RESUMO
Objective: To evaluate and explore the mechanism of the effect of hypertonic pre-injection on postoperative delirium in the aged. Methods: From June 2016 to February 2017, participants scheduled hip arthroplasty surgery were randomly divided into four groups: Group 1 (H1) 30 patients pre-injected 4 ml/kg hypertonic solution were proceeded general anesthesia; Group 2 (H2) 30 patients pre-injected 4 ml/kg hypertonic solution were proceeded spinal canal anesthesia; Group 3 (C1) 30 patients pre-injected 4 ml/kg isotonic saline were proceeded general anesthesia; Group 4 (C2) 30 patients pre-injected 4 ml/kg isotonic saline were proceeded spinal canal anesthesia in Department of Anesthesiology, Third Hospital of Hebei Medical University.All these patients were operated after anesthesia.To avoid electrolyte disorder, the level of Na(+) , Ca(2+) , K(+) in the artery blood was analyzed.Peripheral venous blood was extracted to detect the concentration of inflammatory factors IL-1ß, IL-6, IL-10, TNF-α and nerve injury factor S100ß.In order to evaluate the relationship of these inflammatory fators with monocyte, we used flow cytometry to detect the number of mononuclear in peripheral venous blood.After operation 1 to 3 days, all these patients were assessed cognitive function by Nu-DESC. Results: Electrolytes fluctuationed in the normal range in four groups at different time points.Compared with before infusion, IL-6, IL-1ß and TNF-α of four groups were significantly increased in postoperative.Compared with group H(H1 or H2), IL-1ß, IL-6 and TNF-α were increased and IL-10 was decreased in group C(C1 or C2) after the surgery.S100ß of group C(C1 and C2) was higher than before infusion.No significant changes were found in the cotykines mentioned above between group H1 and H2. The expression of monocytes CD14(+) CD16(+) /CD14(+ +) was decreased and the incidence of postoperative delirium was lower in group H than group C(13.3%, 10.0% vs 33.3%, 36.7%, P<0.05). Conclusion: Hypertonic saline can improve postoperative delirium of the aged and the mechanism may be related to the inhibition of monocyte cells secreting inflammatory factors.
Assuntos
Delírio/prevenção & controle , Complicações Pós-Operatórias/prevenção & controle , Solução Salina Hipertônica/uso terapêutico , Idoso , Citocinas/metabolismo , Feminino , Humanos , Inflamação , Interleucina-1beta , Masculino , Fator de Necrose Tumoral alfaRESUMO
Isoflurane can induce widespread cytotoxicity. We hypothesized that isoflurane induces apoptosis partly by causing excessive calcium release from the endoplasmic reticulum (ER) via direct activation of inositol 1,4,5-trisphosphate receptors (IP3R). Rat pheochromocytoma cells cultured for seven days with nerve growth factor were divided into four groups: control group (C), IP3R antagonist group (X), isoflurane group (I) and isoflurane + IP3R antagonist group (I+X). Groups I and I+X were treated with 1 MAC isoflurane for 12 h. Groups X and I+X were pretreated with IP3R antagonist. Annexin V/PI apoptosis and TUNEL assays were performed to evaluate cell apoptosis. TEM was used to observe changes in cell ultrastructure. Changes in calcium concentration ([Ca(2+)]i) in the cytoplasm were measured by flow cytometry. RT-PCR was performed to evaluate IP3R mRNA expression. TEM showed that isoflurane treatment altered cell ultrastructure. Compared to group C, cell apoptosis rate and [Ca(2+)]i increased in groups I and I+X (P < 0.05). Compared to group C, IP3R mRNA expression was lower in group X and higher in group I (P < 0.05). Compared to group X, cell apoptosis rate, [Ca(2+)]i and IP3R mRNA expression increased in groups I and I+X (P < 0.05). Compared to group I, cell apoptosis rate, [Ca(2+)]i and IP3R mRNA expression decreased in group I+X (P < 0.05). These results suggest that exposure to 1 MAC isoflurane for 12 h causes excessive calcium release partly by direct activation of IP3R on the ER membrane and triggers cell apoptosis.