热缺血期间持续通气对无心跳兔肺的保护作用

目的:研究热缺血期间持续通气对无心跳供者(NHBD)的肺的保护作用。方法:将12只日本大耳白兔作为供者，随机分为两组，在无肝素抗凝处理条件下处死动物，经历热缺血1h。对照组热缺血期间不给予通气，实验组热缺血期间给予持续通气，然后均以4℃ Euro-Collins液灌洗，冷保存2h。另取同种兔12只，建立离体兔肺灌注模型，对保存的兔肺进行再灌注。分别评价血流动力学、肺泡细胞生存能力、组织学改变、血液气体分析及湿干比。结果:实验组与对照组相比，肺血管阻力较低，肺泡细胞生存能力较高，肺血管内血栓数较少，动脉血氧分压较高，湿干比较低。病理学检查，实验组肺损伤程度较对照组轻。结论:热缺血期间的持续通气对无肝素抗凝处理的无心跳供者的肺具有明显的保护作用。     

一贯煎抗急性实验性胃溃疡和促进溃疡愈合作用

观察一贯煎胃溃疡形成与愈合的影响。方法；采用给大鼠胃饲１ｍｌ无水乙醇中０．２ＮＮａＯＨ引起急性胃溃疡的实验模型。结果；分别以６．０，１２．０和２４．０ｇ／ｋｇ的一贯煎煎剂预先胃饲大鼠，均能显著减轻无水乙醇或０．２ＮＮａＯＨ所致的包性胃粘膜损伤，且有一定的量效关系；其中对无水乙醇性胃粘膜损伤的抑制率分别为６．８％，３７．５％和９３．９％；     

金属硫蛋白对供心的保护作用

目的探讨金属硫蛋白(MT)对离体心脏的保护作用。方法16只Wistar大鼠,随机分为2组,对照组腹腔注射蒸馏水0.5ml,24h后取离体心脏行离体灌注(Langendorff模型),测定心功能,然后灌注HTK心脏保护液,4℃下保存3h,再行Langendorff灌注,10min后转为工作心模型15min;实验组腹腔注射36g/LZnSO4(1.5ml/kg),24h后取离体心脏,随后的处理同对照组。测定心肌组织中MT、ATP、丙二醛(MDA)及Ca2 的含量以及超氧化物歧化酶(SOD)的活性,测定心功能指标、心肌含水量(MWC)、心肌肌酸激酶(CK)和乳酸脱氢酶(LDH)漏出率;测定心肌细胞线粒体内Ca2 ATPase活性、Ca2 含量及其合成ATP能力;观察心肌超微结构。结果实验组MT的含量明显高于对照组(P<0.01);实验组心功能指标、心肌组织中ATP含量及SOD活性均优于对照组(P<0.05,P<0.01),实验组MWC、MDA和Ca2 的含量以及CK、LDH漏出率均低于对照组(P<0.05,P<0.01);实验组心肌细胞线粒体内Ca2 ATPase活性及合成ATP能力均优于对照组(P<0.01),Ca2 含量低于对照组(P<0.01);实验组心肌细胞超微结构的损伤较对照组明显减轻。结论MT对鼠离体心脏具有保护作用。     

Cytoprotective agents used in the treatment of patients with cancer

OBJECTIVE: To provide a review of the literature of commonly prescribed cytoprotective agents used in the treatment of patients with cancer. DATA SOURCES: Journal articles, research reports, review articles, and web sites. CONCLUSION: Multiple agents have been theorized to have cytoprotective properties. Significant evidence exists supporting the use of some cytoprotective agents approved by the US Food and Drug Administration (FDA). More research is needed to determine the efficacy of new cytoprotective agents and expanded indications for those agents currently used. IMPLICATIONS FOR NURSING PRACTICE: Knowledge of the indications for and side effect profiles of cytoprotective agents is a necessary component of oncology nursing care. Familiarity with evidence-based research that supports or refutes the use of FDA-approved cytoprotective agents or alternative agents is helpful when suggesting, prescribing, or administering such agents.     

The Nitric Oxide Donor SIN-1 Protects Endothelial Cells from Tumor Necrosis Factor-α-Mediated Cytotoxicity: Possible Role For Cyclic GMP and Heme Oxygenase

In cultured endothelial cells, incubation with TNF-α(50 ng/ml) for 72 h markedly reduced viability of endothelial cells. A 6-h pre-incubation with the nitric oxide (NO) donor linsidomine (SIN-1, 10–150μ ) protected endothelial cells in a concentration-dependent manner and increased viability by up to 59% of control. The unmetabolized parent compound molsidomine and the NO-free metabolite of SIN-1 3-morpholinoiminoacetonitrile (SIN-1C) were without cytoprotective effect. Cytoprotection by SIN-1 was completely abolished by the NO scavenger 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide (PTIO, 30μ ). A cytoprotective effect comparable to SIN-1 was observed when preincubating the cells with dibutyryl cyclic GMP (10–100μ ). Moreover, no protection by SIN-1 occurred in the presence of cycloheximide (1μ ) or 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ, 0.1μ ), a selective inhibitor of soluble guanylyl cyclase. Tin protoporphyrin-IX (SnPP, 25μ ), an inhibitor of heme oxygenase, was found to attenuate SIN-1-induced cytoprotection. Our results demonstrate that SIN-1 produces a long-term endothelial protection against cellular injury by TNF-α, presumably via a cyclic GMP-dependent pathway leading to up-regulation of protective proteins such as heme oxygenase.     

Locally targeted cytoprotection with dextran sulfate attenuates experimental porcine myocardial ischaemia/reperfusion injury.

AIMS: Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may protect damaged tissue from reperfusion injury by functional restoration of HSPG. METHODS AND RESULTS: In a closed chest porcine model of acute myocardial ischaemia/reperfusion injury (60 min ischaemia, 120 min reperfusion), DXS was administered intracoronarily into the area at risk 5 min prior to reperfusion. Despite similar areas at risk in both groups (39+/-8% and 42+/-9% of left ventricular mass), DXS significantly decreased myocardial infarct size from 61+/-12% of the area at risk for vehicle controls to 39+/-14%. Cardioprotection correlated with reduced cardiac enzyme release creatine kinase (CK-MB, troponin-I). DXS abrogated myocardial complement deposition and substantially decreased vascular expression of pro-coagulant tissue factor in ischaemic myocardium. DXS binding, detected using fluorescein-labelled agent, localized to ischaemically damaged blood vessels/myocardium and correlated with reduced vascular staining of HSPG. CONCLUSION: The significant cardioprotection obtained through targeted cytoprotection of ischaemic tissue prior to reperfusion in this model of acute myocardial infarction suggests a possible role for the local modulation of vascular inflammation by glycosaminoglycan analogues as a novel therapy to reduce reperfusion injury.     

乙醇对血管的影响及相关作用机制研究进展

乙醇对血管系统的作用比较复杂,适度饮酒对心脑血管系统疾病可以产生一定的保护作用,而长期过度饮酒可以导致心脑血管相关疾病发生率和死亡率风险升高。越来越多的研究表明乙醇摄入对许多疾病起到双向调节作用,饮酒方式的不同和乙醇摄入剂量的差异对血管系统产生的作用亦有所不同。乙醇作为心脑血管疾病的主要诱因之一,在血管系统疾病的发生发展中起着重要的作用。因此,探讨乙醇对血管系统的作用机制,将为进一步揭示乙醇相关血管系统疾病的发病机制和寻求有效的治疗措施提供重要的参考依据。     

鹿茸多肽对脊髓损伤保护作用的实验研究

目的：观察鹿茸多肽应用于脊髓损伤大鼠的治疗效果。方法：75只雄性Wister大鼠随机分为正常对照组、空白手术组、15、10、5mg治疗组,每组15只。通过脊髓损伤动物模型,各治疗组分别注射15、10、5mg鹿茸多肽,正常对照组皮下注射生理盐水,空白手术组造模后不予处理,给药7d。观察其对脊髓损伤动物的动能测定及脊髓病理变化的影响。结果：15、10、5mg不同剂量鹿茸多肽给药7d后,大鼠运动功能有所恢复,明显高于手术组,差异有统计学意义（P〈0.001）,并且治疗剂量增加,疗效增强。病理组织切片观察显示不同剂量的鹿茸多肽治疗后,组织水肿减轻,炎性细胞浸润减轻;尤以15mg治疗组恢复最明显。结论：鹿茸多肽具有促进脊髓损伤大鼠运动功能恢复的作用,且呈剂量依赖性。     

槲皮素和黄芪甲苷对大鼠缺氧心肌细胞的保护作用

目的 了解并比较槲皮素、黄芪甲苷对体外培养的缺氧心肌细胞的保护作用，寻找其作用的量效关系。方法 将SD乳鼠心肌细胞分成单纯缺氧组（A组）、缺氧＋100mg／L槲皮素组（B组）、缺氧＋50mg／L槲皮素组（c组）、缺氧＋25mg／L槲皮素组（D组）、缺氧＋50．0mg／L黄芪甲苷组（E组）、缺氧＋25．0131mg／L黄芪甲苷组（F组）、缺氧＋12．5mg／L黄芪甲苷组（G组）、缺氧＋10mg／L维生素E组（H组）。各组细胞原代培养后先加入相应浓度的槲皮素、黄芪甲苷、维生素E，再行缺氧处理12h（A组培养后直接行缺氧处理）。检测各组心肌细胞活力和乳酸脱氢酶（LDH）、丙二醛（MDA）、超氧化物歧化酶（SOD）、活性氧（ROS，只检测A、C、F、H组）值。结果B～G组与A组比较，LDH、MDA、ROS（C、F组）值下降，心肌细胞活力、SOD值上升，作用普遍优于H组。在同等高、中、低浓度下，加入黄芪甲苷组的心肌细胞活力和LDH水平总体优于加入槲皮素组（如C、F组的心,肌细胞活力为0．454±0．018、0．471±0．017，LDH为2800±9、2312±52），但两组MDA、SOD和ROS值比较，差异无统计学意义（C、F组的ROS为16．0±5．3、22．4±8．7，P〉0．05）。结论 黄芪甲苷、槲皮素能有效保护缺氧心肌细胞，减轻损伤程度，其作用优于维生素E。黄芪甲苷的保护作用较槲皮素更好，但两者减轻细胞脂质过氧化损伤的作用差异不明显。     

一氧化氮在雷贝拉唑对大鼠胃黏膜损伤保护中的作用

目的:探讨一氧化氮(NO)在雷贝拉唑对大鼠胃黏膜损伤保护中的作用．方法:在乙醇诱导大鼠胃黏膜损伤前,预先给予雷贝拉唑(20 mg/kg)灌胃,1-硝基-精氨酸甲酯(1-NAME,4 mg／kg)、1-精氨酸(250 mg／kg)及d-精氨酸(250 mg／kg)iv．采用激光多普勒血流计(LDF)测定胃黏膜血流量(GMBF),采用镉粒还原和比色法测定胃黏膜和血浆NO-2／NO-3含量,并观察胃黏膜损伤指数(UI)、溃疡坏死组织和中性粒细胞浸润严重程度的变化．结果:与模型损伤组比,雷贝拉唑组大鼠UI明显降低(5．5±0．5 vs 25．2±2.3,P<0．01),溃疡坏死组织和中性粒细胞浸润程度明显减轻(坏死物质 → ／≤ :1／9 vs 8／2,P<0．01;中性粒细胞 → ／≤ :3／7 vs 9／1,P<0．01)．预先用1-NAME处理后,雷贝拉唑保护胃黏膜损伤作用明显减弱;1-NAME抑制作用可被1-精氨酸拮抗,而不被d-精氨酸拮抗．向胃内灌注雷贝拉唑,可增加GMBF、胃黏膜和血浆NO-2／NO-3,1-NAME可逆转这种作用,但对雷贝拉唑抑制酸分泌作用无明显影响．结论:雷贝拉唑对大鼠胃黏膜损伤保护作用与NO有关,而与雷贝拉唑抑制酸分泌作用无关．