Cohler L F, Saba T M, Lewis E P
Ann Surg. 1985 Aug;202(2):240-7. doi: 10.1097/00000658-198508000-00016.
Fibronectin exists in a soluble form in plasma and in an insoluble form in tissues. Plasma fibronectin can modulate phagocytic function as well as incorporate into the tissue matrix where it is believed to influence microvascular integrity and tissue repair. The temporal alterations in plasma and lung lymph fibronectin were studied in relation to increased pulmonary vascular permeability induced by protease infusion. The acute sheep lung lymph fistula model was used. A 39% decrease in plasma fibronectin (control = 421 +/- 67 micrograms/ml) was observed 2.5 hours (255 +/- 43 micrograms/ml) after protease infusion. There was an elevation of lymph fibronectin early after protease infusion, followed by a progressive decline. Concomitant with the decrease in plasma fibronectin, an increase in lymph flow (QL) of greater than 200% (from a control of 6.7 +/- 1.0 ml/hr to 13.9 +/- 1.4 ml/hr) was observed within 2.5 hours. Also, there was a sustained elevation in the total protein lymph/plasma concentration (L/P) ratio, which was maximal at 2.5 hours. The transvascular protein clearance (TVPC = QL X L/P) was 4.5 +/- 0.7 ml/hr at the control period and 13.1 +/- 2.0 ml/hr by 2.5 hours. This was indicative of increased flux of protein-rich fluid across the pulmonary endothelial barrier. Lung vascular permeability stabilized after 2.5 hours as manifested by a slowly declining L/P ratio. Thus, plasma fibronectin deficiency may contribute to the etiology of increased lung vascular permeability with protease infusion. Since the progressive decline in plasma fibronectin was not reflected in a proportional increase in lymph fibronectin, plasma fibronectin may have sequestered in tissues such as the lung, or perhaps in reticuloendothelial cells during the injury phase. Whether the progressive decrease in plasma fibronectin reflects its incorporation into the endothelial barrier matrix where it may mediate stabilization of the pulmonary microvascular barrier remains to be determined.
纤连蛋白以可溶性形式存在于血浆中，以不溶性形式存在于组织中。血浆纤连蛋白可调节吞噬功能，并整合到组织基质中，据信它在其中影响微血管完整性和组织修复。研究了血浆和肺淋巴纤连蛋白的时间变化与蛋白酶注入引起的肺血管通透性增加的关系。使用了急性绵羊肺淋巴瘘模型。蛋白酶注入2.5小时后（对照 = 421±67微克/毫升），观察到血浆纤连蛋白下降39%（255±43微克/毫升）。蛋白酶注入后早期肺淋巴纤连蛋白升高，随后逐渐下降。与血浆纤连蛋白减少同时，在2.5小时内观察到淋巴流量（QL）增加超过200%（从对照的6.7±1.0毫升/小时增加到13.9±1.4毫升/小时）。此外，总蛋白淋巴/血浆浓度（L/P）比值持续升高，在2.5小时时达到最大值。对照期的跨血管蛋白清除率（TVPC = QL×L/P）为4.5±0.7毫升/小时，到2.5小时时为13.1±2.0毫升/小时。这表明富含蛋白质的液体跨肺内皮屏障的通量增加。2.5小时后肺血管通透性稳定，表现为L/P比值缓慢下降。因此，血浆纤连蛋白缺乏可能是蛋白酶注入导致肺血管通透性增加的病因之一。由于血浆纤连蛋白的逐渐下降并未反映在肺淋巴纤连蛋白的相应增加中，血浆纤连蛋白可能在损伤期被隔离在诸如肺等组织中，或者可能在网状内皮细胞中。血浆纤连蛋白的逐渐减少是否反映其整合到内皮屏障基质中，在其中它可能介导肺微血管屏障的稳定，仍有待确定。
