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Updated: Nov 21, 2025

An Experimental Paradigm for the Prediction of Post-Operative Pain PPOP
Published on: January 27, 2010
Effect of dexmedetomidine on CD4+ T cells and programmed cell death protein-1 in postoperative analgesia: a
Yulan Wang1, Yishan Lei1, Yanzheng Gu2
1Department of Anesthesiology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Background:
Surgical trauma inhibits cellular immunity. Dexmedetomidine produces opioid-sparing effect and an impact on immune response.
Methods:
Eighty-six surgical patients were enrolled and received postoperative patient-controlled intravenous analgesia (PCIA) with either fentanyl alone (fentanyl group) or combined with dexmedetomidine (dexmedetomidine group). The percentages of T helper cells (Th1, Th2, and Th17) and regulatory T (Treg) cells, expression levels of programmed cell death protein-1 (PD-1) and its ligand (PD-L1) on the CD4+ T cells, and plasma levels of the cytokines were tested. Postoperative pain was measured by numerical rating scale (NRS), including NRS at rest (NRSR) and movement (NRSM).
Results:
In dexmedetomidine group, Th1 cells were increased significantly at 24 and 48 h following surgery (P=0.011 and P=0.013, respectively) and Treg cells were significantly higher at 48 h postoperatively (P=0.013). PD-1 was significantly lower in dexmedetomidine group at 24 h postoperatively (P=0.046) and interleukin 4 (IL-4) and IL-6 were significantly decreased at 48 h postoperatively (P=0.024 and P=0.035, respectively). Compared with fentanyl group, NRSR scores were lower in dexmedetomidine group at 24 h following surgery (P=0.018) and NRSR and NRSM scores were lower at 48 h postoperatively (P=0.007 and P=0.011, respectively). NRSR exhibited negative correlations with Th1 cells in fentanyl group and dexmedetomidine group (P=0.003 and P=0.005, respectively).
Conclusions:
Dexmedetomidine increases the differentiation of Th1 and Treg cells and reduces the expression of PD-1 on CD4+ T cells. Dexmedetomidine may assist to ameliorate postoperative pain and attenuate proinflammatory response. There might be a negative correlation between pain and Th1 cells.
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