右旋美托咪啶对小鼠肺泡上皮液体清除作用的研究

目的探讨右旋美托咪啶与在体小鼠肺泡液体清除率(AFC)之间的关系,以明确其在肺脏液体清除中的作用。方法应用酶标仪测定伊文思蓝标记的小牛血清白蛋白浓度的方法测定小鼠在体AFC。结果与1mmol/L阿米洛利抑制效应相反,气管内注入1.5μg/kg右旋美托咪啶后,能显著增加小鼠在体AFC。与阿米洛利合用后此增强效应受到抑制,表明右旋美托咪啶能够增加与上皮钠通道有关的阿米洛利敏感性AFC。结论临床上对合并肺脏损害的患者进行镇静时,可以考虑右旋美托咪啶对肺脏液体清除作用的影响,应用其进行相应的治疗。     

咪达唑仑对小鼠肺泡上皮液体清除作用的研究

目的探讨咪达唑仑与在体小鼠肺泡液体清除率(AFC)之间的关系,以及β2肾上腺素受体激动剂特布他林对其作用的影响。方法应用酶标仪测定小牛血清白蛋白浓度的方法测定小鼠在体AFC。结果气管内注入0.1mmol/L咪达唑仑后,能显著降低小鼠AFC。与1mmol/L阿米洛利(特异性钠通道阻断剂)合用后抑制效应未见进一步增强,表明咪达唑仑能够抑制与上皮钠通道有关的阿米洛利敏感性AFC。β2肾上腺素受体激动剂特布他林能明显增加小鼠AFC,与咪达唑仑合用后,特布他林几乎完全逆转咪达唑仑对AFC的抑制作用。结论临床上对合并肺脏损害的患者应用咪达唑仑时应考虑其可能对肺脏液体清除作用的影响,必要时可以考虑应用β2肾上腺素受体激动剂特布他林进行治疗。     

纤溶酶与奥扎格雷钠联合治疗急性脑梗死50例疗效观察

目的观察纤溶酶联合奥扎格雷钠治疗急性脑梗死的临床疗效。方法将100例急性脑梗死患者随机分为观察组与对照组,每组各50例,对照组给予奥扎格雷钠,观察组在此基础上加用纤溶酶,两组疗程均为14d,治疗结束后评定疗效。结果观察组临床总有效率为92.00%,显著优于对照组的78.00%,差异具有统计学意义(P<0.05);观察组的神经功能缺损评分减少程度显著优于治疗前及同期对照组,差异亦均具有统计学意义(P<0.05)。结论纤溶酶联合奥扎格雷钠治疗脑梗死的疗效确切,值得在临床进行推广。     

慢性阻塞性肺疾病患者肺泡液体清除作用机制研究

目的本研究旨在探讨慢性阻塞性肺疾病(COPD)患者离体肺段肺泡液体清除率(AFC)的改变及其与环磷酸鸟苷(cGMP)依赖性蛋白激酶2(PKG2)的关系。方法应用临床外科手术肺切除患者的肺段标本,将药物通过插管注入远端肺组织。应用考马斯亮兰法测定肺泡液体内小牛血清白蛋白浓度的方法测定人离体肺段AFC。应用相关酶联免疫试剂盒检测PKG2。结果 COPD患者肺组织AFC增加,PKG2明显高于对照组。结论 COPD患者气道黏液分泌增多肺脏液体清除作用增强,其机制可能与上皮钠通道功能增强有关。     

间充质干细胞条件培养基对肺泡上皮液体清除能力的影响

目的探讨小鼠骨髓间充质干细胞(BMSCs)条件培养基对小鼠肺泡液体清除的影响和对人肺泡上皮细胞生存能力的作用,并明确小鼠BMSCs条件培养基在肺脏液体清除中的作用机制。方法细胞贴壁法分离培养小鼠BMSCs,应用流式细胞术对小鼠BMSCs的表面标记物进行鉴定;运用酶标仪测定小牛血清白蛋白浓度的方法测定小鼠在体肺泡液体清除率;利用活细胞计数盒(CCK-8)试剂研究小鼠BMSCs条件培养基对人H441肺泡上皮细胞生存能力的影响;采用蛋白质印迹法研究小鼠BMSCs条件培养基对人肺泡上皮细胞钠通道蛋白水平的影响。结果小鼠BMSCs稳定表达CD44,阴性表达CD34;小鼠BMSCs条件培养基能够提升在体小鼠肺泡液体清除率;小鼠BMSCs的条件培养基能够提高人肺泡上皮细胞的生存能力;蛋白质印迹法结果显示小鼠BMSCs条件培养基能够增加人肺泡上皮细胞钠通道的蛋白水平表达。结论小鼠BMSCs条件培养基能够增强肺泡上皮细胞的液体清除并能改善其生存能力,机制可能与肺泡上皮细胞钠通道蛋白表达的增加有关。     

奥扎格雷钠联合纤溶酶治疗脑梗死40例

目的 探讨奥扎格雷钠联合纤溶酶治疗脑梗死的临床疗效。方法 选取2012年3月至2013年11月收治的脑梗死患者80例,随机均分为A组和B组,每组40例。两组在常规治疗基础上,A组予奥扎格雷钠联合纤溶酶,B组单用纤溶酶。比较两组患者治疗有效率、清醒时间、住院时间、神经功能缺损评分。结果 与B组比较,A组的治疗总有效率明显提高(P<0.05);清醒时间和住院时间明显减少,治疗后神经功能缺损评分较治疗前和B组明显降低,差异均有统计学意义(P<0.05)。结论 奥扎格雷钠联合纤溶酶较单用纤溶酶治疗脑梗死疗效确切,可增加有效率,能缩短清醒时间和住院时间,减少治疗后的神经功能损伤。     

纤溶酶辅助治疗急性脑梗死疗效观察

目的:观察纤溶酶辅助治疗脑梗死的疗效和安全性。方法:100例脑梗死患者随机分为两组,对照组50例采用常规治疗,治疗组50例在常规治疗基础上加用纤溶酶治疗。结果:两组治疗后神经功能缺损评分均有明显改善(P<0.05),且治疗组改善程度明显优于对照组(P<0.05)。治疗组总有效率86.0%;对照组总有效率78.0%,差异有统计学意义(P<0.05)。两组均未出现严重出血并发症。结论:纤溶酶辅助治疗急性脑梗死安全有效,值得推广。     

阿替普酶静脉溶栓治疗急性缺血性卒中的疗效及安全性评价

目的探讨采用阿替普酶静脉溶栓治疗急性缺血性卒中的疗效,并评价其安全性。方法选取我院2017年1月～2018年6月收治的60例急性缺血性卒中患者作为研究对象,按照随机数字表法将其分为对照组(n=30)和观察组(n=30),对照组给予尿激酶静脉溶栓治疗,观察组给予阿替普酶静脉溶栓治疗,比较治疗前后两组患者神经功能缺损(NIHSS)评分、巴塞尔指数(ADL)分以及纤溶酶原激活物活性的差异;记录两组患者冠脉再通时间、心力衰竭发生率、出血发生率。结果观察组血管溶栓再通总有效率为93.33%(28/30),明显高于对照组73.33%(22/30),差异有统计学意义(P 0.05);治疗前两组患者神经功能缺损评分、巴塞尔指数以及纤溶酶原激活物活性相比差异均无统计学意义(P 0.05),而治疗后两组患者各项指标均较治疗前改善(P 0.05);且治疗后观察组神经功能缺损评分、巴塞尔指数以及纤溶酶原激活物活性均较对照组治疗后改善(P 0.05);观察者冠脉再通时间明显较对照组缩短(P 0.05);且观察组心力衰竭发生率、出血发生率较对照组降低(P 0.05)。结论阿替普酶静脉溶栓治疗急性缺血性卒中效果显著,可提高纤溶酶原激活物活性,改善患者神经功能,缩短溶栓再通时间,减少并发症发生,值得推广。     

蛇毒纤溶酶静脉滴注联合血府逐瘀片治疗视网膜静脉阻塞的临床观察

目的:探讨蛇毒纤溶酶静脉滴注联合血府逐瘀片治疗视网膜静脉阻塞的临床效果。方法:50例视网膜静脉阻塞患者随机分为研究组和对照组,每组25例,对照组应用蛇毒纤溶酶静脉滴注治疗,研究组应用蛇毒纤溶酶静脉滴注联合血府逐瘀片治疗。观察两组临床疗效、治疗前后视力、视网膜出血吸收情况和不良反应发生情况。结果:研究组总有效率为80.00%显著高于对照组的52.00%(P<0.05)。治疗后2周、4周、6周两组视力均显著提高,研究组视力水平高于对照组(P<0.05)。视网膜出血吸收情况显著优于对照组,组间比较差异有统计学意义(P<0.05)。结论:蛇毒纤溶酶静脉滴注联合血府逐瘀片治疗视网膜静脉阻塞可以促进出血吸收和视力恢复,治疗效果更好。     

腹腔镜胃癌手术与开腹手术对凝血功能的影响

目的探讨腹腔镜胃癌手术与开腹手术对凝血功能的影响。方法 60例胃癌患者随机分为对照组(开腹手术)和观察组(腹腔镜手术),每组30例,于术前、术后24 h,通过凝固法对两组患者的凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)以及纤维蛋白原(FIB)进行检测;同时计算凝血酶原国际标准化值(INR);通过酶联免疫吸附双抗体夹心法,对血浆中D-二聚体含量进行定量测定。结果与术前相比[(12.78±0.64)s VS(12.64±0.70)s],术后24 h两组凝血酶原时间明显缩短[(11.41±0.62)s VS(11.63±0.73)s],差异均有统计学意义(t=46.23 VS t=47.12,P<0.05)。术后24 h与术前相比,两组活化部分凝血活酶时间和凝血酶原国际标准化值,差异无统计学意义(P>0.05)。术后24 h与术前相比,两组纤维蛋白原明显升高,差异有统计学意义(t=46.23 VS t=47.12,P<0.05);术后24 h与术前相比,两组D-二聚体含量明显升高,差异有统计学意义(t=46.54 VS t=46.42,P<0.05);术后24 h与对照组相比,观察组的纤维蛋白原和D-二聚体含量都明显升高,差异有统计学意义(t=47.11 VS t=46.50,P<0.05)。结论与开腹手术相比,腹腔镜胃癌手术更可能导致机体处于高凝状态,增加术后并发静脉血栓的风险,应在围手术期积极进行预防。     

Suppression of the in vitro humoral immune response by chrysotile asbestos

The direct addition of UICC chrysotile B asbestos to spleen cell cultures produced a dose-dependent suppression of the antibody-forming cell (AFC) response to the T-dependent antigen, sheep erythrocytes. Concentrations of 0.1, 1, 10, and 100 micrograms/ml, which had no effect on either cell number or viability, suppressed the in vitro response by 12, 43, 71, and 95%, respectively. By separating spleen cells into nonadherent and plastic-adherent populations, the effects of asbestos on each cell type were studied utilizing reconstituted cultures. Treatment of adherent cells for 1 hr with asbestos and reconstitution with untreated nonadherent cells resulted in a dose-dependent suppression of the AFC response similar to that observed when asbestos was added to whole spleen cultures. Reconstitution studies were also conducted with spleen cell populations from animals administered asbestos in vivo. In cultures reconstituted with adherent cells from asbestos-treated mice and nonadherent cells from saline-treated animals, the AFC response was significantly suppressed. The T-dependent AFC response with reconstitution of adherent cells from saline-treated mice and nonadherent cells from asbestos-exposed animals was no different from reconstituted saline controls. Both adherent alveolar and pleural cells were capable of reconstituting the T-dependent AFC response with nonadherent spleen cells and demonstrated reduced immunological capability when exposed to asbestos fibers. The results of this investigation have identified the adherent spleen cell (macrophage) as the target cell type responsible for asbestos-induced immunosuppression of the in vitro T-dependent antibody-forming cell response.     

Splenic cell targets in gallium arsenide-induced suppression of the primary antibody response

In vivo exposure of female B6C3F1 mice to gallium arsenide (GaAs) was evaluated for its effect on the in vitro IgM antibody-forming cell (AFC) response. In vivo exposure to a single intratracheal dose of GaAs (2.5-200 mg/kg) resulted in a dose-dependent decrease in the in vitro IgM AFC response to the T-dependent antigen sheep red blood cells (SRBC) with a 97% decrease at 200 mg/kg when compared to vehicle controls. The response to the T-independent antigen DNP-Ficoll was significantly reduced at 100 and 200 mg/kg. Spleen cellularity decreased in a dose-related manner with a 54% decrease at 200 mg/kg. Enumeration of splenic subpopulations following GaAs (200 mg/kg) indicated a 58, 61, and 30% decrease in the total number of Thy 1.2 (T cells), Ig (B cells), and F4/80 (macrophages) positive cells, respectively, with no alterations in the percentages of these cells. Mitogenic responsiveness of splenocytes from GaAs-exposed mice was unaltered. To identify the splenic cell populations targeted by GaAs, the AFC response to SRBC was evaluated following cell separation/reconstitution of splenocytes from GaAs- (200 mg/kg, 24-hr exposure) and vehicle-exposed mice. Results demonstrated AFC suppression was due to functional alterations in both adherent (AD; macrophages) and nonadherent, (both T and B lymphocytes) cell populations. Further investigation focused on alterations in the AD population. Separation/reconstitution experiments demonstrated AFC suppression to SRBC was dependent on the concentration of macrophages from GaAs-exposed mice. This macrophage-mediated suppression of the in vitro AFC response could not be attributed to the presence of suppressor macrophages or release of prostaglandins.     

Separation and identification of flavonoid constituent in Humulus Seandens and their effects on alveolar fluid clearance in mice北大核心CSCD

Aims To extract, separate and identify the flavonoid constituents in Humulus Seandens and to explore the relationship of monomers and alveolar fluid clearance (AFC) in mice in vivo. Methods Humulus seandens were extracted with alcohol and then isolated by the technology of Column and the structures were identified by spectrometry. In vivo AFC was measured using bovine serum albumin protein assays affected by luteolin-7-O-β-D-glucoside (LGL) and cosmsiin (AGL). Results The main constituents of flavanones in Humulus seandens were LGL and AGL. Both of them could improve the AFC. Conclusion The AFCs of LGL and AGL, compared to the blank control group, increased which explains the effect of flavonoid constituents on removing edema and promoting water absorption.     

Effect of invertebrate serine proteinase inhibitors on carrageenan-induced pleural exudation and bradykinin release

The carrageenan model of pleurisy is described as temporal plasma exudation (1-5 h) with extensive neutrophil infiltration and release of proteinases into the pleural cavity. The aim of this work was to study the effects of serine proteinase inhibitors on the inflammatory process induced by administration of carrageenan to the rat pleural cavity and on release of kinins in pleural exudate. Pleurisy was induced by injecting carrageenan and serine proteinase inhibitors simultaneously into the pleural cavity. The proteinase inhibitors used were: aprotinin, a plasma kallikrein inhibitor; recombinant leech derived tryptase inhibitor-2PL (LDTI-2PL), a plasmin inhibitor; Boophilus microplus trypsin inhibitors (BmTIs); trypsin; plasma kallikrein; plasmin and neutrophil elastase inhibitors; and a synthetic neutrophil elastase inhibitor (EIsynt). Administration of carrageenan with LDTI-2PL and BmTIs induced a marked increase in exudation (143% and 201%) and leukocyte migration (288% and 408%), respectively, when compared to the control group. Pleural exudate from LDTI-2PL and BmTIs plus carrageenan-treated rats showed a significant increase in plasma kallikrein-like activity, measured by chromogenic substrate hydrolysis. The specific inhibition of enzymatic activity with aprotinin confirmed that 50% of S2302 hydrolysis was produced by plasma kallikrein-like enzymes. Kinin release was increased by 97% and 103% in exudates from LDTI-2PL and BmTIs plus carrageenan-treated rats, respectively. Considering that the plasmin inhibitors LDTI-2PL and BmTIs increased exudation, leukocyte migration and bradykinin release, our results suggest an anti-inflammatory role for plasmin in the pleurisy model.     

硝苯地平对肺泡液体清除率的作用研究

目的探讨硝苯地平与肺泡液体清除率(AFC)之间的关系,进一步阐明硝苯地平所致非心源性肺水肿发生的病理生理学机制。方法应用酶标仪测定小牛血清白蛋白浓度的方法测定小鼠在体AFC。结果硝苯地平气管内给药对AFC无明显抑制作用,为(49±5)%。结论临床上硝苯地平引起的非心源性肺水肿可能不是通过调节肺泡上皮钠主动转运机能,抑制肺水肿液的吸收而起作用的。     

Involvement of tissue plasminogen activator-plasmin system in depolarization-evoked dopamine release in the nucleus accumbens of mice

Tissue plasminogen activator (tPA), a serine protease, catalyzes the conversion of plasminogen to plasmin. In the present study, we investigated the role of the tPA-plasmin system in depolarization-evoked dopamine (DA) and acetylcholine (ACh) release in the nucleus accumbens (NAc) and hippocampus, respectively, of mice, by using in vivo microdialysis. Microinjection of either tPA or plasmin significantly potentiated 40 mM KCl-induced DA release without affecting basal DA levels. In contrast, plasminogen activator inhibitor-1 dose-dependently reduced 60 mM KCl-induced DA release. The 60 mM KCl-evoked DA release in the NAc was markedly diminished in tPA-deficient (tPA-/-) mice compared with wild-type mice, although basal DA levels did not differ between the two groups. Microinjections of either exogenous tPA (100 ng) or plasmin (100 ng) into the NAc of tPA-/-mice restored 60 mM KCl-induced DA release, as observed in wild-type mice. In contrast, there was no difference in either basal or 60 mM KCl-induced ACh release in the hippocampus between wild-type and tPA-/-mice. Our findings suggest that the tPA-plasmin system is involved in the regulation of depolarization-evoked DA release in the NAc.     

Effects of asphalt fume condensate exposure on acute pulmonary responses

OBJECTIVE: The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats. METHODS: For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function. RESULTS: In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages. CONCLUSIONS: These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.     

Effect of endogenous opioid peptides on antibody formation in the primary immune response to sheep erythrocytes

The effects of leu-enkephalin and met-enkephalin on the number of the antibody-forming cells (AFC) in the mouse spleen at the primary immune response to ram erythrocytes depending on the dose and time of the agent administration with relation to the time of immunization were studied. The data indicating diverse effects of these endogenous opioid peptides on antibody genesis were obtained. When administered before immunization, met-enkephalin increased the number of AFC in the CBA mouse spleen and its administration simultaneously with an antigen and afterwards decreased the number of AFC. Leu-enkephalin both decreased and increased the number of AFC in the spleen in the dose-dependent way. The stimulating effect of this agent was more pronounced in the C57BL/6 mice with the initially low immune response as compared to the CBA mice.     

Evidence for arsenic as the immunosuppressive component of gallium arsenide.

Gallium arsenide (GaAs) has been shown previously to suppress the in vivo antibody-forming cell (AFC) response to sheep erythrocytes (SRBC) when administered intratracheally at concentrations between 50 and 200 mg/kg. In the present studies, direct addition of GaAs to in vitro-generated antibody cultures resulted in dose-dependent suppression of the primary antibody response, and was only seen when GaAs was added within 36 hr following immunization. Using atomic absorption spectrophotometry on tissue samples from mice exposed to 200 mg/kg GaAs, arsenic concentrations were found to peak in the spleen at 24 hr and decline, whereas gallium concentrations continue to rise through 14 days. Concentrations of each metal in the spleen at 24 hr are comparable to the concentrations achieved for each metal when GaAs is added at 25 microM to the in vitro model system. The 24 hr time point was chosen for comparison because all in vivo-in vitro studies were conducted using spleens from mice 24 hr after GaAs exposure. NaAsO2 and Ga(NO3)3 suppressed the AFC response dose-dependently, and in a time-dependent manner similar to GaAs when added to the in vitro system. However, based on IC50 values for each salt, the role of the gallium component in the immunosuppression appears weak. Oxalic acid (OA) and meso-2,3-dimercaptosuccinic acid (DMSA), chelators of gallium and arsenic respectively, were added to cultures with GaAs to confirm that arsenic was the primary immunosuppressive component. DMSA dose-dependently blocked GaAs-induced immunosuppression in vitro, while OA had no effect. The metal-binding compounds were determined to be specific for the metals used in these studies and did not cross-react with one another. DMSA was evaluated for its ability to prevent suppression of the AFC response in splenocytes from GaAs-exposed mice and was able to block GaAs-induced suppression of the AFC response when given sc every 4 hr beginning 1 hr prior to GaAs exposure. These data indicate that the arsenic component of GaAs is the major contributor to the GaAs-induced immunosuppression and that this effect occurs within the first 36 hr of the 5-day culture period in a concentration-dependent manner.