Effect of fascia iliaca compartment block combined with general anesthesia on the pain and inflammatory stress mediator secretion after hip replacement

Objective:To investigate the effect of fascia iliaca compartment block combined with general anesthesia on the pain and inflammatory stress mediator secretion after hip replacement. Methods: A total of 170 patients with femoral neck fracture who underwent hip replacement in this hospital between September 2015 and August 2017 were divided into the control group (n=103) who underwent routine general anesthesia and the study group (n=67) who underwent fascia iliaca compartment block combined with general anesthesia after the anesthetic solutions were reviewed. The differences in serum contents of pain mediators, inflammatory factors and stress hormones were compared between the two groups of patients immediately after surgery as well as 12 h and 24 h after surgery.Results: Immediately after surgery, there was no statistically significant difference in serum contents of pain mediators, inflammatory factors and stress hormones between the two groups. 12 h and 24 h after surgery, serum pain mediators NPY, PGE2, 5-HT,β-EP and SP contents of study group were lower than those of control group;serum inflammatory factors CRP, TNF-α and IL-1β contents were lower than those of control group;serum stress hormones Cor, CA and ACTH contents were lower than those of control group.Conclusion: fascia iliaca compartment block combined with general anesthesia can effectively reduce the postoperative pain as well as the systemic inflammatory response and stress response induced by pain in patients with hip replacement.

ClC-3 chloride channel in hippocampal neuronal apoptosis

Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol- lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was es- tablished by 0.5 mmol/L 3-morpholinosyndnomine （SIN-l）, a nitric oxide donor. The models were then cultured with 0.1 mmol/L of 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS; the chloride channel blocker）for 18 hours. Neuronal survival was detected using the 3-（4,5-dimethylthiazol- 2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay, and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining. Western blot analysis and immunochemilumi- nescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins. Real-time PCR was used to detect the mRNA expression of CIC-3. The results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted CIC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-I. Our findings indicate that the increased activities of the CIC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.