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.

[Cohort study of remifentanil-induced hyperalgesia in postoperative patients].

OBJECTIVE: To investigate the incidence of remifentanil-induced hyperalgesia and screen for the relevant influencing factors in the post-operative patients. METHODS: A total of 1620 patients from June 2008 to December 2008 in our hospital undergoing general anesthesia with remifentanil and whose length of operative incision was less than 4 cm were enrolled. The incidence of postoperative hyperalgesia was investigated and recorded at the timepoints of staying at post-anesthesia care unit (PACU), 4 h and 24 h postoperation respectively. The unconditional statistical analysis of Logistic regression was used to explore such possible influencing factors as age, gender, methods of general anesthesia, operative duration, operative sites and remifentanil dose. RESULTS: The incidence of postoperative remifentanil-induced hyperalgesia was 16.1% (n = 261). The incidence of postoperative hyperalgesia was significantly increased in patients < 16 yrs (25.9%) vs ≥ 16 yrs (15.6%) (P < 0.05), males vs females (20.8% vs 13.0%, P < 0.01), operative duration > 2 h (32.7%) vs ≤ 2 h (9.9%) (P < 0.01) and remifentanil dose > 30 µg/kg (41.8%) vs ≤ 30 µg/kg (4.8%) (P < 0.01). And the incidence of limb protective action, touch and cold-induced allodynia were the two highest indicators (39.0%, 34.5%). Analysis of Logistic regression showed that ages under 16 years old, operative duration > 2 h and remifentanil dose > 30 µg/kg were relevant with hyperalgesia (all P < 0.05). CONCLUSION: Ages under 16 years old, operative duration and remifentanil dose are the risk factors for postoperative remifentanil-induced hyperalgesia. Neither methods of general anesthesia nor operative sites has any effect on the occurrence of hyperalgesia.