Effects of methylprednisolone and aprotinin on phospholipase D activity ofleukocytes in systemic inflammatory response induced by cardiopulmonary bypass
M. Wu et al., Effects of methylprednisolone and aprotinin on phospholipase D activity ofleukocytes in systemic inflammatory response induced by cardiopulmonary bypass, ACT PHAR SI, 22(10), 2001, pp. 913-917
Aim: To investigate the role of leukocyte phoshpolipase D (PLD) in systemic
inflammatory response induced by cardiopulmonary bypass (CPB) and the effe
cts 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. Arte
rial blood (10 mL) was collected for assay of leukocyte PLD activity, myelo
peroxidase (MPO) activity, and CD11b expression at 8 different time points
in perioperative period. Plasma IL-6, IL-8, and C-reactive protein levels w
ere also determined. Results: At the time point of ascending aorta declampe
d, 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<plus/minus>6) nmol choline.h(-1).mg(-1
) that was lower than control (P<0.05), while it had no statistical differe
nce compared with that of pre-CPB. In methylprednisolone group, PLD activit
y elevation was postponed to the time point of CPB stopped. There was no st
atistical 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 act
ivity decreased by different extent. Conclusion: Leukocyte PID activity was
elevated significantly in systemic inflammatory response induced by CPB an
d methylprednisolone partially blunted the CPB-induced inflammatory respons
e by inhibiting PLD activity.