镉对大鼠睾丸中乳酸脱氢酶同工酶活性的影响

采用聚丙烯酚胺凝胶垂直板电泳结合光密度扫描法，分析在四种镉中毒浓度（0．2、04、0．8和1．6mg／kg）下的SD大鼠睾丸中乳酸脱氨酶（LDH）同工酶活性的变化。结果表明：LDH各同工酶的活性在对照组和四种镉染毒组之间均有显著性差异（P＜0．05），LDH－X酶活性受锻中毒抑制最明显，LDH1、LDH2、LDH3和LDH4酶活性随镉中毒浓度的升高而逐渐抑制，而LDH5酶的活性在镉浓度0．2～0．8mg／kg范围内时升高而在1．6mg／kg剂量时则下降的特殊反应，LDH同工酶总活性随镉中毒浓度的升高而降低。结果提示：镉可能对LDH同工酶H、M和C亚基的基因表达影响不一。     

镉对大鼠四种器官乳酸脱氢酶同工酶的影响

目的：观察镉对大鼠器官乳酸脱氢酶（ＬＤＨ）同工酶的影响；方法：采用聚丙稀酰胺凝胶垂直板电泳法结合光密度扫描法，分析在四咱镉中毒浓度（０．２ｍｇ／ｋｇ、０．４ｍｇ／ｋｇ、０．８ｍｇ／ｋｇ和１．６ｍｇ／ｋｇ）下的ＳＤ大鼠心、肝、肾和脑中ＬＤＨ同工酶的变化。结果：随着镉中毒浓度的升高，心脏ＬＳＨ各同工酶的活性显著升高，而肾脏ＬＤＨ各同工酶的活性显著下降，脑中的ＬＤＨ１和ＬＤＨ２的活性出现选知高后下降现象     

朱砂、雄黄对感染性脑损伤大鼠乳酸脱氢酶及其同工酶的影响

背景：要提高含重金属和砷化物矿物药(如朱砂、雄黄)中药制剂的用药安全和排除该类药物的出口障碍，有必要对朱砂、雄黄进行有效性和安全性评价。目前，对复方中朱砂、雄黄的药效作用机制尚不清楚。目的：研究生理、病理状态下安宫牛黄丸中的朱砂、雄黄对机体作用的差异，探讨其药理作用机制。设计：随机对照研究。单位：一所大学的临床药理研究所。材料：实验于2003—01在广州中医药大学临床药理研究所完成。选用第一军医大学实验动物中心提供的体质量为250～300gSD雄性大鼠51只。方法：SD大鼠随机分成6组(8～10只／组)：正常组，正常+安宫牛黄散(下简称整方)组(278mg／kg)；正常+除去朱砂、雄黄的安宫牛黄散(下简称拆方)组(222．7mg／kg)；脑水肿模型组(一侧大鼠颈总动脉注射百日咳杆菌250亿／kg)；模型+整方组(造模前1h给药278mg／kg)；模型+拆方组(造模前1h给药222．7mg／kg)。一次给药后5h(模型组注菌后4h)采血、制备脑匀浆。主要观察指标：脑组织、血清中乳酸脱氢酶(LDH)总活力，血清中乳酸脱氢酶同工酶LDH1—5百分酶活力。结果：与正常组比较，正常+整方组、正常+拆方组LDH总活力显著升高32．4％～38．4％(P&;lt;0．05)，LDH1.2百分酶活力均显著升高(P&;lt;0．01)，LDH4.5百分酶活力下降(P&;lt;0．01)，但除LDH5外，两组同工酶酶活间无显著差异。与模型组比较，模型+整方组、模型+拆方组LDH总活力显著下降23．4％～38．5％(P&;lt;0．01)，LDH5百分酶活力显著升高(P&;lt;0．01)，但两组间无显著差异；模型+整方组LDH2.3，百分酶活力显著下降(P&;lt;0．01)，LDH1.4百分酶活力无显著变化；模型+拆方组LDH1.4百分酶活力显著下降(P&;lt;0．05，0．01)，而LDH2.3百分酶活力变化不显著。结论：正常生理状态下服用安宫牛黄散，对心肌、肾等有一定的损伤作用。感染性脑水肿病理状态下，整方和拆方均可抑制被过度激活的LDH酶，两者之间无显著差异；复方中的朱砂、雄黄对LDH同工酶水平有不同程度的影响。     

肌肽抗全身性缺血/再灌注损伤作用的研究

目的通过失血性休克大鼠血液回输后造成的全身性缺血／再灌注损伤（IRI）模型，研究肌肽对全身性IRI的保护作用。方法36只Wistar大鼠随机分成假手术组、休克损伤组、再灌损伤组和肌肽治疗组。制作大鼠IRI模型：大鼠失血至40mmHg→维持20min→放置1h→全血回输→维持3h→处死。假手术组大鼠手术后处死；休克损伤组大鼠输血前处死；再灌损伤组和三个肌肽治疗组输血前分别静脉推注生理盐水或90mg／kg肌肽，大鼠放置3h后处死。大鼠处死后取血浆检测乳酸脱氢酶（LDH）活性及丙二醛（MDA）浓度；取肝、脑、肺、心、肾组织制作石蜡切片，观察组织病理改变，取肝组织制作肝细胞悬液检测肝细胞凋亡率。结果与休克损伤组相比，再灌损伤组血浆LDH活性及MDA浓度显著升高（P〈0．01，P〈0．05）、组织病理损伤明显加重。与再灌损伤组相比，肌肽治疗组血浆LDH活性及MDA浓度显著降低（P〈0．01）；肝、脑、肺、心、肾组织切片病理损伤明显减轻；肝细胞凋亡率显著降低（P〈0．05）。结论肌肽对全身性IRI具有保护作用。     

毒鼠强对鼠心肌、骨骼肌的作用及与血清酶升高的关系

目的 研究毒鼠强对鼠心肌、骨骼肌的影响及与血清酶升高的关系。方法 用同种大鼠30只，将其分成3组：对照组、半致死量组（0．02mg／kg）及致死量组（0．04mg／kg）；每组雌雄各半。按大鼠的体重将毒鼠强粉溶于生理盐水后灌入胃内，对照组则灌入等量的生理盐水。于死亡立即或1h后取血清测心肌肌钙蛋白TnⅠ及肌酸激酶（CK）、天门冬酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、α-羟丁酸脱氢酶（α-HBDH），并取死亡或处死大鼠的心肌和大腿骨骼肌做病理检查。结果大鼠中毒后10～60min出现四肢或全身抽搐；致死量组6只大鼠于中毒后20-60分钟死亡。血清心肌肌钙蛋白TnⅠ中毒组较对照组增高（P〈0．01），致死量组较半致死量组增高（P〈0．01）；CK、AST、LDH、α-HBDH中毒组高于对照组（P〈0．01），致死量组高于半致死量组（P〈0．01）；中毒大鼠心肌、骨骼肌组织均有变性、坏死；中毒剂量越大，损伤越明显；骨骼肌的损害比心肌损害更严重的。结论毒鼠强急性中毒后，血清酶学异常升高；其心肌和骨骼肌组织均有显著损伤。异常升高的血清酶是毒鼠强对心肌和骨骼肌双重损伤的结果。     

何首乌提取物对大鼠脑缺血再灌注损伤的保护作用

目的：观察何首乌提取物对大鼠局灶性脑缺血再灌注后超氧化物歧化酶活性、丙二醛及一氧化氮含量的影响，探讨其对脑损伤的保护作用。方法：实验于2003—04／05在山东大学医学院实验室完成。40只Wistar雄性大鼠随机分为4组：假手术组、缺血组、20mg／kg何首乌组和40mg／kg何首乌组，每组10只。制造人鼠火脑中动脉缺血再灌沌模型。20mg／kg何首乌组和40mg／kg何首乌组于缺血前30min及缺血后1h分别给予何首乌提取物20mg／kg、40mg／kg腹腔内注射。各组大鼠于再灌注后24h检测脑缺血组织超氧化物歧化酶活件、丙二醛和一氧化氮含量。结果：40只大鼠均进入结果分析。①超氧化物歧化酶活性：20mg／kg何首乌组、40mg／kg何首乌组明显高于缺血组[（85．1&;#177;10．2），（103．2&;#177;12、9），（62．8&;#177;8．7）NU／mg，P〈0．01]，高剂量组高于低剂量组（P〈0．05）。②丙二醛和一氧化氮含量：20mg／kg何首乌组、40mg／kg何首乌组明显低于缺血组[丙二醛含量：（6．58&;#177;0．62），（5．41&;#177;0．58），（9．24&;#177;0．88）μmol／g，P〈0．01；一氧化氮含量：（5183&;#177;0．77），（4．71&;#177;0．59），（7．65&;#177;0．86）mmol／g，P〈0．011，高剂量组高于低剂量组（P〈0．05）。结论：①何首乌提取物可抑制脑缺血再灌注损伤后超氧化物歧化酶活性的下降及丙二醛、一氧化氮含量的升高，表明何首乌提取物可以清除体内过多的氧自由基，对脑缺血再灌注损伤起保护作用。②何首乌提取物的疗效与剂昔有关．高剂量的疗效明显好于低剂量．     

大枣多糖对大鼠气血双虚模型胸腺、脾脏中淋巴细胞超微结构影响的可能途径

目的：观察大枣多糖对放血和环磷酰胺并用所致气血双虚模型大鼠免疫器官淋巴细胞超微结构的影响，分析大枣补气血作用的可能途径。 方法：实验于2002—02／05在河南中医学院动物实验中心完成，选用Wistar雄性大鼠60只，按二次随机分组法分为6组（每组按1～10编号）。①大枣多糖200，100，50mg／kg组、当归补血口服液组及气血双虚模型组大鼠均经尾部放血及腹腔注射环磷酰胺制备气血双虚模型。分别灌服200，100，50mg／kg的大枣多糖（鼠李科植物枣Ziziphus jujuba Mill干燥成熟果实的提取精制物）水溶液（10mL/kg）、当归补血口服液3．3mL／kg（原药液稀释1．5倍）及同体积生理盐水。②正常对照组大鼠不放血仅腹腔注射同体积生理盐水，灌服同体积的生理盐水。各组大鼠给药1次／d，连续14d。于末次给药后2h，麻醉处死大鼠，每组各取5只大鼠（编号为2，4，6，8，10），取胸腺和脾脏作病理切片，电学显微镜观察组织超微结构变化。按Weibel点计数法及立体学公式对胸腺皮质和脾脏的淋巴细胞超微结构指标进行定量分析。 结果：进入分析保持为6组，每组选择5只大鼠，实验过程中无脱失。①与正常对照组相比，气血双虚模型组大鼠胸腺皮质淋巴细胞的线粒体体密度、比表面、比膜面、常染色质体密度均显著降低（P〈0．01），核比表面及异染色质体密度显著升高（P〈0．01）；脾脏淋巴细胞的比表面、异染色质体密度、核比表面均显著升高（P〈0．01），线粒体体密度、比膜面、常染色质体密度均显著降低（P〈0．01），说明代谢功能显著降低，造模成功。②与气血双虚模型组相比，大枣多糖200，100，50mg／kg组大鼠胸腺皮质淋巴细胞的线粒体体密度、比表面、比膜面、常染色质体密度显著升高（P〈0．05-0．01），异染色质体密度、核比表面显著降低（P〈0．01）；当归补血口服液组比膜面显著升高（P〈0．01），核比表面及异染色质体密度显著降低（P〈0．01）。③与气血双虚模型组大鼠相比，大枣多糖200，100，50mg／kg组大鼠脾脏淋巴细胞的线粒体体密度、比膜面、常染色质体密度显著升高（P〈0．01），异染色质体密度显著降低（P〈0．01）；大枣多糖50mg／kg组比表面显著降低（P〈0．01），大枣多糖100，50mg／kg组核比表面显著降低（P〈0．01）；当归补血口服液组比膜面、常染色质体密度显著升高（P〈0．01），异染色质体密度、核比表面显著降低（P〈0．01）。 结论：200，100，50mg／kg的大枣多糖均能明显减轻气血双虚模型大鼠胸腺、脾脏组织淋巴细胞超微结构的病理改变，改善细胞能量代谢，从而起到补气生血的作用。     

盐酸小檗碱对亚硝酸盐中毒小鼠脑急性缺氧的保护作用

目的观察盐酸小檗碱对小鼠脑急性缺氧的保护作用。方法利用亚硝酸钠（NaNO2）中毒和断头实验复制缺氧模型，用盐酸小檗碱3个剂量组即2．0mg／kg、4．0mg／kg、8．0mg／kg连续灌胃6d，观察小鼠存活时间、断头张口次数和喘息时间；用试剂盒测量脑组织超氧化物岐化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）和乳酸脱氢酶（LDH）含量。HE染色观察脑组织形态学变化。结果盐酸小檗碱能明显延长急性缺氧条件下小鼠的存活时间（P〈0．05，P〈0．01）、断头喘息时间（P〈0．05，P〈0．01），提高缺氧小鼠脑组织SOD和LDH的活性，减少MDA和NO的含量；镜下可见模型组小鼠脑膜出血，皮质细胞坏死，脑水肿；盐酸小檗碱治疗组小鼠除脑膜血管扩张外未见明显异常。结论盐酸小檗碱对亚硝酸盐中毒小鼠脑急性缺氧具有一定的保护作用。     

葡萄籽原花青素对脑缺血再灌注损伤的保护作用

目的：观察不同剂量葡萄籽原花青素对大鼠局灶性脑缺血再灌注损伤的神经保护作用及其作用的不同途径。 方法：实验于2004-10／2005-07在安徽医科大学神经生物实验室完成。取SD大鼠160只随机分成假手术组、模型组和葡萄籽原花青素50，100，200mg／kg组5组，每组32只．①缺血前30min模型组大鼠腹腔注射lmL生理盐水，葡萄籽原花青素50，100，200mg／kg组腹腔注射相应浓度的葡萄籽原花青素液1mL，6h后重复给药一次；假手术组不给药。②采用线栓法制备脑缺血再灌注大鼠模型，假手术组不栓塞动脉。各组随机取8只大鼠在再灌注12h断头处死测脑组织含水量；其余大鼠在再灌注24h断头处死取脑，分别检测脑梗死体积比、缺血侧脑组织超氧化物歧化酶活性和丙二醛含量。 结果：160只大鼠全部进入结果分析。①脑梗死体积比：葡萄籽原花青素100，200mg／kg组显著低于模型组（0．3077&;#177;0．0206，0．2972&;#177;0．0248．0．4594&;#177;0.0399，P〈0．01）。②脑含水量：葡萄籽原花青素50，100，200mg／kg组均低于模型组[（79．97&;#177;0．76）％，（79．63&;#177;0.92）％，（79．67&;#177;0．51）％．（81．41&;#177;1．28）％，P〈0．01]。③超氧化物歧化酶活性：葡萄籽原花青素50，100，200mg／kg组均高于模型组[（64．35&;#177;2．29），（64．52&;#177;2．20），（64．43&;#177;2．38）．（39．72&;#177;6．94）NU／mg，P〈0．01]。④丙二醛含量：葡萄籽原花青素50，100，200mg／kg组均低于模型组[（1．15&;#177;0．07），（1．11&;#177;0．16），（1．01&;#177;0．13）．（1．42&;#177;0．23）μmol／g，P〈0．011。 结论：①葡萄籽原花青素≥100mg/kg时可使局灶性脑缺血大鼠脑梗死体积减小，发挥有效的脑保护作用。②≥50mg／kg时即能增强抗氧化酶活性，减轻脂质过氧化损伤，减轻脑水肿程度。     

吴茱萸碱对大鼠胃黏膜损伤的保护作用及其机制

【目的】研究吴茱萸碱对大鼠胃黏膜损伤的保护作用及其机制。【方法】采用乙醇诱发的大鼠胃黏膜损伤模型，用吴茱萸碱处理后，检测胃黏膜溃疡指数（UI），血清中一氧化氮（N0）水平和胃组织中非对称性二甲基精氨酸（ADMA）水平及二甲基精氨酸一二甲胺水解酶（DDAH）的活性。【结果】乙醇诱发大鼠胃黏膜损伤的同时伴有ADMA水平显著升高以及DDAH活性和N0水平下降，而用吴茱萸碱（0．5mg／kgor1．0mg／kg）预处理后则可显著减轻胃黏膜损伤，降低ADMA水平和升高DDAH活性及N0水平。【结论】吴茱萸碱对乙醇诱导的胃黏膜损伤具有保护作用，其机制与抑制ADMA的生成从而升高N0水平有关。     

Effects of various anesthetic protocols on 18F-flurodeoxyglucose uptake into the brains and hearts of normal miniature pigs (Sus scrofa domestica)

This study used positron emission tomography-computed tomography (PET-CT) to evaluate the effects of 4 anesthetic protocols on 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) accumulation in the brains and hearts of miniature pigs (Sus scrofa domestica). The 18F-FDG standard uptake value was quantified by dividing the brain into 6 regions: cerebellum, brainstem, and frontal, parietal, temporal, and occipital lobes. Five (2 female and 3 male) clinically normal miniature pigs were premedicated with medetomidine (200 μg/kg IM) after which the following 4 anesthetic protocols were administered by using a crossover design: 1) propofol (4 mg/kg IV)-isoflurane inhalation; 2) propofol (4 mg/kg IV); 3) ketamine (5 mg/kg IV); 4) tiletamine-zolazepam (4.4 mg/kg IM). Compared with levels after other protocols, brain accumulation of 18F-FDG increased during propofol anesthesia but decreased with tiletamine-zolazepam. Relative to that due to other protocols, heart accumulation of 18F-FDG increased with propofol-isoflurane anesthesia but decreased with tiletamine-zolazepam. Comparing glucose accumulation in the brain and heart of miniature pigs by using PET-CT, we found that glucose accumulation varied according to the anesthetic protocol and between the 2 organs. These results can be used to evaluate how different anesthetic agents affect glucose metabolism in brain and heart of miniature pigs. Furthermore, these data should be considered when selecting an anesthetic agent for miniature pigs that will undergo PET-CT imaging with 18F-FDG.     

The effects of anesthesia on the clinical chemistry of New Zealand White rabbits.

The effects of four anesthetics on various plasma biochemical parameters were investigated in the New Zealand White rabbit. Fifty animals were assigned to five treatment groups (n = 10 per group): control (1 ml normal saline intravenously [i.v.]); ketamine (10 mg/kg i.v.) with either xylazine (3 mg/kg i.v.) or diazepam (2 mg/kg i.v.); pentobarbitone (30 mg/kg i.v.); and thiopentone (20 mg/kg i.v.). Plasma cholesterol, triglycerides, lactate dehydrogenase (LDH), sodium, potassium, chloride, calcium and phosphorus concentrations were measured by an autoanalyzer. Blood samples were obtained at six time-points: before injection and at 10, 30, 60, and 120 min and 24 h after injection of the anesthetic or saline. Plasma biochemical levels were compared to control group and baseline (time 0) levels. Plasma cholesterol concentrations significantly increased in the ketamine-diazepam (P<0.01) and pentobarbitone (P<0.05) groups, whereas plasma triglycerides significantly increased in the ketamine-xylazine (P<0.01) and ketamine-diazepam (P<0.01) groups. Plasma LDH significantly increased in the ketamine-diazepam group (P<0.001) and decreased in the pentobarbitone group (P<0.01). Plasma sodium levels significantly increased after ketamine-xylazine (P<0.05), ketamine-diazepam (P<0.05), and thiopentone (P<0.05) administration; plasma potassium significantly increased after ketamine-xylazine (P<0.05) and decreased in the pentobarbitone group (P<0.05); plasma chloride (P<0.01) and phosphorus (P<0.05) significantly increased after ketamine-diazepam treatment whereas plasma calcium levels increased (P<0.05) after ketamine-xylazine injection. From the results observed so far, we concluded that plasma levels of some biochemical parameters significantly increased or decreased after anesthetic administration. Therefore, caution is required in interpreting data on plasma biochemical parameters from anesthetized rabbits, particularly during the recovery period.     

Hepatoprotective Activity of Licorice Water Extract against Cadmium-induced Toxicity in Rats

Licorice is commonly used as a cure for digestive disorders and as a detoxification agent in East Asia. This study investigated the protective effect of licorice water extract against cadmium (CdCl(2), Cd)-induced liver toxicity in rats. To induce acute toxicity, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously (i.v.) injected into rats. The rats then received either a vehicle or licorice water extract (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd 24 h after the last licorice/vehicle treatment. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with licorice reduced ALT, AST and LDH. In histopathological analysis, licorice decreased the central necrosis around central veins, the peripheral hemorrhage around portal triads, the percentage of degenerative hepatic regions (%/mm(2) hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cells). Licorice also inhibited the increment of Bad (a BH3 domain-containing protein) translocation by Cd in liver cells. These results demonstrate that licorice could have a hepatoprotective effect by inhibiting the translocation of Bad to the mitochondria in Cd-intoxificated rats.     

不同粒径纳米和常规微米SiO_2对大鼠肺、肝、心、睾丸组织的氧化损伤作用

目的探讨不同粒径纳米和常规微米SiO2对大鼠肺、肝、心、睾丸组织的氧化损伤作用。方法采用气管直接滴注法给大鼠染毒,滴注后48 h处死大鼠,测定肺、肝、心、睾丸组织超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活性及脂质过氧化作用(LPO)水平。结果①在67.5 mg/kg剂量下,20 nm SiO2、60 nm SiO2均可引起肺、肝、睾丸组织SOD活性显著降低(P0.05),微米SiO2只引起肺组织SOD酶活性降低(P0.05)。各实验组大鼠心脏SOD活性无显著性变化(P0.05)。②在67.5 mg/kg剂量下,20 nm SiO2、60 nm SiO2及微米SiO2均可引起肺、肝脏GSH-Px活性显著降低(P0.05),且20 nm SiO2还引起心肌组织GSH-Px活性显著降低(P0.05),微米SiO2只引起肺组织GSH-Px活性降低(P0.05)。③20 nm SiO2、60 nm SiO2均可引起肺、肝和睾丸组织LPO水平显著升高(P0.05),且20 nm SiO2还引起心肌组织LPO水平显著升高(P0.05),微米SiO2只引起肺组织LPO水平显著升高(P0.05)。结论微米SiO2只引起肺组织的氧化损伤,而20 nm SiO2、60 nm SiO2均可引起肺、肝、心、睾丸组织不同程度的氧化损伤作用,且20 nm SiO2的毒性作用强于60 nm SiO2的毒性作用。     

Protection against ischemia/reperfusion injury and myocardial dysfunction by antisense-oligodeoxynucleotide directed at angiotensin-converting enzyme mRNA.

Angiotensin-converting enzyme (ACE) activity in the myocardium and angiotensin-II (Ang-II) levels in plasma increase after myocardial ischemia, which lead to exacerbation of myocardial injury and cardiac dysfunction. We examined the protective role of novel antisense-oligodeoxynucleotide (AS-ODN) directed at ACE mRNA in myocardial ischemic injury. Sprague-Dawley rats were treated with ACE-AS-ODN (200 microg per rat, n = 8, i.v.) or inverted-ODN (IN-ODN, 200 microg per rat, n = 8, i.v.), given with 600 microg per rat of liposome DOTAP/DOPE. Hearts from AS-ODN- or IN-ODN-treated rats were excised, perfused in vitro, and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Parallel groups of rats were given ACE inhibitor captopril (5 mg/kg, n = 8) or saline (n = 8) before excising the hearts. Ischemia/reperfusion resulted in myocardial dysfunction (increase in coronary perfusion pressure and LV end-diastolic pressure and a decrease in developed LV pressure) in the saline-treated rats. Myocardial dysfunction was associated with evidence of lipid peroxidation and enzyme leakage (MDA and LDH levels in the myocardium) and up-regulation of ACE protein expression. Administration of AS-ODN or captopril, but not IN-ODN, reduced Ang-II levels in the plasma, decreased ischemia/reperfusion-mediated cardiac functional deterioration and lipid peroxidation, and preserved LDH in the myocardium (all P < 0.05 versus the saline group). AS-ODN and captopril had equipotent effects on cardiac dynamics. ACE protein expression (western blot) was decreased in the hearts of the AS-ODN-treated group, but not in IN-ODN-treated rat hearts. In contrast, ACE protein expression was significantly increased in captopril-treated rat hearts. These observations suggest that AS-ODN directed at ACE mRNA can ameliorate myocardial dysfunction and injury after ischemia/reperfusion, and its use is associated with decreased expression of ACE protein in the ischemic myocardium.     

朱砂、雄黄对感染性脑损伤大鼠乳酸脱氢酶及其同工酶的影响

背景要提高含重金属和砷化物矿物药(如朱砂、雄黄)中药制剂的用药安全和排除该类药物的出口障碍,有必要对朱砂、雄黄进行有效性和安全性评价.目前,对复方中朱砂、雄黄的药效作用机制尚不清楚.目的研究生理、病理状态下安宫牛黄丸中的朱砂、雄黄对机体作用的差异,探讨其药理作用机制.设计随机对照研究.单位一所大学的临床药理研究所.材料实验于2003-01在广州中医药大学临床药理研究所完成.选用第一军医大学实验动物中心提供的体质量为250～300 g SD雄性大鼠51只.方法SD大鼠随机分成6组(8～10只/组)正常组,正常+安宫牛黄散(下简称整方)组(278 mg/kg);正常+除去朱砂、雄黄的安宫牛黄散(下简称拆方)组(222.7 mg/kg);脑水肿模型组(一侧大鼠颈总动脉注射百日咳杆菌250亿/kg);模型+整方组(造模前1 h给药278 mg/kg);模型+拆方组(造模前1 h给药222.7 mg/kg).一次给药后5 h(模型组注菌后4 h)采血、制备脑匀浆.主要观察指标脑组织、血清中乳酸脱氢酶(LDH)总活力,血清中乳酸脱氢酶同工酶LDH1-5百分酶活力.结果与正常组比较,正常+整方组、正常+拆方组LDH总活力显著升高32.4%～38.4%(P＜0.05),LDH1 2百分酶活力均显著升高(P＜0.01),LDH4,5百分酶活力下降(P＜0.01),但除LDH5外,两组同工酶酶活间无显著差异.与模型组比较,模型+整方组、模型+拆方组LDH总活力显著下降23.4%～38.5%(P＜0.01),LDH5百分酶活力显著升高(P＜0.01),但两组间无显著差异;模型+整方组LDH2,3百分酶活力显著下降(P＜0.01),LDH1,4百分酶活力无显著变化;模型+拆方组LDH1,4百分酶活力显著下降(P＜0.05,0.01),而LDH2,3百分酶活力变化不显著.结论正常生理状态下服用安宫牛黄散,对心肌、肾等有一定的损伤作用.感染性脑水肿病理状态下,整方和拆方均可抑制被过度激活的LDH酶,两者之间无显著差异;复方中的朱砂、雄黄对LDH同工酶水平有不同程度的影响.     

大黄抗内毒素性休克大鼠炎性介质作用的实验研究

目的：研究大黄对内毒素性休克大鼠炎性介质作用的机制。方法：选用大鼠内毒素性休克模型。随机分为６组：单纯手术组、内毒素组、大黄预防用药组（１５０ｍｇ／ｋｇ组和７５０ｍｇ／ｋｇ组）和大黄治疗组（１５０ｍｇ／ｋｇ组和７５０ｍｇ／ｋｇ组）。检测磷脂酶Ａ２（ＰＬＡ２）和血小板活化因子（ＰＡＦ）的活性。结果：内毒素注射前６组大鼠平均动脉压（ＭＡＰ）无显著性差异；注射内毒素后４小时ＭＡＰ明显降低；大黄预防用药组和大黄治疗组ＭＡＰ则与注射内毒素前及单纯手术组比较均无明显变化，并均显著高于内毒素组注射内毒素４小时后。注射内毒素后４小时，血清和小肠组织中ＰＬＡ２活性及ＰＡＦ含量均明显增高；与内毒素组注射内毒素后４小时比较，大黄预防组和治疗组则血清和小肠组织中ＰＬＡ２活性和ＰＡＦ含量显著降低。结论：大黄对内毒素性休克所致炎症反应有明显的预防和治疗作用     

卞丝肼对6-OHDA损毁大鼠纹状体AADC活性的影响

目的观察卞丝肼对6-羟多巴胺（6-OHDA）所致帕金森病模型大鼠纹状体芳香L-氨基酸脱羧酶（AADC）活性的影响。方法采用6-OHDA建立帕金森病大鼠模型（黑质纹状体去神经支配）,用生理盐水制作假损毁大鼠作为对照;注射卞丝肼60分钟后,处死大鼠,迅速摘除大脑,并取出纹状体,进行匀浆处理。取匀浆上清液加入到培养基中培养后用高效液相色谱柱（HPLC）进行DA含量测试。结果在假损毁大鼠中,10 mg/kg卞丝肼和50 mg/kg卞丝肼可以使纹状体AADC活性明显降低（P〈0.01）。在6-OHDA损毁大鼠纹状体中,10 mg/kg卞丝肼和50 mg/kg卞丝肼明显降低AADC活性,分别为对照物组的25%和12%（P〈0.01）。然而,10 mg/kg卞丝肼和50 mg/kg卞丝肼组之间无统计学差异。结论卞丝肼降低6-OHDA损毁大鼠黑质纹状体AADC活性,影响L-DOPA代谢。     

Nisoldipine Cardioplegia in the Isolated Rabbit Heart

BACKGROUND: The metabolic and hemodynamic effects of nisoldipine supplementation in cardioplegia after ischemic injury were investigated in 13 isolated rabbit hearts. Group 1 consisted of 6 hearts, which received St. Thomas II cardioplegic solution. In group 2, nisoldipine was added to the cardioplegic solution at a concentration of 0.1 mg/kg in 7 hearts. METHODS: The explanted hearts were suspended from Langendorff apparatus and were perfused with Krebs-Henseleit solution. Left ventricular pressure, heart rate, malondialdehyde, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidized glutathione, creatine kinase MB, (CK-MB), aspartate transaminase, and lactate dehydrogenase (LDH) were measured before and after 60 minutes of ischemia. Peak generated pressure after ischemia was significantly higher in group 2 versus group 1 while end-diastolic pressure was significantly lower in group 2 after ischemic arrest (P <.05). RESULTS: Malondialdehyde levels were lower in group 2 (P <.05). Glutathione peroxidase and glutathione reductase levels were significantly higher in group 2 (P <.05). The only enzymatic significant difference was observed between the preischemic and postischemic levels of aspartate transaminase in group 2 (P <.05). CONCLUSIONS: These findings show beneficial effects of nisoldipine cardioplegia, although its use as a cardioplegic additive is not yet possible. We believe, however, the effects of oral nisoldipine before cardiac surgery can be studied in a clinical setting.