Brus F, Van Oeveren W, Heikamp A, Okken A, Oetomo S B
Beatrix Childrens Hospital, Division of Neonatology, University Hospital Groningen, The Netherlands.
Pediatr Res. 1996 Jun;39(6):958-65. doi: 10.1203/00006450-199606000-00006.
We investigated whether leakage of protein in lungs of preterm ventilated rabbits of 28- and 29-d gestational age is correlated with activation of clotting, complement, and polymorphonuclear leukocytes (PMN) in plasma. We found signs of systemic activation of clotting, complement and PMN in ventilated 28-d gestational age rabbits, as indicated, respectively, by increased median plasma fibrin monomer concentrations (83 versus 40% of normal adult rabbit plasma in nonventilated 28-d gestational age rabbits, p < 0.01), decreased median plasma CH50 activity (112 versus 122 U/L in nonventilated 28-d gestational age rabbits, p < 0.05), and increased median plasma beta-glucuronidase concentrations (159 versus 97% of maximal activated adult rabbit plasma in nonventilated 28-d gestational age rabbits p < 0.05). We did not find signs of systemic activation in the ventilated 29-d gestational age group. Higher median total protein concentrations in alveolar wash of the ventilated 28-d gestational age rabbits (2.7 versus 1.3 mg/mL in the nonventilated rabbits. p < 0.01) indicated protein leakage into the lungs, and this protein leakage was more pronounced in the lungs of ventilated 28-d gestational age rabbits than in those of ventilated 29-d gestational age rabbits (2.1 mg/mL, p < 0.01). The total protein concentration in the alveolar wash of all 28-d gestational age rabbits was correlated with the concentration of fibrin monomers (p = 0.51, p = 0.035) and beta-glucuronidase (p = 0.61, p = 0.011), and the CH50 activity (p = -0.73, p = 0.002) in plasma. We conclude that leakage of protein in lungs of preterm ventilated rabbits of 28-d gestational age is correlated with activation of clotting, complement, and PMN in plasma. This activation process may contribute to lung injury by intravascular and intraalveolar deposition of fibrin and formation of proteinaceous edema.
我们研究了胎龄28和29天的早产通气兔肺中蛋白质渗漏是否与血浆中凝血、补体和多形核白细胞（PMN）的激活相关。我们发现，通气的胎龄28天兔存在凝血、补体和PMN全身激活的迹象，分别表现为血浆纤维蛋白单体浓度中位数增加（通气的胎龄28天兔为正常成年兔血浆的83%，未通气的胎龄28天兔为40%，p<0.01）、血浆CH50活性中位数降低（未通气的胎龄28天兔为122 U/L，通气的胎龄28天兔为112 U/L，p<0.05）以及血浆β-葡萄糖醛酸酶浓度中位数增加（未通气的胎龄28天兔为最大激活成年兔血浆的97%，通气的胎龄28天兔为159%，p<0.05）。我们在通气的胎龄29天组未发现全身激活的迹象。通气的胎龄28天兔肺泡灌洗中总蛋白浓度中位数较高（未通气兔为1.3 mg/mL，通气兔为2.7 mg/mL，p<0.01），表明有蛋白质渗漏到肺中，且这种蛋白质渗漏在通气的胎龄28天兔肺中比通气的胎龄29天兔肺中更明显（2.1 mg/mL，p<0.01）。所有胎龄28天兔肺泡灌洗中的总蛋白浓度与血浆中纤维蛋白单体浓度（p = 0.51，p = 0.035）、β-葡萄糖醛酸酶浓度（p = 0.61，p = 0.011）以及CH50活性（p = -0.73，p = 0.002）相关。我们得出结论，胎龄28天的早产通气兔肺中蛋白质渗漏与血浆中凝血、补体和PMN的激活相关。这一激活过程可能通过血管内和肺泡内纤维蛋白沉积以及蛋白质性水肿的形成导致肺损伤。
