Kiener J L, Cho E, Saba T M
J Trauma. 1986 Nov;26(11):1013-23. doi: 10.1097/00005373-198611000-00010.
Fibronectin is found in plasma as well as in association with connective tissue and cell surfaces. Depletion of plasma fibronectin is often observed in septic trauma and burned patients, while experimental rats often manifest hyperfibronectinemia with sepsis. Since Factor XIII may influence the rate of clearance and deposition of plasma fibronectin into tissues, we evaluated the temporal changes in plasma fibronectin and plasma Factor XIII following bacteremia and RE blockade in rats in an attempt to understand the mechanism leading to elevation of fibronectin levels in bacteremic rats, which is distinct from that observed with RE blockade. Clearance of exogenously administered fibronectin after bacteremia was also determined. Rats received either saline, Pseudomonas aeruginosa (1 X 10(9) organisms), gelatinized RE test lipid emulsion (50 mg/100 gm B.W.), or emulsion followed by Pseudomonas. Plasma fibronectin and Factor XIII were determined at 0, 2, 24, and 48 hours post-blockade or bacteremia. At 24 and 48 hr following bacteremia alone or bacteremia after RE blockade, there was a significant elevation (p less than 0.05) of plasma fibronectin and a concomitant decrease (p less than 0.05) of plasma factor XIII activity. Extractable tissue fibronectin from liver and spleen was also increased at 24 and 48 hours following R.E. blockade plus bacteremia. In addition, the plasma clearance of human fibronectin was significantly prolonged (p less than 0.05) following bacterial challenge. Infusion of activated Factor XIII (20 units/rat) during a period of hyperfibronectinemia (908.0 +/- 55.1 micrograms/ml) resulted in a significant (p less than 0.05) decrease in plasma fibronectin (548.5 +/- 49.9 micrograms/ml) within 30 min. Thus Factor XIII deficiency in rats with bacteremia may contribute to the elevation in plasma fibronectin by altering kinetics associated with the clearance of fibronectin from the blood.
纤连蛋白存在于血浆中，也与结缔组织和细胞表面相关。败血症创伤患者和烧伤患者常出现血浆纤连蛋白减少，而实验大鼠败血症时常表现为高纤连蛋白血症。由于因子 XIII 可能影响血浆纤连蛋白清除率及其在组织中的沉积速率，我们评估了大鼠菌血症和网状内皮（RE）阻断后血浆纤连蛋白和血浆因子 XIII 的时间变化，以试图了解菌血症大鼠纤连蛋白水平升高的机制，这与 RE 阻断时观察到的情况不同。还测定了菌血症后外源性给予纤连蛋白的清除情况。大鼠分别接受生理盐水、铜绿假单胞菌（1×10⁹ 个菌）、凝胶化的 RE 试验脂质乳剂（50 mg/100 gm 体重）或脂质乳剂后再给予铜绿假单胞菌。在阻断或菌血症后 0、2、24 和 48 小时测定血浆纤连蛋白和因子 XIII。单独菌血症或 RE 阻断后菌血症的 24 和 48 小时，血浆纤连蛋白显著升高（p<0.05），同时血浆因子 XIII 活性降低（p<0.05）。RE 阻断加菌血症后 24 和 48 小时，肝脏和脾脏中可提取的组织纤连蛋白也增加。此外，细菌攻击后，人纤连蛋白的血浆清除率显著延长（p<0.05）。在高纤连蛋白血症期间（908.0±55.1μg/ml）输注活化因子 XIII（20 单位/大鼠）导致 30 分钟内血浆纤连蛋白显著降低（p<0.05）（548.5±49.9μg/ml）。因此，菌血症大鼠的因子 XIII 缺乏可能通过改变纤连蛋白从血液中清除的动力学而导致血浆纤连蛋白升高。
