Background:  Both cardiopulmonary bypass (CPB) and operative trauma are associated with increased
            expression of proinflammatory cytokines. We assessed the relative contribution of
            CPB on activation of various proinflammatory cytokines in patients undergoing coronary
            revascularization by comparing them with patients receiving coronary artery bypass
            grafts using off-pump (OPCAB) techniques. Methods:  Twenty-six patients were assigned to either the OPCAB procedure using a suction device
            and regular sternotomy (n = 13) or were treated conventionally using extracorporeal
            circulation, blood cardioplegia and hypothermic arrest (29 - 31°C; n = 13). C-reactive
            protein and systemic levels of TNF-α, TNF specific receptors Rp1 and Rp2, Interleukin-6
            (IL-6) and soluble IL-2 receptors (sIL-2r) were assayed by ELISA or EIA. To account
            for systemic nitric oxide production, total nitrate/nitrite (NOx) was measured using
            the Griess reaction. Results:  Coronary revascularization with CPB was associated with a significant expression increase
            in the TNF-system and sIL-2r when compared to the OPCAB patients. Although IL-6 expression
            did not differ between both groups, C-reactive protein levels were significantly lower
            in the OPCAB group. Moreover, systemic NOx levels as the stable end-product of nitric
            oxide were lower in the OPCAB group. Conclusions:  The data of the present study indicate that, despite comparable surgical trauma,
            the OPCAB revascularization procedure without the use of CPB and cardioplegic arrest
            significantly reduces the systemic inflammatory response syndrome and early catecholamine
            requirement. This may contribute to improved organ function, subsequently resulting
            in improved postoperative recovery from surgical revascularization procedures, particularly
            in critically ill patients.
         
         
         
            
Key words: 
         
         
            OPCAB - Inflammation - Cytokines
          
       
    
   
      
         References 
         
         
             
         
         wildhirt@hch.med.uni-muenchen.de