Velky T S, Greenburg A G, Yang J C, Forbes S
Surgery. 1984 Aug;96(2):190-5.
Plasma fibronectin (PFN) depletion has been associated with poor outcome in patients with sepsis or those who have experienced trauma; restoration of normal levels appears beneficial. PFN synthesis is increased after cecal ligation even in malnourished animals with sepsis, implying that stimulation of endogenous PFN synthesis is possible. One hundred rats received either a single therapeutic agent (gelatin, heparin, indomethacin, urokinase, captopril, or endotoxin) or the combination of a cecal ligation and a single agent (cimetidine, methylprednisolone, epsilon-aminocaproic acid (EACA), or transaminomethyl cyclohexane carboxylic acid. PFN levels were measured by enzyme-linked immunosorbent assay at 0, 24, and 48 hours. Only endotoxin alone caused significant PFN elevation at 24 to 48 hours (p less than 0.01); however, its multiplicity of effects precludes localization of regulatory pathways. Methylprednisolone results in an accelerated rise in PFN levels after operation (p less than 0.05), probably through an intracellular augmentation PFN synthesis. EACA attenuates the postoperative response while transaminomethyl cyclohexane carboxylic acid augments the PFN rise. This effect of EACA implies the existence of a proteolytic fragment capable of stimulating PFN synthesis. If a nontoxic factor can be identified, the use of exogenous PFN may be avoided.
血浆纤连蛋白（PFN）耗竭与脓毒症患者或经历创伤的患者预后不良有关；恢复正常水平似乎有益。即使在患有脓毒症的营养不良动物中，盲肠结扎后PFN合成也会增加，这意味着刺激内源性PFN合成是可能的。100只大鼠接受单一治疗剂（明胶、肝素、吲哚美辛、尿激酶、卡托普利或内毒素）或盲肠结扎与单一药剂（西咪替丁、甲基强的松龙、ε-氨基己酸（EACA）或转氨酶甲基环己烷羧酸）的组合。在0、24和48小时通过酶联免疫吸附测定法测量PFN水平。仅内毒素在24至48小时导致显著的PFN升高（p<0.01）；然而，其多种作用妨碍了调节途径的定位。甲基强的松龙导致术后PFN水平加速升高（p<0.05），可能是通过细胞内增强PFN合成。EACA减弱术后反应，而转氨酶甲基环己烷羧酸增强PFN升高。EACA的这种作用意味着存在能够刺激PFN合成的蛋白水解片段。如果能够鉴定出无毒因子，则可以避免使用外源性PFN。
