Introduction: Acute pain is a common complication following cesarean section under general anesthesia. Post–cesarean section pain management is important for both the mother and the newborn. This study compared the effects of patient-controlled intravenous analgesia (PCIA) using sufentanil or tramadol on postoperative pain control and initiation time of lactation in patients who underwent cesarean section under general anesthesia. Methods: Primiparas (n=146) scheduled for cesarean section under general anesthesia were randomized to receive PCIA with sufentanil or tramadol. Movement-evoked and rest-pain intensity were assessed by the Numerical Rating Scale (NRS) postoperatively. The number of PCIA attempts, amount of drug consumed, initiation time of lactation, and Quality of Recovery Score 40 (QoR-40) were recorded at 4, 8, 12, and 24 h postoperatively. Pre- and postoperative serum prolactin levels were recorded. Results: No between-group difference existed in the NRS at rest at any time point postoperatively. Patients on sufentanil had more movement-evoked pain and a higher sedation score at 4, 8, and 12 h postoperatively, as compared with the tramadol group. At 24 h, the QoR-40 was higher in the tramadol group compared with the sufentanil group. No significant between-group differences were present in patient satisfaction and nausea/vomiting scores. Postpartum prolactin levels were significantly higher in the tramadol group versus the sufentanil group, corresponding with a significant delay in initiation of lactation in the latter. Conclusion: PCIA with tramadol may be preferred due to lower movement-evoked pain, higher quality of recovery, and earlier lactation in patients following cesarean section under general anesthesia.

Although the underlying mechanisms of renal IRI have been extensively studied, the corresponding effective treatments are still lacking. HMGB1, an important nuclear factor that is secreted outside cells when experiencing stress conditions, acts as a DAMP and exerts crucial effects on renal IRI. Many studies have suggested that the effect of HMGB1 on kidney damage is mediated mainly through the interaction of HMGB1 with pattern recognition receptors such as TLR4 and RAGE, which then results in the aggravation of local inflammatory response, increased infiltration of leukocytes, and finally renal tubular damage. Preclinical studies using animal models have demonstrated that inhibition of HMGB1 and downstream signal pathways can attenuate renal injury. This review critically evaluates HMGB1 in renal IRI across redox state, subcellular localization, temporal and cell-specific release, receptor usage, integrated stress pathways, autophagy, and regulated cell death. It also compares direct neutralization, inhibition of release or translocation, epigenetic/RNA-based regulation, and receptor-directed strategies. The evidence is predominantly derived from short-term rodent studies, with one large-animal antibody study and no therapeutic human trials. Accordingly, HMGB1 is best regarded as a biologically compelling but clinically unvalidated target whose therapeutic value will depend on redox- and phase-selective inhibition, kidney-directed delivery, and rigorous pharmacokinetic and safety evaluation.