Glucocorticoid reduction of bronchial epithelial inflammation during cardiopulmonary bypass

Gary E. Hill, Sandra Snider, Timothy A. Galbraith, Stephanie Forst, Richard A. Robbins

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Tumor necrosis factor-α (TNF-α) is released in inflammatory lung conditions, raising airway nitric oxide (NO) concentrations through the cytokine-mediated induction of nitric oxide synthase (NOS). Cardiopulmonary bypass (CPB) creates an inflammatory state, characterized by the release of TNF-α, that may result in lung injury following CPB. This study measured plasma levels of TNF-α and interleukin-6 (IL-6) as well as airway NO concentrations during CPB, and the effect of methylprednisolone (MPSS) on the levels of these inflammatory products. Twenty adult males scheduled for coronary artery bypass grafting (CABG) were anesthetized and randomized to a group given MPSS at 1 gm intravenously 5 min before CPB (Group S) or a group not given MPSS (Group N). Plasma levels of TNF-α and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) and the airway NO concentration by chemiluminescence. TNF-α was significantly (p < 0.05) increased at 30 min after the termination of CPB, while IL-6 was significantly (p < 0.05) increased at 50 min into CPB and 30 min after the end of CPB in Group N as compared with controls in the same group and with Group S at the same time intervals. A group of 10 patients undergoing repair of infrarenal aortic aneurysms, which served as a control group for plasma levels of TNF-α, showed no significant changes in TNF-α concentrations at any time during aneurysm repair. Airway NO increased significantly (p < 0.01) in Group N as compared with Group S at 5, 20, 35, and 50 min of CPB. These results demonstrate that CPB is a state characterized by systemic cytokine release and increased endogenous airway NO production that is reduced by MPSS. Since lower airway NO is thought to be produced by the bronchial epithelium during inflammation, this study suggests that the bronchial epithelium is a likely target of CPB-induced lung injury.

Original languageEnglish (US)
Pages (from-to)1791-1795
Number of pages5
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume152
Issue number6 I
StatePublished - Dec 1995

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Cardiopulmonary Bypass
Glucocorticoids
Inflammation
Tumor Necrosis Factor-alpha
Nitric Oxide
Interleukin-6
Lung Injury
Epithelium
Cytokines
Aortic Aneurysm
Methylprednisolone
Luminescence
Coronary Artery Bypass
Nitric Oxide Synthase
Aneurysm
Enzyme-Linked Immunosorbent Assay
Lung
Control Groups

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Glucocorticoid reduction of bronchial epithelial inflammation during cardiopulmonary bypass. / Hill, Gary E.; Snider, Sandra; Galbraith, Timothy A.; Forst, Stephanie; Robbins, Richard A.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 152, No. 6 I, 12.1995, p. 1791-1795.

Research output: Contribution to journalArticle

Hill, Gary E. ; Snider, Sandra ; Galbraith, Timothy A. ; Forst, Stephanie ; Robbins, Richard A. / Glucocorticoid reduction of bronchial epithelial inflammation during cardiopulmonary bypass. In: American Journal of Respiratory and Critical Care Medicine. 1995 ; Vol. 152, No. 6 I. pp. 1791-1795.
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