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J Thorac Cardiovasc Surg 1995;110:1658-1662
© 1995 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Omaha, Neb.
Received for publication Feb. 28, 1995. Accepted for publication April 6, 1995. Address for reprints: Gary E. Hill, MD, FCCM, Department of Anesthesiology and Internal Medicine, University of Nebraska Medical Center, 600 S. 42 St., Box 984455, Omaha, NE 68198-4455.
Abstract
Cardiopulmonary bypass induces an inflammatory state characterized by tumor necrosis factor-
release. Integrin CD11b is a neutrophil surface adhesive glycoprotein integrin that is rapidly and permanently unregulated by tumor necrosis factor-exposure. The CD11b integrin is known to be the primary neutrophil integrin responsible for neutrophil lung and myocardial entrapment after cardiopulmonary bypass and subsequent reperfusion injury. Twenty-four adults admitted to the hospital for myocardial revascularization were equally randomized to one of three groups: group A (control), group B (methylprednisolone before cardiopulmonary bypass), and group C (low-dose aprotinin protocol). Blood was collected at three times: (1) baseline, (2) 50 minutes of cardiopulmonary bypass duration, and (3) 30 minutes after cardiopulmonary bypass termination. Neutrophil CD11b integrin expression was measured by fluorescence-activated cell sorter analysis and plasma tumor necrosis factor-levels measured by enzyme-linked immunosorbent assay. Group A demonstrated significant (p <0.05) increases in CD11b expression at times 2 and 3 when results were compared with those of the same group baseline and with those of groups B and C at similar times. No significant changes were noted between groups B and C at any time. Group A demonstrated a significant (p <0.05) increase in levels of tumor necrosis factor-at time 3 when results were compared with those of the same group baseline and of groups B and C at the same time. No significant changes were noted between groups B and C at any time. These results demonstrate low-dose aprotinin has a similar antiinflammatory effect to that of methylprednisolone in blunting cardiopulmonary bypass–induced systemic tumor necrosis factor-release and neutrophil integrin CD11b upregulation. (J THORAC CARDIOVASC SURG 1995;110:1658-62)
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