Effect of acute normovolemic hemodilution on anesthetic effect, plasma concentration, and recovery quality in elderly patients undergoing spinal surgery.

OBJECTIVE: To explore the effect of acute normovolemic hemodilution (ANH) on the anesthetic effect, plasma concentration, and postoperative recovery quality in elderly patients undergoing spinal surgery. METHODS: A total of 60 cases of elderly patients aged 65 to 75 years who underwent elective multilevel spinal surgery were assigned randomly into the ANH group (n = 30) and control group (n = 30). Hemodynamic and blood gas analysis indexes were observed and recorded before ANH (T1), after ANH (T2), immediately after postoperative autologous blood transfusion (T3), 10 min (T4), 20 min (T5), 30 min (T6), 40 min (T7), and 50 min (T8) after the transfusion, and at the end of the transfusion (i.e., 60 min; T9). At T3 ~ 9, bispectral index (BIS) and train-of-four (TOF) stimulation were recorded and the plasma propofol/cisatracurium concentration was determined. The extubation time and recovery quality were recorded. RESULTS: The ANH group presented a lower MAP value and a higher SVV value at T2, and shorter extubation and orientation recovery time (P < 0.05) compared with the control group. BIS values at T8 and T9 were lower in the ANH group than those in the control group (P < 0.05). TOF values at T7 ~ 9 were lower in the ANH group than those in the control group (P < 0.05). There were no statistically significant differences in the postoperative plasma concentrations of propofol and cisatracurium between the groups (P > 0.05). CONCLUSION: During orthopedic surgery, the plasma concentration of elderly patients is increased after autologous blood transfusion of ANH, and the depth of anesthesia and muscle relaxant effect are strengthened, thus leading to delayed recovery of respiratory function and extubation.

Exploration of the mechanism of reinfusion of fresh autologous blood in type 2 diabetes mice to induce macrophage polarization and inhibit erythrocyte damage.

AIMS/INTRODUCTION: Type 2 diabetes triggers an inflammatory response that can damage red blood cells. M2 macrophages have inhibitory effects on inflammation, and play an important role in tissue damage repair and fibrosis. Autologous blood transfusion has the potential to inhibit red blood cell damage by mediating macrophage polarization. MATERIALS AND METHODS: Swiss mice were used to establish a suitable type 2 diabetes model, and autologous blood transfusion was carried out. The mice were killed, the blood of the mice was collected and CD14+ monocytes were sorted. The expression levels of phenotypic molecules CD16, CD32 and CD206 in CD14+ monocytes were analyzed by flow cytometry. The proportion of M1 and M2 macrophages were analyzed by flow cytometry. The Q value, P50 , 2,3-diphosphoglycerate and Na+ -K+ -ATPase of red blood cells were detected. The red blood cell osmotic fragility test analyzed the red blood cell osmotic fragility. Western blot analysis was used to analyze the expression changes of erythrocyte surface membrane proteins or transporters erythrocyte membrane protein band 4.1, sphingosine-1-phosphate, glycolipid transfer protein and signal peptide peptidase-like 2A. RESULTS: Autologous blood transfusion induced a significant increase in the number of macrophages. The state and capacity of blood cells improved with autologous blood transfusion. Reinfusion of fresh autologous blood in type 2 diabetes mice made erythrocytes shrink. The expression of erythrocyte-related proteins proved that the erythrocyte injury in the reinfusion of fresh autologous blood + type 2 diabetes group was significantly reduced. CONCLUSION: The reinfusion of fresh autologous blood into the body of patients with type 2 diabetes can induce macrophage polarization to M2, thereby inhibiting red blood cell damage.

Regulation of Macrophage Polarization by miR-449a/Cripto-1-PI3K/AKT/NF-κB Signaling Pathway in Allogeneic Transfusion Mice.

In this study, the expression of Cripto-1 and the role of macrophage polarization in immune response after allogeneic transfusion were analyzed by constructing a mouse model of allogeneic transfusion. In order to analyze the effects of miR-449a on the PI3K/AKT/NF-κB signaling pathway and the expression of downstream related regulatory factors under normal and abnormal conditions, we adopt in vitro and in vivo experiments separately. The molecular mechanism of PI3K/AKT/NF-κB signaling pathway was analyzed by blocking or activating gene expression and western blotting. Experiment in vitro has confirmed that inhibition of miR-449a increased the protein expression of Cripto-1. In vivo experiments confirmed that allogeneic transfusion reduced the expression of Cripto-1, which further inhibited NF-κB signaling pathway through AKT/PI3K phosphorylation, regulated macrophage polarization, inhibited M1 polarization of macrophages, promoted M2 polarization, and thus affected immune response of the body.

Autologous blood transfusion impedes glycolysis in macrophages to inhibit red blood cell injury in type 2 diabetes through PI3K/Akt/PKM2 signaling axis.

AIMS: To explore the effect and mechanism of autologous blood transfusion impeding glycolysis in macrophages and inhibiting red blood cells (RBCs) injury in type 2 diabetes through PI3K/Akt/PKM2 signaling axis. METHODS: Cell transfection were performed and diabetic mice model was constructed. The group were divided into control (NC) and type 2 diabetes model (T2D). T2D model mice were injected with preserved autologous blood, si-PI3K, si-PKM2, si-NC Tran+T2D, (Tran+T2D+si-PI3K, Tran+T2D si-PKM2, Tran+T2D+si-NC) through tail vein. The anti-oxidative effects of transfusion of autologous blood in CD14+ monocytes were detected. The expression of PI3K/Akt/PKM2 protein in CD14+ monocytes were examined by western blot. Effect of autologous blood transfusion ameliorating RBCs injury by regulating PI3K and PKM2 in T2D mice were detected. RESULTS: Effects on oxidative stress in T2D mice were all overturned after autologous blood transfusion in T2D mice. The results manifested that the levels of PI3K, pAkt and PKM2 were downregulated, while the expression of HIF-1α was upregulated in CD14+ monocytes from T2D mice, whereas these influences were all effectively reversed by autologous blood transfusion in T2D mice. The survival rate of RBCs in the serum of T2D mice was declined in the serum of T2D mice, while the effect was reversed by the autologous blood transfusion. CONCLUSION: Autologous blood transfusion can reduce glycolysis in macrophages and inhibit the release of inflammatory factors through the PI3K/PKM2 signal axis, thereby inhibiting red blood cell damage and improving the oxygen-carrying capacity and survival activity of RBCs in diabetic patients.

Exploration of the effect of PUM1/Cripto-1 pathway on ferroptosis by regulating macrophage polarization in allogeneic blood transfused mice.

BACKGROUND: To study the link between macrophage polarization, PUM1/Cripto-1 pathway and ferroptosis in the allogeneic blood transfusion setting. METHODS: This is an exploratory research. The purpose of this study was to investigate the effect of PUM1/Cripto-1 pathway on ferroptosis by regulating macrophage polarization in allogeneic blood transfused mice. Establish in vitro cell models and in vivo rat models. To find out whether PUM1 and Cripto-1 were expressed, RT-qPCR and Western blot analyses were employed. The macrophage polarization markers iNOS, TNF-, IL-1, IL-6, Arg-1, and IL-10 were utilized to identify M1 and M2 macrophages. JC-1 staining was used to detect ATP membrane potential in peripheral blood macrophages. RESULTS: In animal experiments, expression of Cripto-1 was negatively regulated by PUM1 and promoted M1 type polarization of macrophages. Allogeneic blood transfusion assured good state of macrophage mitochondria. Allogeneic blood transfusion inhibited ferroptosis in macrophages by affecting the PUM1/Cripto-1 pathway. In cell experiments, PUM1 regulated Cripto-1 in mouse macrophage RAW264.7. Polarization of RAW264.7 cells was regulated by the PUM1/Cripto-1 pathway. The effect of PUM1/Cripto-1 pathway on macrophage ferroptosis in cell experiments was consistent with that in animal experiments. CONCLUSIONS: In this study, through in vivo cell experiments and in vitro animal experiments, it was successfully proved that PUM1/Cripto-1 pathway affected ferroptosis by regulating macrophage polarization in allogeneic blood transfused mice.