Thoracoabdominal aortic surgery can cause systemic inflammatory response and ischemia occurs when the blood flow through the major arteries that supply blood to remote organs slowed or stopped [9, 10]. So, microthrombus formation associated with blood flow slowing or stopping causes widespread inflammation and severe ischemia. This process causes of multiorgan disorders and associates with histopathological and functional changes [11, 12]. Thoracoabdominal aortic clamping can cause transient ischemia may be an inevitable consequence of descending or thoracoabdominal aortic surgery due to microthrombus formation for inadequate heparin dose. Especially, when the hematocrit level is higher than 40 mg/dl microthrombus may easily form. It was suggested that microcirculatory disturbances such as higher blood viscosity due to hemoconcentration and microthrombus formation were related to the ischemia . Heparin has beneficial effects on organs injury in the events due to its anticoagulant activity .
The present study showed that levels of HSP-70, IL-6 and MPO at the tissue level after ischemia/reperfusion were increased. Intensity of edema, cellular degeneration and congestion in the lung tissue after I/R was decreased after heparin treatment and the histopathologic protective effect of heparin was shown in the present study. Myeloperoksidaz and IL-6 are acute phase proteins and increases with inflammation [15, 16]. HSP-70 is a well known cytoprotective agent and increases after I/R and its level is directly related with the degree of tissue injury and inflammation. In the present study, HSP-70 level was highest in the control group, followed by heparin, high dose- heparin and sham groups.
Heat shock protein 70 (Hsp70) has been shown to have an anti-apoptotic function, but its mechanism is not clear in heart. Histopathologic changes were mild in heart. Only cellular degeneration showed significant difference among groups after I/R [17, 18]. The changes in IL-6 and HSP-70 should be studied in larger cohorts.
Lower levels of MPO in heart and lung tissue after I/R in the heparin ve high dose heparin groups, showed that the inflammation and injury was significantly lower with this treatment. The decrease in HSP-70 in these groups also was an indirect proof of lower tissue injury and better cellular protection. Markers of injury and repair were analyzed together in the present study.
The half-life of heparin increases from approximately 30 min following an IV bolus of 25 U/kg, to 60 min with a bolus of 100 U/kg, and to 150 min with a bolus of 400 U/kg . We administer heparin dose 100 u/kg bolus and maintain ACT level as 200 in abdominal aortic surgery, routinely. In the present study there was no significant difference between heparin groups (ACT: 200 and ACT: 600) in terms of histopathologic changes or biochemical inflammatory response in the lungs and heart. Also, clinical pattern was not different between the groups. The HSP-70 expression was significantly higher and MPO activity was significantly lower in ischemic control group compared with heparin groups.