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Objective:To evaluate the relationship between early postoperative recovery and frailty after digestive endoscopy-assisted minimally invasive surgery under intravenous anesthesia in the elderly.Methods:This study retrospectively selected hospitalized patients, aged ≥65 yr, scheduled for elective gastrointestinal endoscopic treatment.Early postoperative recovery time was defined as the period from the end of propofol administration to the achievement of a modified Aldrete score of 9.All the patients were divided into 2 groups according to whether the early recovery time after operation was less than 75%: normal early postoperative recovery time group and delayed early postoperative recovery time group.Frailty was assessed using the frailty phenotype (FP score 0-5), and the patient was diagnosed as frail (FP ≥3) or non-frail (FP 0-2). The age, sex, height, weight, smoking history, American Society of Anesthesiologists (ASA) Physical Status classification, type of operation, and baseline mean arterial pressure and heart rate were recorded.Logistic regression analysis was used to identify the risk factors for delayed early postoperative recovery time after minimally invasive digestive endoscopy under intravenous anesthesia in elderly patients.Results:A total of 214 patients were enrolled and divided into normal early postoperative recovery time group ( n=169) and delayed early postoperative recovery time group ( n=45). There were significant differences in frailty, age, drinking history of more than 10 yr, preoperative ASA Physical Status classification and propofol administration time between delayed early postoperative recovery time group and normal early postoperative recovery time group ( P<0.05). The results of logistic regression analysis indicated that frailty, age, ASA Physical Status classification Ⅲ, and propofol administration time were independent risk factors for the occurrence of delayed early postoperative recovery ( P<0.05). Conclusions:Frailty, age, ASA Physical Status classification Ⅲ and propofol administration time are independent risk factors for delayed early postoperative recovery time following digestive endoscopy-assisted minimally invasive surgery under intravenous anesthesia in elderly patients.
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Objective:To design a modified S1PR3 specific agonist, GPS-725.017, and investigate its protective effect on acute lung injury by promoting macrophage clearance of bacteria.Methods:A short peptide derived from the intracellular region of S1PR3 receptor was named GPS725.017, which was modified with norleucine (Nle) and myristicacid (myr) at its N terminus. Mice were divided into the sham operation group, solvent group and GPS-725.017 treatment group. The acute lung injury model was induced by endotracheal injection of E. coli (5×10 6 CFU), and the experimental group was treated with GPS-725.017 (10 mg/kg). The 48-h survival rate of mice was recorded. After 5 h of modeling, the bacterial load and inflammatory cytokines in peripheral blood and lung were detected, and Vps34 protein content in alveolar macrophages was determined by Western blot. After 12-h of modeling, lung tissues were collected for H&E staining and pathological scores. Results:Compared with the solvent group, the survival rate of mice in the GPS-725.017 treatment group was significantly improved ( P<0.01), the bacterial CFU in blood and alveolar lavage fluid was significantly lower than that in the solvent group ( P<0.001), and the levels of TNF-α and IL-1β in blood and alveolar lavage fluid were significantly lower than those in the solvent group ( P<0.001). Western blot showed that the expression level of Vps34 protein in alveolar macrophages was significantly higher than that in the solvent group ( P<0.01). Histopathology result showed that the pathological damage of lung in the treatment group was significantly less than that in the solvent group ( P<0.001). Conclusions:The modified synthetic S1PR3 specific agonist GPS-725.017 could specifically activate the S1PR3 receptor on the membrane of alveolar macrophages and up-regulate the expression level of intracellular Vps34 protein, which can promote the removal of bacteria in alveolar macrophages, significantly reduce the degree of lung injury and improve the survival rate in ALI mice.
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Objective RY-15, a specific agonist of Sphingosine 1-phosphate Receptor 3, was synthesized for investigating the function and mechanism of S1PR3 in bacterial clearance. Methods Measure the ability of RY-15 with FITC to enter the THP-1 cell after coculture for 5 min, 10 min, 20 min, 30 min through confocal microscopy. The function of GY-5 and RY-15 in bacterial clearance was observed by gentamicin protection test. The phosphorylation level of ERK and p-ERK in THP-1 cell was detected by Western Blot after GY-5 and RY-15 stimulation for different times. Results According to confocal microscopy, RY-15 started to enter the THP-1 cell after stimulating for 10 min and the effect of entering cell was very obvious after stimulating for 30 min. Compared to GY-5 group, live bacteria in the macrophage were largely decreased in the RY-15 group( P<0.05). Conmpared to GY-5 group, the p-ERK level raised largely at different poins. Conclusions RY-15, a specific agonist of Sphingosine 1-phosphate Receptor 3, can promote bacterial clearance through entering cell and the phosphorylation level of ERK is a possible mechanism.
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Objective To screen the risk factors for blood coagulation abnormality in patients undergoing off-pump coronary artery bypass grafting (OPCABG).Methods A total of 140 patients undergoing elective OPCABG were included in this study,and combined intravenous-inhalational anesthesia was performed during operation.The patients were divided into normal group and abnormal group according to whether or not blood coagulation abnormality developed during operation and within 48 h after operation.The data such as gender,age,body mass index,American Society of Anesthesiologists physical status,the number of operation per year for surgeons,comorbidities (hypertension and diabetes mellitus),preoperative hematocrit (Hct),left ventricular ejection fraction,arterial oxygen pressure,liver function,operation time and requirement for intraoperative continuous cardiac output monitoring,positive end expiratory pressure,tranexamic acid,ulinastatin and hydroxyethyl starch,postoperative acidosis and hypothermia were recorded.Results Blood coagulation abnormality was found in 43 patients,and the incidence was 31％.The results of logistic regression analysis showed that the number of operation per year for surgeons＜ 50,preoperative abnormal liver function,preoperative Hct＜35％,surgery time≥240 min,no use of continuous cardiac output monitoring during operation and postoperative hypothermia were risk factors for blood coagulation abnormality in patients undergoing OPCABG.Conclusion The number of operation per year for surgeons＜50,preoperative abnormal liver function,preoperative Hct ＜ 35％,operation time ≥ 240 min,no use of continuous cardiac output monitoring during operation and postoperative hypothermia are risk factors for blood coagulation abnormality in patients undergoing OPCABG.
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Objective The purpose of this research is to study the preventive and therapeutic effects of suramin on lipopolysaccharide (LPS)-induced mouse model of acute lung injury and its molecular mechanism.Methods A total of 24 healthy male C57BL/6 mice were randomly divided into two groups: Control group and suramin group.LPS (5 mg/kg, iv) induced acute lung injury model was used in this study.The severity of lung injury was evaluated using haematoxylin-eosin (HE) staining after the injection of LPS for 0, 24 and 72 hours.The expression of TNF-α and IL-6 mRNA levels were also detected by RT-PCR.In vitro, THP-1 cells were stimulated by LPS (100 ng/mL) with saline or suramin pre-treatment.The expressions of p-ERK1/2, p-JNK and p-P38 were analyzed by Western blot at 10 min, 20 min and 30 min after LPS insult.A 2-tailed Student's t test was used to compare difference between two independent groups.Results Compared with the saline group, the lung tissues injury were significantly decreased in the suramin group of 72 hours after the injection of LPS (saline 3.90 ±0.35;suramin 2.50 ±0.12) (t =7.668, P ＜ 0.01).The expressions of TNF-α (saline 8.35 ± 1.63;suramin 4.62 ± 0.70) (t =4.187, P＜0.01) andIL-6 (saline10.53 ± 2.10;suramin5.53±1.10) (t=4.224, P＜0.01) mRNA were also obviously reduced in suramin group after the injection of LPS for 24 hours.The expression levels of pERK1/2, p-JNK and p-P38 were obviously down-regulated by suramin at 10 min, 20 min and 30 min after LPS stimulation.Conclusion Suramin protected LPS-induced acute lung injury through down-regulating the expression of pro-inflammatory factors, which was closely relative to the inhibition of the MAPK pathway.