Objective To investigate the effect of dexmedetomidine on the outcome of rats with acute lung injury following blunt chest trauma.Method Forty male SD rats weighing 250～300 g were randomly (random number)divided into 5 groups(n=8 each),namely,group C(normal),group D(normal plus dexmedetomidine),group T(trauma),group TD(trauma plus dexmedetomidine),group TDY(trauma plus dexmedetomidine plus yohimbine).Au rats were sacrificed by using exsanguination from arteria femoralis 6 hours later.The TNF-α and IL-1β levels in plasma were examined by using ELISA.Lung wet/dry(W/D)weight and the percentage of neutrophil in leucocytes in bronehoalveolar lavage fluid(BALF)of rats were detected.HE staining was performed to observe the injury of lung tissue under microscope.Results There was significant lung injury after blunt chest trauma.The serum concentrations of TNF-α and IL-1β,PMN%and lung wet/dry(W/D)weight were significantly higher in traumatic group(P<0.05,P<0.01).chest trauma,but this protective effect of dexmedetomidine could be blocked by yohimbine,at least in part,via the inhibition of α2-adrenergie receptor.Conclusions Dexmedetomidine has a certain protective effect on acute traumatic acute lung injury in rats.

0.05).The value of J of negative group was(6.180?0.214) ?g?cm-2?h-1,while there was significant difference between trial group and negative group(P

By introducing an electro-withdrawing antipyrine group, N-(p-toluenesulfonyl)-N-(4-antipyrine)-10-methylacridinium-9-carboxamide triflate was prepared. The UV, FL and CL properties of the target compound and of its precursor were investigated by comparing with those of the model compound N-(p-toluenesulfonyl)-N-phenyl-10-methylacridinium-9-carboxamide triflate and the corresponding precursor respectively. The results show that acridine sulfonamide with a heterocyclic antipyrine group exhibits blue shift of both UV absorption and of maximum excitation wavelength(λex) and emission wavelength(λem) in FL spectra, comparing with the corresponding model compound. The λex of the final target and its precursor are 268 and 274 nm, respectively; and the λem are 321 and 327 nm, respectively, while λex of the model compound and its unmethylated precursor are 365 and 359 nm, respectively; and the λem are 504 and 440 nm, respectively. Moreover, the chemiluminescence of the final target compound triggered by H2O2 could finish within 1.1 s; and the quantum yield is similar to that of the model compound, being 5.6 times high as that of luminol.

Objective To investigate the effects of penehyclidine hydrochloride (PHCD) on acute lung injury (ALI) induced by blunt chest trauma and Toll-like receptor 4 (TLR4) expression in the lung tissues in rats.Methods Ninety-six male SD rats weighing 250-300 g were randomly divided into 3 groups ( n = 32 each):control group (group C), ALI group and PHCD group. ALI was induced by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs in anesthetized rats according to the method described by Raghavendran et al. PHCD 2 mg/kg was injected intraperitoneally immediately after ALI was induced in group PHCD. Eight rats were selected at 2, 8, 12 and 24 h after ALI was induced, and arterial blood samples were collected for determination of the serum TNF-α concentration. Eight rats were selected at 8 h after ALI was induced, arterial blood samples collected for blood gas analysis and then the rats sacrificed. The lungs were immediately removed for determination of W/D lung weight ratio, myeloperoxidase (MPO) activity and TLR4 expression, and microscopic examination. Results The pH value and PaO2 were significantly lower, and the PaCO2, lactic acid level, MPO activity, W/D ratio, TLR4 expression and serum TNF-α concentration higher in groups ALI and PHCD than in group C (P ＜ 0.01 ). The pH value and PaO2 were significantly higher, and the PaCO2, lactic acid level, MPO activity, W/D ratio, TLR4 expression and serum TNF-α concentration lower in group PHCD than in group ALI ( P ＜ 0.05). The lung histopathologic damage was significantly ameliorated in PHCD group as compared with ALI group. Conclusion PHCD can protect the lungs against blunt chest trauma-induced ALI, and the down-regulation of TLR4 expression in lung tissues and reduction of inflammatory response are involved in the mechanism.

Objective To investigate the effect of penehyclidine hydrochloride on the cell apoptosis in lung tissues in a rat model of traumatic acute lung injury (ALI) .Methods Fifty-four SD rats weighing 225-275 kg were randomly divided into 3 groups ( n = 18 each) : control group (group C) , ALI group, penehyclidine hydrochloride group ( group P) . Traumatic ALI was induced by dropping a self-made impact device on the chest of anesthetized rats according to the technique described by Raghavendran et al. Intraperitoneal penehyclidine hydrochloride 2 mg/kg was injected immediately after blunt chest trauma and at 12 h after blunt chest trauma in group P. Six rats in each group were sacrificed at 3, 12 and 24 h after blunt chest trauma and the lung tissues collected for microscopic examination and determination of cell apoptosis (by TUNEL) and expression of Bax and Bcl-2 (by immuno-histochemical staining) . The apoptosis index was calculated. Results The apoptosis index and expression of Bax and Bcl-2 were significantly higher, while the ratio of Bcl-2/Bax was significantly lower at each time point in groups ALI and P than in group C ( P ＜ 0.05) . The apoptosis index and Bax expression were significantly lower,while the Bcl-2 expression and ratio of Bcl-2/ Bax higher at each time point in group P than in group ALI.The microscopic examination showed that penehyclidine hydrochloride injection significantly attenuated the pathologic changes. Conclusion Penehyclidine hydrochloride can reduce the traumatic ALI through inhibiting the cell apoptosis in rat lung tissues.

Objective To investigate the mechanism of myocardial ischemia and reperfusion-induced acute lung injury (ALl) and protective effect of ischemic postconditioning.Methods Forty SD rats were allocated to sham group,myocardial ischemia/reperfusion group (reperfusion group),ischemic postconditioning group (postconditioning group),and ischemic postconditioning + phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibiting group (inhibitor group) according to the random number table,with 10 rats per group.Myocardial ischemia/reperfusion was induced by left anterior descending coronary artery occlusion.Postconditioning was performed within 1 minute before reperfusion consisting of 3 10 s cycles of reperfusion followed by 10 s occlusion.Lung was immediately removed 120 minutes after reperfusion for HE stain,immunohistochemical detection of inflammatory factors and apoptosis factors,TUNEL assay of cell apoptosis,and Western blot of protein kinase B (Akt),phospho-Akt (p-Akt),glycogen synthase kinase-3β (GSK-3β),and phospho-GSK-3β (p-GSK-3β).Results Down-regulated B-cell lymphoma-2 (Bcl-2) and IL-10 and up-regulated Bcl-2 associated X protein (Bax),cysteinyl aspartate specific proteinase-3 (Caspase-3),IL-6 as well as IL-8 were observed in other 3 groups compared with sham group (P ＜0.01).Moreover,down-regulated Bax,Caspase-3,IL-6,IL-8 as well as TUNEL and up-regulated Bcl-2 as well as IL-10 were observed in reperfusion group compared to postconditioning group and tensor group (P ＜ 0.01).No statistical differences were found among the four groups in levels of Akt,p-Akt,and GSK-3β,but level of p-GSK-3β was significantly down-regulated in reperfusion group compared to other 3 groups(P ＜ 0.01).Conclusion Development of ALI may relate to down-regulation of p-GSK-3β evoked directly by the release of inflammation factors in early period of myocardial ischemia/reperfusion and ischemic postconditioning may attenuate the condition.

Objective:To explore the application value of transesophageal echocardiography (TEE)in secondum atri-al septal defect (ASD)intervention and minimally invasive occlusion surgery in adult patients.Methods:A total of 134 cases adult patients (>15 years)with pure secondum ASD (including 91 cases undergoing interventional occlu-sion and 43 cases undergoing minimally invasive occlusion surgery),who were screened via transthoracic echocardio-graphy (TTE)and TEE from Jan 2012 to Dec 2012,were selected.Intervention group and minimally invasive sur-gery group received TTE and TEE monitoring respectively during operation.Preoperative TTE and TEE parameters and operation results were compared and analyzed.Results:The parameters of ASD diameter measured by TEE were significantly higher than those measured by TTE in two groups (P <0.01 all).Maximum defect diameter of ASD measured by TEE was significantly higher than that of measured by TTE [(19.8±5.2)mm vs.(18.7±4.9)mm], P <0.01. The correlation between maximum defect diameter measured by TTE and occluder size (intervention group r =0.926,minimally invasive surgery group r =0.215)was all lower than that of TEE (intervention group r=0.965,minimally invasive surgery group r =0.627),P <0.01 both.Conclusion:TEE is better than TTE in as-sessment of ASD size.It should be regarded as a routine preoperative screening method for adult ASD patients.It has important value in real-time monitoring,guidance and immediate evaluation of therapeutic effects during mini-mally invasive ASD occlusion surgery.

Objective To investigate the role of gamma-aminobutyric acid (GABA) A receptor (GABAAR) in lung tissues in lipopolysaccharide (LPS)-induced acute lung injury in rats.Methods Thirty-two male Wistar rats,aged 8 weeks,weighing 200-230 g,were randomly divided into 4 groups (n =8 each) ∶ control group (group C),group LPS,GABA pretreatment + LPS group (group GABA) and GABAAR antagonist bicuculline pretreatment + LPS group (group BIC).Acute lung injury was induced by intravenous LPS 5 mg/kg in groups LPS,GABA and BIC,while the equal volume of normal saline was given in group C.GABA 50 mg/kg and bicuculline 10 μmol/kg were injected intraperitoneally 30 min before LPS injection in GABA and BIC groups,respectively.Arterial blood samples were collected at 6 h after LPS injection for measurement of arterial partial pressure of oxygen (PaO2).The animals were then sacrificed and lungs removed for determination of W/D lung weight ratio,GABAAR expression,contents of interleukin-6 (IL-6),tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissues and for microscopic examination.Results Compared with group C,PaO2 was significantly decreased in the other three groups,and W/D lung weight ratio,TNF-α,IL-6 and MDA contents were significantly increased,GABAAR expression was up-regulated,and SOD activity was decreased in groups LPS and GABA (P ＜ 0.05).Compared with group LPS,W/D lung weight ratio,TNF-α,IL-6 and MDA contents were significantly increased,GABAAR expression was up-regulated,and SOD activity was decreased in group GABA (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group BIC and in PaO2 in groups GABA and BIC (P ＞ 0.05).Conclusion GABAA R in lung tissues is involved in the development of acute lung injury induced by LPS.

Objective To compare the roles of Toll-like receptor 4 (TLR4)/NF-κB signal pathway in acute lung injury (ALl) induced by blunt chest trauma and by blunt chest trauma-hemorrhagic shock and resuscitation (double hits) in rats.Methods Forty male Sprague-Dawley rats,aged 8 weeks,weighing 240-280 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma group (T group),and blunt chest trauma and hemorrhagic shock and resuscitation group (group THSR).Lung contusion was induced in anesthetized rats by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.At 6 h after the model was established,the arterial blood samples were collected for blood gas analysis and detection of tumor necrosis factor-alpha (TNF-α) concentrations in serum.Oxygenation index (PaO2/FiO2) was calculated.The rats were then sacrificed and pulmonary specimens were obtained for determination of TLR4 expression and NF-κB ac tivity (by immunohistochemistry and Western blot) in lung tissues and for microscopic examination.Results Compared with group S,PaO2 and PaO2/FiO2 were significantly decreased,PaCO2 and TNF-α concentrations in serum were increased,TLR4 expression was up-regulated,and NF-κB activity was enhanced in T and THSR groups (P ＜ 0.05).Compared with group T,PaO2 and PaO2/FiO2 were significantly decreased,PaCO2 and TNF-α concentrations in serum were increased,TLR4 expression was up-regulated,and NF-κcB activity was enhanced in THSR group (P ＜ 0.05).The histopathological damage to lung tissues was aggravated in THSR group as compared with T group.Conclusion The role of TLR-4/NF-κB signal pathway in ALI induced by blunt chest traumahemorrhagic shock and resuscitation (double hits) is significantly stronger than that in ALI induced by blunt chest trauma alone in rats.

To improve the solubility of quercetin ( QT) , one of flavonoids that can inhibit the proliferation of vari-ous types of cancer cells, the novel amphiphilic polymer N-( 4-methylimidazole)-hydroxyethyl-chitosan ( MHC) , synthetized by chemical derivatization from chitosan, was used as the self-assembly micelles of QT. The formed polymer was characterized by 1 H NMR, elemental analysis and pyrene fluorescence spectrometry. The formulation of MHC micelles loading quercetin was optimized through single factor experiment. Then the optimized formulation was obtained as follows:the concentration of MHC was 0. 67% and the ratio of drug and carrier was 1 ∶10. The micelles particle size was ( 99. 21 ± 1. 71) nm, Zeta potential was +( 20. 01 ± 0. 72) mV and drug loading was ( 5. 42 ± 0. 32 )%. The in vitro release curve was investigated and was found to conform to Higuchi equation of Q=0. 1101 t1/2 -0. 064. The results of in vivo experiment showed that the mean rentention time and bioavail-ability of the MHC-QT micelles were 21. 42 h and 57. 49 μg h/mL, respectively, compared to 0. 30 h and 2. 50 μg h/mL of the free QT solution. These indicated that the MHC micelles could significantly improve the solubility of QT, the drug sustained-release effect and bioavailability, which would used as carrier for the anti-tumor drugs.