COMPLEMENT ACTIVATION CONTRIBUTES TO VENTILATOR-INDUCED LUNG INJURY IN RATS

被引：2

作者：

Petersen, B. ^{[1
]}

Busch, T. ^{[1
]}

Gaertner, J. ^{[2
]}

Haitsma, J. J. ^{[3
,7
,8
]}

Krabbendam, S. ^{[3
]}

Ebsen, M. ^{[4
]}

Lachmann, B. ^{[3
,5
,6
]}

Kaisers, U. X. ^{[1
,9
]}

机构：

[1] Univ Leipzig, Fac Med, Dept Anesthesiol & Intens Care Med, Leipzig, Germany

[2] Schoen Clin, Dept Anesthesiol & Intens Care Med, Vogtareuth, Germany

[3] Erasmus Univ, Med Ctr, Dept Anesthesiol, Rotterdam, Netherlands

[4] Community Hosp, Inst Pathol, Kiel, Germany

[5] Charite, Med Ctr, Dept Anesthesiol & Intens Care, Campus Virchow Klinikum, Berlin, Germany

[6] Campus Charite Mitte, Berlin, Germany

[7] Vrije Univ Amsterdam Med Ctr, Dept Anesthesiol, Amsterdam, Netherlands

[8] Vrije Univ Amsterdam Med Ctr, Dept Intens Care, Amsterdam, Netherlands

[9] Univ Hosp, Ulm, Germany

来源：

JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | 2016年 / 67卷 / 06期

关键词：

complement system; ventilator-induced; lung injury; Cl esterase inhibitor; animal model; arterial carbon dioxide tension; arterial oxygen tension; END-EXPIRATORY PRESSURE; MECHANICAL VENTILATION; PULMONARY-EDEMA; MODEL; EXPRESSION; PROTEASE; INHIBITOR; ADHESION; PATHWAY; STRESS;

D O I：

暂无

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

The complement system contributes to ventilator induced lung injury (VILI). We hypothesized that pretreatment with the Cl esterase inhibitor (C1INH) Berinert constrains complement activation consecutively inducing improvements in arterial oxygenation and histological pulmonary damage. At baseline, male Sprague-Dawley rats underwent mechanical ventilation in a conventional mode (PIP 13 cm 1120, PEEP 3 cm H2O). In the Control group, the ventilator setting was maintained (Control, n = 15). The other animals randomly received intravenous pretreatment with either 100 units/kg of the C1-INH Berinert (R) (VILI-C1INH group, n = 15) or 1 ml saline solution (VILI-C group, n = 15). VILI was induced by invasive ventilation (PIP 35 cm H2O, PEEP 0 cm H2O). After two hours of mechanical ventilation, the complement component C3a remained low in the Control group (258 +/- 82 ng/ml) but increased in both VILI groups (VILI-C: 1017 +/- 283 ng/ml; VILIC1INH: 817 +/- 293 ng/ml; P < 0.05 for both VILI groups versus Control). VILI caused a profound deterioration of arterial oxygen tension (VILI-C: 193 +/- 167 mmHg; VILI/C1-INH: 154 +/- 115 mmHg), whereas arterial oxygen tension remained unaltered in the Control group (569 +/- 26 mmHg; P < 0.05 versus both VILI groups). Histological investigation revealed prominent overdistension and interstitial edema in both VILI groups compared to the Control group. C3a plasma level in the VILI group were inversely correlated with arterial oxygen tension (R =-0.734; P < 0.001). We conclude that in our animal model of VILI the complement system was activated in parallel with the impairment in arterial oxygenation and that pretreatment with 100 units/kg Berinert (R) did neither prevent systemic complement activation nor lung injury.

引用

页码：911 / 918

页数：8

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