Abstract
To investigate the effects of cardiopulmonary bypass (CPB) on the differentiation of T lymphocyte subsets and the expression of specific transcription regulator T-bet/GATA binding protein 3 (GATA3). A prospective double-blind study was conducted. Patients with CPB pulmonary repair of ventricular septal defect (observation group) or off-pump ligation of ductus arteriosus (control group) with 20 cases each in the 150th Military Hospital from February 2015 to February 2016 were enrolled. The blood sampled was collected on the time of before operation, at the end of CPB or operation, 4 hours after operation, and 24 hours after operation. T lymphocytes were isolated, the helper T cell 1 (Th1) specific transcription factor T-bet mRNA, helper T cell 2 (Th2) specific transcription factor GATA3 mRNA expression and cytokine γ-interferon (IFN-γ) mRNA, interleukin-4 (IL-4) mRNA expression were measured by Northern Blot. Compared with before operation, expression levels of T-bet mRNA [integral gray values: (1.39±0.52)×105 vs. (2.92±0.88)×105], IFN-γ mRNA [integral gray values: (3.68±0.65)×105 vs. (6.10±0.93)×105] were decreased transiently at the end of CPB in the observation group (both P < 0.05), returned to preoperative levels at 24 hours after operation [integral gray values: (2.77±0.74)×105, (6.22±1.25)×105, respectively, both P > 0.05]; expression levels of GATA3 mRNA [integral gray values: (4.96±0.88)×105 vs. (3.21±0.68)×105], IL-4 mRNA [integral gray values: (3.52±1.13)×105 vs. (1.85±0.63)×105] were increased (both P < 0.05), recovered to the preoperative levels at 24 hours after operation [integral gray values: (3.11±0.51)×105, (1.93±0.84)×105, respectively, both P > 0.05]. There were no significant differences in the expressions of T-bet, GATA3, IFN-γ and IL-4 mRNA in the control group at each time points (all P > 0.05). CPB causes the imbalance of Th1, Tc1/Th2, Tc2 and pro-inflammatory and anti-inflammatory reactions specially, which participate the complication occurrence after CPB. The changing of T-bet/GATA3 may be the internal mechanism for these changes.
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