Heparin attenuates visceral apoptosis in a swine model of hemorrhagic shock and reperfusion injury.

Abstract Objectives The use of unfractionated heparin in hypovolemic shock, aortic clamping and visceral reperfusion is still not established, despite evidence of inhibition of early cell damage. This study investigated the potential protective effect of unfractionated heparin on hepatic and renal apoptosis in a porcine ischemia and reperfusion model. Methods Twenty-one male swine (Sus scrofa) were divided into three groups: sham (n = 5), heparin (n = 8) and non-heparin (n = 8). The heparin and non-heparin groups underwent hypovolemic shock for 30 min, supraceliac aortic clamping for 1 h and reperfusion for 3 h. Unfractionated heparin 200 mg/kg was administered to the heparin group during aortic clamping. Hemodynamic and laboratory parameters were monitored, including aminotransferase and serum urea. Histological lesion scores were applied to hematoxylin & eosin-stained liver and kidney sections. Apoptosis quantification was performed by caspase-3 immunohistochemistry. Results The proposed model caused a severe cardiocirculatory disturbance in the heparin and non-heparin groups, observed by the carotid–femoral pressure gradient and lactic acidosis. There was no significant difference in hemodynamic and laboratory parameters between these two groups. The mean values of liver and renal histological lesion scores did not present any significant differences. Caspase-3 immunoexpression was lower in the heparin than the non-heparin group for both liver and kidney. Conclusions Attenuation of liver and kidney cell apoptosis in pigs undergoing systemic heparinization suggests a potential use for heparin in modulating cell death under critical hemodynamic conditions.