Effects of methylprednisolone and aprotinin on phospholipase D activity of leukocytes in systemic inflammatory response induced by cardiopulmonary bypass
Abstract
Aim: To investigate the role of leukocyte phospholipase D (PLD) in systemic inflammatory response induced by cardiopulmonary bypass (CPB) and the effects of methylprednisolone and aprotinin on leukocyte PLD activity.
Methods: Forty-two patients who received CPB open heart surgery were divided into 3 groups: methylprednisolone group, aprotinin group, and control group. Arterial blood (10 mL) was collected for assay of leukocyte PLD activity, myeloperoxidase (MPO) activity, and CD11b expression at 8 different time points in perioperative period. Plasma IL-6, IL-8, and C-reactive protein levels were also determined.
Results: At the time point of ascending aorta declamped, leukocyte PLD activity for control group was (18 +/- 8) nmol choline . h-1 . mg-1, which was higher than that of pre-CPB (P < 0.01); the PLD activity for methylprednisolone group was (10 +/- 6) nmol choline . h-1 . mg-1 that was lower than control (P < 0.05), while it had no statistical difference compared with that of pre-CPB. In methylprednisolone group, PLD activity elevation was postponed to the time point of CPB stopped. There was no statistical difference in PLD activity between aprotinin group and control (P > 0.05). After administration of methylprednisolone or aprotinin, leukocyte CD11b expression, plasma IL-6, IL-8, C-reactive protein levels, and MPO activity decreased by different extent.
Conclusion: Leukocyte PLD activity was elevated significantly in systemic inflammatory response induced by CPB and methylprednisolone partially blunted the CPB-induced inflammatory response by inhibiting PLD activity.
Keywords:
Methods: Forty-two patients who received CPB open heart surgery were divided into 3 groups: methylprednisolone group, aprotinin group, and control group. Arterial blood (10 mL) was collected for assay of leukocyte PLD activity, myeloperoxidase (MPO) activity, and CD11b expression at 8 different time points in perioperative period. Plasma IL-6, IL-8, and C-reactive protein levels were also determined.
Results: At the time point of ascending aorta declamped, leukocyte PLD activity for control group was (18 +/- 8) nmol choline . h-1 . mg-1, which was higher than that of pre-CPB (P < 0.01); the PLD activity for methylprednisolone group was (10 +/- 6) nmol choline . h-1 . mg-1 that was lower than control (P < 0.05), while it had no statistical difference compared with that of pre-CPB. In methylprednisolone group, PLD activity elevation was postponed to the time point of CPB stopped. There was no statistical difference in PLD activity between aprotinin group and control (P > 0.05). After administration of methylprednisolone or aprotinin, leukocyte CD11b expression, plasma IL-6, IL-8, C-reactive protein levels, and MPO activity decreased by different extent.
Conclusion: Leukocyte PLD activity was elevated significantly in systemic inflammatory response induced by CPB and methylprednisolone partially blunted the CPB-induced inflammatory response by inhibiting PLD activity.