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Neutrophil expression of CD11b/CD18 and IL-8 secretion during normothermic cardiopulmonary bypass.

作者信息

Paugam C, Chollet-Martin S, Dehoux M, Chatel D, Brient N, Desmonts J M, Philip I

机构信息

Département d'Anesthésie et de Réanimation Chirurgicale et INSERM U408, Centre hospitalo-universitaire Bichat, Paris, France.

出版信息

J Cardiothorac Vasc Anesth. 1997 Aug;11(5):575-9. doi: 10.1016/s1053-0770(97)90007-0.

Abstract

OBJECTIVE

To assess blood polymorphonuclear neutrophil (PMN) activation status during normothermic cardiopulmonary bypass (CPB), the expression of the PMN adhesion molecule CD11b/CD18 was measured. Basal state as well as ex vivo capacity of PMN to be stimulated by a bacterial peptide (FMLP) were investigated. Because interleukin-8 (IL-8) is known to induce CD11b/CD18 expression in vitro in PMN, IL-8 plasma levels were concomitantly measured.

DESIGN

Prospective study.

SETTING

University hospital.

PARTICIPANTS

Thirteen patients scheduled for cardiac surgery.

INTERVENTIONS

Systemic arterial and pulmonary arterial blood samples were withdrawn at the same moment during the first 4 hours after the onset of CPB.

MEASUREMENTS AND MAIN RESULTS

Twenty minutes after the onset of CPB, basal expression of PMN CD11b/CD18 was upregulated, whereas IL-8 plasma levels remained unchanged. The increase in PMN CD11b expression was maintained until the fourth hour after the onset of CPB. At this time, elevation of IL-8 plasma levels was maximal. No differences were found between pulmonary and systemic arterial IL-8 plasma levels, even after aortic unclamping. The capacity of PMN to be stimulated ex vivo by FMLP remained normal.

CONCLUSIONS

Normothermic CPB induced a fast increase in CD11b expression, which appeared to be similar to that observed during hypothermia. IL-8 was probably not related to the very early CD11b upregulation, but could be involved in pulmonary PMN sequestration during pulmonary reperfusion and contribute to the maintained expression of PMN CD11b. Although partially activated, PMNs maintain a normal capacity to respond to a further FMLP stimulation and thus to bacterial infection.

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