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Objective@#To compare the effects of various interventions on the incidence of central line-associated bloodstream infection (CLABSI) .@*Methods@#The clinical data of 218 patients with central venous catheterization were retrospectively analyzed. Infected patients were treated as CLABSI group and non-infected patients as control group.@*Results@#Of the 218 patients, 24 patients were developed CLABSI. There was no significant difference in sex, age, primary infection status and puncture site between CLABSI group and control group. Univariate analysis showed that axillary vein puncture could significantly reduce the incidence of CLABSI (P=0.028), and the infection rate of axillary vein puncture per 1000 days under B-ultrasound was significantly reduced by 0.93‰. The average indwelling days of deep venous catheter in patients with pulse puncture were significantly longer than those in other groups (47.32 days vs 19.90 days). The average indwelling days in patients with axillary vein puncture positioned by B ultrasound were longer than those in patients with other parts of vein puncture positioned by B ultrasound (P < 0.05). Logistic multiple regression analysis showed that the main risk factors for CLABSI were anatomically located puncture (P = 0.031) and non-axillary venous catheterization (P = 0.068).@*Conclusions@#Choosing axillary vein as the position of deep venous catheterization and using ultrasound-guided central venous puncture can reduce the incidence of CLABSI and prolong the average catheterization time.
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BACKGROUND: Acute pulmonary embolism (APE) is a disorder involving the pulmonary circulation resulting from a blockage of the pulmonary artery. The present study aimed to investigate the effects of aspirin on the nuclear factor-κB (NF-κB) activity in a rat model of APE. METHODS: A total of 108 healthy male Sprague-Dawley rats were randomly assigned into six groups (n=18 rats per group): control group, sham operation group, APE model group, and low-, medium- and high-dose aspirin groups. Six, 24, and 72 hours after the induction of APE, rats in the low-, medium- and high-dose aspirin groups were given aspirin at a respective daily dose of 150, 300, and 600 mg/kg by gavage for three consecutive days. Rats in the other groups were treated with equal volumes of normal saline. Six rats in each group were anesthetized with 10％ chloral hydrate solution at each time point, and then the lung tissues were colected and analyzed using immunohistochemical staining. RESULTS: Positive immunohistochemical staining was present in the bronchial epithelial cells, alveolar cells, macrophages, and surrounding bronchial smooth muscle cells. When compared with the APE model group, the number of positive cells was significantly lower in the other groups at each time point (P<0.001). Statistically significant differences were also observed among the aspirin-treated groups at 6 hours (P<0.05,P<0.001). Compared with the APE model group, NF-κB protein expression was reduced in the other groups at each time point (P<0.05,P<0.001). Rats from the APE model group had thrombosis, damaged alveolar walls, and pulmonary hemorrhage, along with different degrees of infl ammatory cellular infiltration at each time point. However, pathological changes such as pulmonary hemorrhage and infiltration of inflammatory cells were attenuated after the aspirin treatment. CONCLUSION: Aspirin can significantly inhibit NF-κB activity in the lung of rats with APE in a dose-dependent manner, and can alleviate lung injury after APE.
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<p><b>OBJECTIVE</b>To explore the expression of Ghrelin and high mobility group protein B1 (HMGB1) in the serum and the intestinal tissue of sepsis model rats, and to evaluate the effect of electro-acupuncture (EA) at Zusanli (ST36) on the expression of HMGB1 and Ghrelin.</p><p><b>METHODS</b>Forty-eight male Wistar rats were randomly divided into four groups, i.e., the sham-operation (sham), the cecal ligation and puncture group (CLP), the CLP + EA at Zusanli (ST36) group (EA), and the CLP + Ghrelin receptor blocking agent + EA group (GHSRA), 12 in each group. A sepsis rat model was prepared by CLP. The incision of the abdominal wall was immediately sutured along the ventral midline for rats in the Sham group. In the EA group EA at Zusanli (ST36) was performed 20 min after CLP surgery with the constant voltage (2 - 100 Hz, 2 mA) for 30 min. In the GHSRA group, Ghrelin receptor blocking agent, [D-Arg1, D-Phe5, D-Trp79, Leu11]-substance P (700 nmol/kg), was administered through intravenous injection immediately after CLP, and 20 min later, EA at Zusanli (ST36) was performed in the same way as for rats in the EA group. Blood samples were withdrawn 12 h after CLP. The serum levels of Ghrelin and HMGB1 were detected using ELISA. Ghrelin expressions and the number of Ghrelin immunopositive cell in the jejunum were determined by immunohistochemistry. HMGB1 contents of the jejunum tissue were detected by Western blotting.</p><p><b>RESULTS</b>Compared with the Sham group, the number of serum immunopositive cells and the expression of HMGB1 in the jejunum tissue significantly increased and levels of Ghrelin and the expression rate of immunopositive cells significantly decreased in the CLP group (P < 0.05). Compared with the CLP group, the number of serum immunopositive cells and the expression of HMGB1 in the jejunum tissue significantly decreased, but levels of Ghrelin and the expression rate of immunopositive cells significantly increased in the EA group (P < 0.05). Compared with the EA group, the number of serum immunopositive cells and the expression of HMGB1 in the jejunum tissue significantly increased in the GHSRA group (P < 0.05), but there was no statistical difference in levels of Ghrelin between the two groups (P > 0.05). The serum level of HMGB1 was negatively correlated with Ghrelin in the Sham group, the CLP group, and the EA group (r = -0. 528, P < 0.01).</p><p><b>CONCLUSIONS</b>EA at Zusanli (ST36) could inhibit the expression of HMGB1 in the jejunum of septic rats, and promote the expression of Ghrelin. The expression of HMGB1 was inhibited by Ghrelin receptor blocking agent, which suggested that the anti-inflammation of EA at Zusanli (ST36) might be associated with Ghrelin.</p>
Subject(s)
Animals , Male , Rats , Disease Models, Animal , Electroacupuncture , Ghrelin , Metabolism , HMGB1 Protein , Metabolism , Jejunum , Metabolism , Rats, Wistar , Sepsis , MetabolismABSTRACT
Objective To study the influence of electro-acupuncture(EA)at Zusanli points(足三里穴) on the apoptosis of thymocytes in rats with abdominal infection and its mechanism.Methods A total of 40 Sprague-Dawley(SD)rats were randomly divided into four groups,including normal control group,model group,non-acupoint group and Zusanli group.The abdominal infection model of rat was made by cecal ligation and puncture(CLP).After abdominal cavity infection for 36 hours,the apoptosis of thymocytes was observed under electron microscope and light microscope,and the apoptosis ratio of thymocytes was determined by Annexin V-PI method with flow cytometry technique.The content of Bcl-2 protein of thymocytes and concentration of corticosterone in plasma were determined.Results Abdominal infection resulted from CLP could significantly increase the apoptosis of thymocytes and lead to the typical histopathological changes of apoptosis of thymocytes under electron microscope and light microscope.Apoptosis ratios of thyrnocytes in model group[(44.7?3.3)%],non-acupoint group[(42.7?3.0)%]and Zusanli group[(32.6?3.3)%] were significantly higher than the ratio in the control group[(21.2?2.3)%,all P0.05).Abdominal infection resulted from CLP also could reduce the content of Bcl-2 protein of thymocytes.The content of Bcl-2 protein of thymocytes in model group(71.2?5.6),non-acupoint group(73.5?5.9)and Zusanli group(82.4?6.8) were significantly lower than normal control group(95.3?6.3,all P