心麻痹液

摘要： 目的：研究St.Thomas No.2液中添加左卡尼汀（LCN）对老年大鼠离体心脏再灌注损伤的影响。方法使用 Langendorff 灌注装置建立老年大鼠离体心脏再灌注损伤模型，将SD老年大鼠24只随机分成3组，对照组采用 St.Thomas No.2液作为心脏停搏液，LCN1组、LCN2组采用含6、12 g/L左卡尼汀的St.Thomas No.2液为心脏停搏液。离体心脏保存30min再恢复灌注，观察心功能恢复情况，比较冠脉流出液心肌酶浓度以及心肌组织匀浆三磷酸腺苷（ATP）和丙二醛（MDA）含量。结果离体心脏灌注30 min 时各组心功能恢复率差别无统计学意义，灌注60 min 时LCN1组左心室收缩峰压（LVSPP）恢复率较对照组高（P＜0.05），其他指标差异无统计学意义（P＞0.05），LCN2组心功能恢复率较LCN1组和对照组高（P＜0.05）。冠脉流出液心肌酶浓度和心肌丙二醛含量以对照组最高，LCN2最低（P＜0.05）；LCN1组、LCN2组心肌组织ATP含量较对照组明显增高（P＜0.05）。结论 St.Thomas No.2液中添加左卡尼汀可以减轻老年大鼠离体心脏的缺血再灌注损伤，该保护效果与使用剂量与再灌注时间有关。

摘要： 目的 比较晶体停搏液与含血停搏液在成人心脏手术心肌保护的效果,为优化心肌保护策略提供理论依据.方法 计算机检索Cochrane图书馆(2011年第3期)、MEDLINE、EMBase、PubMed、HighWire、中国生物医学文献数据库(CBM)及中国期刊全文数据库(CNKI)等中外生物医学数据库,收集关于比较晶体与含血停搏液在成人心脏手术中心肌保护的效果的临床随机对照试验,检索日期为1985年1月至2011年12月.按Cochrane系统评价方法,评价所纳入研究的文献质量,并提取有效数据后采用RevMan 5.1软件进行meta分析.结果 纳入16项研究,共计3934例患者,其中含血停搏液组2004例,晶体停搏液组1930例.各研究间无统计学异质性,采用固定效应模型.Meta分析显示:晶体停搏液与含血停搏液组在术后30 d病死率(OR=1.11,95％CI:0.59 ～2.08,P=0.74)、术后低心排血量综合征发生率(OR =0.98,95％ CI:0.41 ～2.33,P=0.85)、围手术期心肌梗死发生率(OR =0.85,95％ CI:0.55 ～ 1.29,P=0.44)、术后正性肌力药物使用率(OR=1.05,95％ CI:0.81 ～1.38,P=0.70)方面,差异均无统计学意义.结论 在中低风险择期成人心脏手术中,含血停搏液与晶体停搏液心肌保护效果无差异.%Objectives To compare the cardioprotection effect between blood and crystalloid cardioplegia during cardiac surgery in adult patients,and provide a theoretical basis for optimal myocardial protection strategies.Methods A meta-analysis of randomized controlled trials (RCT) studies about comparing blood and crystalloid cardioplegia in adult patients undergoing cardiac surgery were performed.Cochrane library(Issue 3,2011),MEDLINE,EMBase,PubMed,HighWire,CBM and CNKI were searched from January 1985 to December 2011.Studies were assessed according to the Cochrane Handbook for systematic reviews.Data were extracted from these trials and analyzed by RevMan5.1 software.Results Sixteen trials involved 3934 patients were included,2004 cases were in blood group,and 1930 were in crystalloid group.There was no statistical heterogeneity between studies using a fixed effects model.Meta-analysis indicated that,there were no significant differences between blood and crystalloid group in the incidence of postoperative 30 days mortality (OR =1.11,95％ CI:0.59-2.08,P =0.74),the incidence of postoperative low cardiac output (OR =0.98,95％ CI:0.41-2.33,P =0.85),the incidence of perioperative myocardial infarctions (OR =0.85,95％ CI:0.55-1.29,P =0.44),and inotropic support requirement (OR =1.05,95％ CI:0.81-1.38,P =0.70).Conclusion The blood cardioplegia is no difference with crystalloid cardioplegia in adult patients undergoing cardiac surgery.

摘要： BACKGROUND: On-pump beating-heart technique has been promoted as better systemic protection compared with the technique of cardioplegic arrest, and the attenuated inflammatory reaction may play an important role in the protective effect of the on-pump beating-heart technique.OBJECTIVE: To observe the protective effects of St. Thomas No.2 solution supplemented with levocarnitine on preservation of hypothermic rat hearts ex vivo.METHODS: Isolated rat heart Langendorff model and working model were established . Thirty-two Sprague-Dawley rats were randomized to four groups with eight rats in each group. In two groups, the hearts were arrested with St.Thomas No.2 solution and preserved in the same solution for 4 hours or 6 hours, while in the other two groups, the hearts were arrested with St.Thomas No.2 solution supplemented with levocarnitine (12 g/L) and preserved in the same solution for 4 hours or 6 hours.RESULTS AND CONCLUSION: Compared with St. Thomas No.2 solution group, after the hearts were preserved for 4 hours,there were no differences in heart rate, coronary artery flow, left ventricular systolic pressure peak, +dp/dt max, water content in myocardium, and adenosine triphosphate (P ＞ 0.05), but creatine kinase release was significantly reduced (P ＜ 0.05) in the St.Thomas No.2 solution supplemented with levocarnitine group. After the hearts were preserved for 6 hours, the measurement results above-mentioned were superior in the St.Thomas No.2 solution supplemented with levocarnitine group than in the St.Thomas No.2 solution group (P ＜ 0.05). These results suggest that St.Thomas No.2 solution supplemented with levocarnitine provides better effects on preservation of hypothermic rat hearts ex vivo.%背景:在心脏瓣膜置换中应用添加左卡尼汀的心脏停搏液可明显减轻心肌线粒体的脂质过氧化反应,保护心肌细胞.目的:观察加入左卡尼汀的St.Thomas No.2液对大鼠离体心脏低温保存的效果.方法:利用Langendorff 灌注装置建立SD大鼠离体心脏灌注和工作模型,随机分成4组,其中2组采用 St.Thomas No.2 液作为心脏停搏液与保存液分别保存心脏4 h、6 h,另2组采用添加左卡尼汀的St.Thomas No.2液作为心脏停搏液与保存液分别保存心脏4 h、6 h.结果与结论:与St.Thomas No.2 液保存4 h组比较,添加左卡尼汀的St.Thomas No.2液保存 4 h组心脏心率、冠状动脉流量、左心室收缩峰压和左心室内最大上升速率及心肌含水量、ATP含量差别无显著性意义(P > 0.05),但心肌酶漏出量明显减少(P < 0.05);添加左卡尼汀的St.Thomas No.2液保存 6 h组上述指标检测结果均优于St.Thomas No.2保存6 h组 (P < 0.05).提示左卡尼汀强化的St.Thomas No.2液可显著提高大鼠离体心脏的低温保存效果.

摘要： 目的:观察含左西孟旦(Levo)的停搏液对大鼠离体缺血再灌注心肌的保护作用.方法:32只雄性Wistar大鼠随机分为10、L0.03、L0.3、LG共4组,每组8只,在去极化停搏液STH-2中分别加入Levo 0、0.03、0.3 μmol/L以及Levo 0.3 μmol/L+格列苯脲10 μmol/L.平衡灌注30 min后分别用25°C的4种不同停搏液停搏,2 h后重新灌注30 min,观察对比各组停搏前后不同时间点心功能指标、再灌注末冠脉流出液中乳酸脱氢酶(LDH)和肌酸激酶(CK)含量的不同.结果:各组心功能基础值差异无统计学意义(P＞ 0.05),再灌注期各组心功能都有不同程度的降低,L0.3组左心室舒张末压(LVDP)、心室内压力上升/下降速率(±dp/dtmax1的恢复率均高于其他3组(P＜0.01或P＜0.05),HR的恢复率明显高于L0组(p＜0.01),L0.03组、LG组与L0组比较心率(HR)、+dp/dtmax的恢复率差异无统计学意义(P＞0.05),-dp/dtmax恢复率在T2时点高于L0组(P＜0.05或P＜ 0.01).再灌注末CK和LDH漏出量L0.3组明显低于其他各组(P＜ 0.05或P＜ 0.01).结论:Levo加入STH-2停搏液能够明显减轻缺血再灌注心肌的损伤.%Objective: To observe the protective effect of levosimendan (Levo) in cardioplegic solution on isolated rat heart. Methods: Thirty-two male Wistar rats were randomly divided into four groups: no Levo (LO) group, 0.03 μmol/L Levo (L0.03) group, 0.3 μmol/L Levo (L0.3) group, 0.3 μmol/L Levo and 10 μmol/L glibenclamide (LG) group. The hearts was connected to Langendorff perfusion apparatus immediately after perfused with K-H solution for 30 minutes. Hearts were then perfused by different cardioplegic solutions at 25 °C for 2 h, and then were reperfused with K-H solution for 30 minutes. The changes of hemodynamics, myocardial enzyme leakage in the coronary effluent were observed. Results: There were no significant differences in hemodynsmics, creatine kinase(CK)and lactate dehydrogenase(LDH) before hearts stopped beating in all groups (P > 0.05). After reperfusion, the recovery values of heart rate (HR), left ventricular developed pressure (LVDP)and the rate of pressure development(±dp/dumax) were higher in group L0.3 than that of group L0 (P 0.05). The recovery of ±dp/dtmax, was higher at T2 in groups L0.03 and LG than that of group L0 (P < 0.05). The levels of LDH and CK were significantly decreased at the end stage of reperfusion in group L0.3 compared with those of other groups (P < 0.05). Conclusion: There was a protective effect on myocardial ischemia-reperfusion injury with Levo added into STH-2 cardioplegic solution.

摘要： 目的:利用Langendorff离体灌注模型研究缺血预处理(IPC)单独应用和与心麻痹液联合应用对兔未成熟心脏全心缺血再灌注的影响,以了解心麻痹液在IPC心肌保护效应中的作用.方法:新西兰幼兔,体重220g~280g,兔龄14d~21d.麻醉及肝素化后,快速开胸取出心脏,浸入4°CKrebs-Henseleit缓冲液,30s内主动脉插管行Langendorff灌注,用39°C经混合气(O2:CO2=9%:5%)平衡的Krebs-Henseleit缓冲液灌注.32只兔未成熟心脏随机分为四组:对照组Ⅰ(conⅠ,n=8),全心接受30min缺血、40min再灌注;IPC组(IPC,n=8),接受5min缺血、10min再灌注预处理(IPC)和30min缺血、40min再灌注;对照组Ⅱ(conⅡ,n=8),接受4°C的St.ThomasⅡ心麻痹液使心脏停跳和45min缺血、40min再灌注;IPC复合心麻痹液(IPC+St.Ⅱ,n=8),接受IPC、St.Ⅱ灌注和45min缺血、40min再灌注.记录心脏停跳前平稳灌注时冠脉流量(CF)、心率(HR)、左室发展压(LVDP)、左室压力最大上升和下降速度率(±dp/dtmax)作为基础值,并分别把再灌注后5、10、20、30、40min的CF、HR、LVDP、±dp/ dtmax测定值表达为对其相应基础值的恢复率.记录IPC组与conⅠ在主动脉停灌后心脏缺血跳动时间,测定各组再灌注后冠脉流出液中肌酸激酶同工酶(CK-MB)及再灌注末心肌组织ATP含量.结果:复灌后IPC组与对照组Ⅰ相比在冠脉流出量(CF)、心率(HR)、左室发展压(LVDP)、左室最大上升和下降速度率(±dp/ dtmax)恢复率无明显差别,肌酸激酶同工酶(CK-MB)漏出量有增多趋势(但P＞0.05);IPC组在全心停灌后心脏缺血跳动时间明显延长(P＜0.01),再灌注末心肌ATP含量显著减少(P＜0.001).而在IPC复合心麻痹液组HR 、CF、LVDP及±dp/dtmax恢复率较对照组Ⅱ明显得以改善,且保存心肌ATP含量,肌酸激酶同工酶(CK-MB)漏出减少.结论:IPC在单独应用时不足以保护经历全心缺血再灌注损伤的兔未成熟心脏,反而有可能导致心肌细胞的损伤;而在与心脏停搏液合用时,IPC对经历全心缺血再灌注的兔未成熟心肌具有明显的保护作用.因此,在Langendorff离体灌注心脏模型,本研究首次观察到IPC心肌保护效应的获得需要心麻痹液的参与.

摘要： Objective To evaluate the protective effect on lung by using continuous pulmonary artery perfusion with oxygenated blood and L-arginine during cardiopulmonary bypass(CPB).Methods Forty five cases received mitral valve replacement were randomly divided into 3 groups and each group involved 15 cases. Group I(control group), patients received routine procedure of CPB. Proup Ⅱ, patients received rcontinuous pulmonary artery perfusion with oxygenated blood. Group Ⅲ,continuous pulmonary artery perfusion with oxygenated blood containing L-arginine (200 mg/kg) (n=15). All cases received routine procedure of CPB and continuously infused from the root of pulmonary artery until releasing aortaoaic clamp. Blood samples were collected from the radial artery respectively at the following time points:after the induction of anaesthesia, 1 hour after opening of aorta, 0, 6, 12, 24 hours after patients being taken back to ICU. ELISA test was used to detected the expression of tmmor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10). Lung tissue samples (1.0 cm ×1.0 cm×1.0 cm) were obtained from right lower lobe. The pathologicl changes of lung tissues were observed under light mi-croscope by using HE staining. Results at each time points, the expression of TNF-α, IL-6 in group Ⅱ and group Ⅲ weresignificantly lower than that in group Ⅰ (P<0.05). The level of TNF-α, IL-6 in group Ⅲ were lower than in group Ⅱ(P<0.05). However, the expression of IL-10 in group Ⅱ and group Ⅲ were higher than in group Ⅰ, and the level of IL-10 in group Ⅲ were higher than that in group Ⅱ(P<0.05). In the group Ⅰ: HE staining showed marked pulmonary interstitial edema, intra-alveolus neutrophilic granulocyte exudation with karyorrhexis. In the group Ⅱ, light capillary vessel hyperaemia and pulmonary interstitial lymphocyte exudation were detected. Nearly normal lung tissue were observed in group Ⅲ. Conclusion Continuous pulmonary artery perfusion with oxygenated blood and L-arginine could inhibit the synthesis of inflammatory factors significantly and increase the releasing of anti-inflammatory factors during CPB. Therefore, it may reduces pulmonary inflammatory reaction and have protective effects on lung tissue.%目的 体外循环(CPB)期间观察肺动脉持续灌注氧合血及氧合血内加入L-精氨酸对肺组织的保护作用.方法 45例择期常规行二尖瓣置换术病人纳入临床对照研究,随机分成对照组,常规体外循环;灌注组,肺动脉持续灌注氧合血;加药组,肺动脉持续灌注含L-精氨酸(200 mg/kg)的氧合血;每组各15例.3组病人均采用常规CPB,灌注组和加药组从肺动脉根部持续灌注氧合血至CPB开放主动脉结束.分别在麻醉后、开放主动脉1 h,回ICU 0、6、12、24 h取桡动脉血,采用双抗体夹心酶联免疫吸附试验(ELISA法)测定肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)、白细胞介素10(IL-10)的表达.征得病人本人及家属同意,于CPB前及停机后30min取1.0 cm×1.0cm×1.0cm右下肺组织.光镜观察肺组织结构变化.结果 45例术中及术后经过顺利,均痊愈出院.开放主动脉后,加药组和灌注组血浆中TNF-α、IL-6水平明显低于对照组(P<0.05),加药组优于灌注组;IL-10水平高于对照组,加药组优于灌注组.对照组光镜下见肺泡间质水肿,肺泡内大量中性粒细胞渗出,细胞核碎裂;灌注组肺泡毛细血管轻度充血,肺间质淋巴细胞浸润;加药组基本保持了正常的肺组织结构.结论 CPB期间持续肺动脉灌注氧合血对肺组织有保护作用;L-精氨酸对肺组织也有保护作用.

摘要： 目的 观察含维拉帕米、普奈洛尔的钾("钾维普")停搏90 min对幼大鼠心脏功能影响,并与缺血、高钾液停搏及连续灌流不停搏心脏比较.方法 离体幼大鼠心脏Langendorff法灌流20 min,分4组(n=8):正常灌注组(CON),连续灌流150 min;缺血-再灌注组(I/R),无糖不充氧修正洛氏液灌3 min停灌27 min连续3阵(缺血90 min)再灌注60 min;高钾停搏液保护组(ST.T)和"钾维普"停搏液保护组(KVP),缺血期间每次3 min灌注分别采用ST.ThomasⅡ停搏液、含维拉帕米6.8×10-7mol/L和普奈洛尔1.1×10-7mol/L的ST.ThomasⅡ停搏液.实验全程170 min维持37°C,实时监测心率、心肌张力、收缩力、最大收缩速度、最大舒张速度及冠脉流量等参数.结果 CON组幼大鼠心脏离体灌流150 min,心率、收缩力、冠脉流量呈下降性变化,心肌张力无明显改变;I/R组缺血90 min期间心肌张力升高,复灌后呈紊乱的颤动未能复搏;与CON组比较,ST.T组缺血60 min后心肌张力升高明显(P＜0.05),复灌后收缩力小(P＜0.05);与ST.T组比较,KVP组缺血90 min期间心脏张力低(P＜0.05),复灌后心搏各参数恢复好(P＜0.05),冠脉流量高(P＜0.05),其中心率、收缩力、收缩舒张速度、冠脉流量均高于CON组(P＜0.05).结论 "钾维普"停搏保护的未成熟心脏功能优于连续灌流不停搏和缺血、高钾液停搏的心脏功能.

摘要： 目的 探讨不同剂量的左卡尼汀(LCN)添加至St.Thomas No.2液后对长时间冷保存离体大鼠心脏能量代谢的影响.方法 利用Langendorff灌注装置建立离体大鼠心脏模型.SD大鼠56只随机分为4组:对照组8只、St组16只(该组使用St.Thomas No.2液为心脏停搏液和保存液)、LCN 1组16只(St.Thomas No.2液加LCN 12g/L为心脏停搏液和保存液)和LCN 2组16只(St.Thomas No.2液加LCN 6g/L为心脏停搏液和保存液).对照组直接取左心室心肌组织,其他各组16只大鼠中8只在4°C条件下保存心脏7h后取左心室心肌,另外8只建立离体左心工作模型,再灌注30min后取左心室心肌.检测心肌三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)、总腺苷(TNA)含量并计算能荷(EC);提取心肌线粒体后检测线粒体内Ca2+含量([Ca2+]m)及线粒体呼吸功能.结果 St组冷保存后心肌ATP含量和EC显著下降,[Ca2+]m显著增高,线粒体呼吸控制率(RCR)明显降低(P<0.05);再灌注后心肌ATP含量及EC无明显改善,[Ca2+]m进一步增高,RCR进一步降低(P<0.05).LCN 1组及LCN 2组各项指标较St组显著改善(P<0.05),两治疗组之间比较差异亦有统计学意义.结论 不同剂量的左卡尼汀添加至St.Thomas No.2液可减轻线粒体钙超载,改善心肌能量代谢,对心肌细胞线粒体有较好的保护作用.此保护作用与LCN剂量有关.

摘要： 目的 评价含左西孟旦的STH-2心脏停搏液对大鼠离体心脏缺血再灌注损伤的影响.方法 雄性Wistar大鼠32只,制备离体Langendorff灌注模型,随机分为4组(n=8),采用K-H液平衡灌注30 min时,C组采用STH-2心脏停搏液进行灌注,L1组、L2组和L2+G分别用含0.03μmol/L左西孟旦、0.3 μmol/L左西孟旦和0.3 μmol/L左西孟旦+10μmol/L格列苯脲(ATP敏感性钾通道阻断剂)的STH-2心脏停搏液进行灌注,灌注2 h时采用K-H液再灌注30 min.分别于灌注心脏停搏液前即刻(基础状态)、再灌注10 min、20 min、30 min时收集冠脉流出液,测定乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性.再灌注30 min时,取心肌组织,测定ATP、MDA、SOD水平及含水量.结果 与C组比较,L1组CK、LDH的活性和MDA含量降低,SOD活性升高,L2组CK、LDH的活性和MDA含量降低,ATP含量和SOD活性升高(P＜0.05或0.01);与L1组比较,L2组CK和IDH的活性和MDA含量降低,SOD活性升高(P＜0.05或0.01);与L2组比较,L2+G组MDA含量、CK和LDH的活性升高,ATP含量和SOD活性降低(P＜0.05或0.01).结论 含左西孟旦的STH-2心脏停搏液可减轻大鼠心肌缺血再灌注损伤,且与浓度有关,其机制与开放ATP敏感性K+通道有关.%Objective To investigate the effect of STH-2 cardioplegic solution containing levosimendan on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Thirty-two male Wistar rats weighing 250-300 gwere anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg. The hearts were rapidly excised and perfused with oxygenated (95% O2-5% CO2) K-H solution for 30 min in a Langendorff apparatus and then divided into 4groups (n = 8 each) according to the composition of cardioplegic solution: group Ⅰ control (group C) was perfused with STH-2 cardioplegic solution; group Ⅱ , Ⅲ and Ⅳ were peffused with STH-2 cardioplegic solution containing levosimendan 0.03 μmol/L (L1), 0.3 μmol/L (L2) and levosimendan 0.3 μmol/L + glibenclamide 10 μmol/L (L2+ G) respectively. The isolated hearts were first perfused with different cardioplegic solutions for 2 h and then with K-H solution for 30 min. The coronary effluent was collected before ischemia (baseline) and at 10, 20 and 30 min of reperfusion for measurement of creatine kinase (CK) and lactate dehydrogenase (LDH)activities. Myocardial specimens were obtained from apex at 30 min of reperfusion for determination of myocardial ATP and MDA contents and SOD activity. Results Perfusion with STH-2 cardioplegic solution significantly increased CK and LDH activities and MDA content, and significantly decreased SOD activity. Levosinendan 0.03or 0.3 μmol/L significantly attenuated the cardioplegia-induced increase in LDH,CK and SOD activities and MDA content. The protective effects of levosimendan on myocardium against I/R injury were reversed by glibenclamide to some extent. Conclusion Levosimendan can protect myocardium from I/R injury in a dose-dependent manner by opening KATP channel.

摘要： 本发明公开了一种天然气水合物孔底冷冻绳索取心钻具及取心方法，本发明适用于深海和陆地永冻层的天然气水合物钻探取心。本发明采用单纯的冷冻取样，采用干冰为冷源，酒精为助冷催化剂和载冷剂，能过实现天然气水合物岩心快速冷冻；将绳索取心与孔底冷冻结合，实现不提钻快速取心；采用钻井液压力来驱动控制阀机构实现冷源注入冷冻机构的过程，具有较高的可行性。钻进时内管总成不回转，因而在较大程度上避免了因钻具回转产生的机械力对水合物岩心的破坏，更有效地提高了岩心采取率。

摘要： 本发明公开了一种天然气水合物孔底冷冻绳索取心钻具及取心方法，本发明适用于深海和陆地永冻层的天然气水合物钻探取心。本发明采用单纯的冷冻取样，采用干冰为冷源，酒精为助冷催化剂和载冷剂，能过实现天然气水合物岩心快速冷冻；将绳索取心与孔底冷冻结合，实现不提钻快速取心；采用钻井液压力来驱动控制阀机构实现冷源注入冷冻机构的过程，具有较高的可行性。钻进时内管总成不回转，因而在较大程度上避免了因钻具回转产生的机械力对水合物岩心的破坏，更有效地提高了岩心采取率。

摘要： 本发明提供一种心脏麻痹液，相较于现有的心脏麻痹液，本发明于pH值、微粒物质形成及渗透压方面表现得更加稳定，且同时对于维护心脏功能的能力也表现较佳。该心脏麻痹液包含溶于水中的钾离子(K+)、镁离子(Mg2+)、钠离子(Na+)、氯离子(Cl‑)、葡萄糖酸根离子、醋酸根离子、硫酸根离子(SO42‑)、三羟甲基氨基甲烷(THAM)及甘露醇。

摘要： 本发明提供贝类中麻痹性贝类毒素的液相色谱‑串联质谱检测方法，包括如下步骤：1.1试样提取：贝类试样加入甲酸溶液，超声提取，离心，取上清液，定容，得到试样提取液；1.2 试样净化：所述试样提取液加入二氯甲烷，混匀，离心，取上清液加入已活化的C18固相萃取柱中，洗脱，收集流出液与洗脱液，合并后定容，静置，离心，取上清液过滤膜，得到试样检测液；1.3 试样检测：取所述试样检测液，进行液相色谱‑串联质谱检测，外标法定量。本发明属于食品安全检测技术领域，简化了操作，减少了有机溶剂消耗，试样的净化效果好，无需超滤步骤，同时还实现了PSTs中部分结构类似物的有效分离和检测，拓宽了对PSTs的检测种类。

摘要： 本发明公开了一种麻痹性贝毒毒素的高效液相色谱‑串联质谱检测方法，其特征在于，包括下列步骤：（1）提取；（2）净化；（3）色谱条件；（4）质谱条件。利用本发明建立的方法对具有证书的参考阳性样品进行检测，获得了较为满意的结果，回收率如表6所示。液相色谱‑串联质谱检测PSP毒素方法操作简便、灵敏度强，重现性好，准确性高，可以满足日常对于PSP毒素的检测要求。

摘要： 本发明涉及医药学、更具体涉及心脏外科，且当在正常体温条件下、也在低体温条件下施行心脏麻痹时，可用于保护心脏免于缺血。通用心脏麻痹液包含以下可药用物质：钾离子；镁离子；提供7.1‑8.9的范围内的pH缓冲的碱和酸；提供275‑460mOsmol/kg的范围内的渗克分子浓度的利尿剂。所述溶液用于在人工血液循环条件下维持心功能，尤其用于实现和保持心搏停止。使用所述通用心脏麻痹液的方法通过以下提供转变来维持心搏停止(一旦实现了心搏停止)：降低所述溶液的初始组分的供应速度(相对于自体血的供应速度)，由此降低溶液的组分对于自体血的比例。

摘要： 一种外用化骨刺除肩周炎解麻痹液是粮食、中草药发酵制剂，又是外用药，不会有副作用。这是外用药贴在皮肤上通过毛孔经由细胞把药效运送到筋骨层刺激化骨刺除肩周炎症，打通血脉解除麻痹，胜过口服药。

摘要： 本发明公开了一种治疗麻痹的精华液，其特征在于：每剂该精华液组成如下：龟甲15克，地黄10克，白求10克，枸杞15克，冬虫夏草5克，荷叶10克，蜈蚣15克。本发明的精华见效快，长久服用可以治愈麻痹症。

摘要： 一种外用化骨刺除肩周炎解麻痹液是粮食、中草药发酵制剂，又是外用药，不会有副作用。这是外用药贴在皮肤上通过毛孔经由细胞把药效运送到筋骨层刺激化骨刺除肩周炎症，打通血脉解除麻痹，胜过口服药。

摘要： 本发明涉及改进的心麻痹液。本发明提供能够产生一种易可逆的，快速电气化学捕获的，并伴有最小组织缺血性的心麻痹液和其组合物。心麻痹液及其组合物被用作停止，保护和/或保存器官，特别是在进行心内直视手术，移植，心血管诊断或治疗干预过程中，停搏，保护和/或保存心脏。