Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass.
Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass.
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体外循环中可溶性补体受体 1 型的补体抑制。
DOI：
10.1016/0003-4975(93)90264-i
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Herskowitz,A
中科院分区：
文献类型：
--
作者：
Gillinov,AM;DeValeria,PA;Winkelstein,JA;Wilson,I;Curtis,WE;Shaw,D;Yeh,CG;Rudolph,AR;Baumgartner,WA;Herskowitz,A
虽然体外循环(CPB)中补体的激活已被充分证实，但其在灌流后器官损伤中的致病作用尚未得到证实。本研究利用补体激活的有效抑制剂--可溶性人补体受体1型(SCR1)，研究补体激活在猪体外循环肺损伤中的作用。体外实验表明，sCR1抑制猪体内的经典和替代补体途径。7头对照仔猪和6头静脉注射sCR1(12 mg/kg)的仔猪接受2小时低温(28℃)体外循环，然后进行2小时的观察。对照仔猪体外循环2小时后，C3、C5的总溶血补体活性和功能活性分别降至转流前的61.3%、67.8%和61.4%。用sCR1处理的动物的血浆几乎没有溶血活性(总溶血补体活性和基线的5%)，显示出有效的补体抑制作用。两组患者在CPB期间出现相似程度的中性粒细胞减少，CPB后肺组织髓过氧化物酶水平无差异。CPB后2小时，对照组仔猪肺血管阻力增加338%，而sCR1组仅增加147%(p<；0.05)，肺泡-动脉梯度在对照组(331±52 mm Hg)和sCR1组(290±85 mm Hg)之间无显著差异，组织学检查显示两组均有相似程度的肺水肿。这些数据构成了补体激活在CPB后肺损伤中起致病作用的直接证据。尽管sCR1可减轻CPB后肺损伤，降低肺高压，但抑制补体不能改善CPB后氧合，对白细胞动力学和肺组织学无明显影响。因此，补体参与了CPB后肺损伤的发病机制，但并不是所有肺损伤的原因。
Although complement activation during cardiopulmonary bypass (CPB) is well documented, its pathogenic role in postperfusion organ injury is unproven. In this study, soluble human complement receptor type 1 (sCR1), a potent inhibitor of complement activation, was used to determine the contribution of complement activation to pulmonary injury in a porcine model of CPB. In vitro experiments demonstrated that sCR1 inhibits both classic and alternative complement pathways in the pig. Seven control piglets and 6 piglets treated with sCR1 (12 mg/kg intravenously) underwent 2 hours of hypothermic (28 °C) CPB followed by 2 hours of observation. In control piglets, total hemolytic complement activity and functional activities of C3 and C5 declined to 61.3%, 67.8%, and 61.4% of prebypass values, respectively, after 2 hours of CPB. Plasma from animals treated with sCR1 had virtually no hemolytic activity (total hemolytic complement activity < 5% of baseline), demonstrating effective complement inhibition. Similar degrees of neutropenia developed in the two groups during CPB, and there was no difference in post-CPB lung tissue myeloperoxidase level. Two hours after CPB, pulmonary vascular resistance increased 338% in control piglets but only 147% in piglets pretreated with sCR1 (p< 0.05); the alveolar-arterial gradient was not significantly different between controls (331 ± 52 mm Hg) and piglets receiving sCR1 (290 ± 85 mm Hg), Histologic examination revealed similar degrees of pulmonary edema in both groups. These data constitute direct evidence that complement activation plays a pathogenic role in lung injury after CPB. Although pretreatment with sCR1 ameliorated lung injury after CPB, resulting in decreased pulmonary hypertension, complement inhibition did not improve post-CPB oxygenation and had no significant effect on leukocyte kinetics or lung histology. Thus, complement participates in the pathogenesis of lung injury after CPB, but is not responsible for all of the pulmonary damage.
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可溶性 CR1 在补体和中性粒细胞介导的组织损伤中的保护作用。
DOI：
--
发表时间：
1992
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Mulligan,MS;Yeh,CG;Rudolph,AR;Ward,PA
通讯作者：
Ward,PA
体外循环期间补体激活。
影响因子：
6
作者：
Nicholas C. Cavarocchi;James R. Pluth;H. V. Schaff;T. A. Orszulak;Henry A. Homburger;Eduardo Solis;Michael P. Kaye;M.S. Clancy;Jacob Kolff;G. Michael Deeb;Louis Brounstein;W. A. Schnell
通讯作者：
W. A. Schnell
DOI：
10.1016/s0022-5223(19)40771-x
发表时间：
1973
期刊：
The Journal of thoracic and cardiovascular surgery
影响因子：
--
作者：
Norman B. Ratliff;W. Glenn Young;Donald B. Hackel;Eileen Mikat;James W. Wilson
通讯作者：
James W. Wilson
可溶性补体受体1型对超急性同种异体移植排斥的影响。
DOI：
10.1016/0022-4804(91)90202-w
发表时间：
1991
期刊：
The Journal of surgical research
影响因子：
--
作者：
Pruitt,SK;Bollinger,RR
通讯作者：
Bollinger,RR
影响因子：
4.6
作者：
KIRKLIN, JK;CHENOWETH, DE;SAMUELSON, PN
通讯作者：
SAMUELSON, PN