APROTININ AND METHYLPREDNISOLONE EQUALLY BLUNT CARDIOPULMONARY BYPASS-INDUCED INFLAMMATION IN HUMANS

Cardiopulmonary bypass induces an inflammatory state characterized by tumor necrosis factor-alpha release, Integrin CD11b is a neutrophil su rface adhesive glycoprotein integrin that is rapidly and permanently u nregulated by tumor necrosis factor-alpha exposure, The CD11b integrin is known to be the primary neutrophil integrin responsible for neutro phil lung and myocardial entrapment after cardiopulmonary bypass and s ubsequent reperfusion injury. Twenty-four adults admitted to the hospi tal for myocardial revascularization were equally randomized to one of three groups: group A (control), group B (methylprednisolone before c ardiopulmonary bypass), and group C (low-dose aprotinin protocol), Blo od was collected at three times: (1) baseline, (2) 50 minutes of cardi opulmonary bypass duration, and (3) 30 minutes after cardiopulmonary b ypass termination. Neutrophil CD11b integrin expression was measured b y fluorescence-activated cell sorter analysis and plasma tumor necrosi s factor-alpha levels measured by enzyme-linked immunosorbent assay, G roup A demonstrated significant (p < 0.05) increases in CD11b expressi on 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 s ignificant changes were noted between groups B and C at any time, Grou p A demonstrated a significant (p < 0.05) increase in levels of tumor necrosis factor-alpha 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. The se results demonstrate low-dose aprotinin has a similar antiinflammato ry effect to that of methylprednisolone in blunting cardiopulmonary by pass-induced systemic tumor necrosis factor-alpha release and neutroph il integrin CD11b upregulation.