determine phagocytic activity over 8 postoperative days (POD). Products of the oxidative burst (i.e., myeloperoxidase) reduced the phagocytic activity of nonseptic swine PMN. Phagocytic activity was augmented by inhibiting the nonseptic swine oxidative burst with 10 mM sodium azide (an inhibitor of myeloperoxidase). In swine with untreated intraabdominal sepsis, PMN Fc receptor-mediated phagocytosis exhibited a biphasic response. An initial (between POD1 and POD4) increase in PMN function was followed by a subsequent (between POD4 and POD8) decrease in PMN function. Partial preservation of phagocytic capability was seen when swine were reexplored on POD4 and had their intraabdominal sepsis treated. These results indicate that (1) as in humans, nonseptic swine PMN Fc receptor-mediated phagocytosis is augmented by inhibition of the PMN respiratory burst; (2) untreated intraabdominal sepsis produces an initial increase and subsequent decrease in PMN Fc receptor-mediated phagocytosis; (3) early treatment of intraabdominal sepsis results in partial restoration of PMN Fc receptor-mediated phagocytosis.
体外研究表明，吞噬细胞能够响应炎症信号而被激活，并且激活过程相当复杂。在人类中已观察到多形核白细胞（PMN）Fc受体介导的吞噬作用与氧化代谢之间的关系。我们依次检查了总共13只术后猪的循环多形核白细胞（PMN），这些猪分别有无败血症、未治疗的腹腔内败血症或治疗后的腹腔内败血症，以确定术后8天（POD）内的吞噬活性。氧化爆发产物（即髓过氧化物酶）降低了非败血症猪PMN的吞噬活性。用10 mM叠氮化钠（一种髓过氧化物酶抑制剂）抑制非败血症猪的氧化爆发可增强吞噬活性。在患有未治疗的腹腔内败血症的猪中，PMN Fc受体介导的吞噬作用表现出双相反应。PMN功能最初（在POD1和POD4之间）增加，随后（在POD4和POD8之间）PMN功能下降。当猪在POD4接受再次探查并治疗腹腔内败血症时，观察到吞噬能力部分保留。这些结果表明：（1）与人类一样，抑制PMN呼吸爆发可增强非败血症猪PMN Fc受体介导的吞噬作用；（2）未治疗的腹腔内败血症会导致PMN Fc受体介导的吞噬作用先增加后降低；（3）腹腔内败血症的早期治疗可导致PMN Fc受体介导的吞噬作用部分恢复。
