BACKGROUND: We aimed to demonstrate the positive effects of the serine protease inhibitor aprotinin on neural ischemia-reperfusion injury and apoptosis in a rat model. METHODS: There were 18 rats divided into 3 groups: group A (sham, n = 6), group B (ischemia-reperfusion, n = 6), and group C (ischemia-reperfusion + aprotinin, n = 6). The systolic blood pressure of the group B and C rats was decreased to 40% to 50% of the normal level by taking blood from the femoral vein to develop hemorrhagic shock. The blood was retained and given to the remaining group B and C rats for reperfusion 20 minutes after the procedure. In group B, isotonic solution and, in group C, aprotinin was administered to the rats 5 minutes before reperfusion. After the rats were killed, the brain tissue samples were fixed for histopathologic examination. Brain tissue superoxide dismutase, malondialdehyde, and tissue myeloperoxidase level and apoptotic cell analyses were performed in all groups. RESULTS: Superoxide dismutase level decreased from group A to group B and increased from group B to group C (p < 0.05). Malondialdehyde and myeloperoxidase levels and apoptotic cells increased from group A to group B and decreased from group B to group C (p < 0.05). CONCLUSION: The results suggest that the systemic use of aprotinin in ischemic neural tissue prevents reperfusion injury and also protects the morphologic, functional, and biochemical integrity of the neural tissue.
BACKGROUND: We aimed to demonstrate the positive effects of the serine protease inhibitor aprotinin on neural ischemia-reperfusion injury and apoptosis in a rat model. METHODS: There were 18 rats divided into 3 groups: group A (sham, n = 6), group B (ischemia-reperfusion, n = 6), and group C (ischemia-reperfusion + aprotinin, n = 6). The systolic blood pressure of the group B and C rats was decreased to 40% to 50% of the normal level by taking blood from the femoral vein to develop hemorrhagic shock. The blood was retained and given to the remaining group B and C rats for reperfusion 20 minutes after the procedure. In group B, isotonic solution and, in group C, aprotinin was administered to the rats 5 minutes before reperfusion. After the rats were killed, the brain tissue samples were fixed for histopathologic examination. Brain tissue superoxide dismutase, malondialdehyde, and tissue myeloperoxidase level and apoptotic cell analyses were performed in all groups. RESULTS: Superoxide dismutase level decreased from group A to group B and increased from group B to group C (p < 0.05). Malondialdehyde and myeloperoxidase levels and apoptotic cells increased from group A to group B and decreased from group B to group C (p < 0.05). CONCLUSION: The results suggest that the systemic use of aprotinin in ischemic neural tissue prevents reperfusion injury and also protects the morphologic, functional, and biochemical integrity of the neural tissue.
Authors: Sophie Dunberry-Poissant; Kim Gilbert; Caroline Bouchard; Frédérique Baril; Anne-Marie Cardinal; Sydnée L'Ecuyer; Mathieu Hylands; François Lamontagne; Guy Rousseau; Emmanuel Charbonney Journal: Intensive Care Med Exp Date: 2018-11-12
Authors: Yusuke Iwata; Toru Okamura; Nobuyuki Ishibashi; David Zurakowski; Hart G W Lidov; Richard A Jonas Journal: J Thorac Cardiovasc Surg Date: 2009-04-21 Impact factor: 5.209
Authors: André R Greenidge; Kiana R Hall; Ian R Hambleton; Richelle Thomas; Dougald M Monroe; R Clive Landis Journal: Patholog Res Int Date: 2013-01-28