高血压病程及血脂对冠状动脉造影病变程度的影响

目的探讨高血压病程及血脂与冠状动脉造影病变程度的关系。方法502例住院患者作为研究对象,所有病例均经选择性冠状动脉造影分组,按照有无冠状动脉狭窄及其程度分为：无病变及狭窄性病变、斑块浸润性病变、单支病变、双支病变、三支病变及弥漫病变五组;所有患者入院后测量血压,并对每一个患者进行高血压和糖尿病病史的调查,测定血脂水平;经桡动脉或股动脉途径进行选择性冠状动脉造影。结果随着冠状动脉造影病变程度分级的加重,高血压组患者数逐渐增加,卡方检验示P＆lt;0.01,有显著性统计学意义。在冠状动脉造影病变程度的分级各组中,随着病变程度的加重高血压患者的比例逐渐增多,说明高血压病是冠状动脉病变严重程度的相关因素。高血压病患者的发病病程,随着冠状动脉造影病变程度分级的加重,高血压组患者病程数值逐渐增加,One-WayANOVA过程检验示P＆lt;0.01,有显著性统计学意义。随着冠状动脉狭窄程度的加重,血浆总胆固醇、低密度脂蛋白胆固醇、载脂蛋白B、三酰甘油、脂蛋白（a）水平呈逐渐增高趋势;载脂蛋白A1（ApoAl）、高密度脂蛋白胆固醇有下降的趋势;年龄愈大,冠脉病变的严重程度愈重;体质量、三酰甘油水平在冠心病各组中无明显差别。结论高血压病是冠状动脉病变严重程度的相关因素,高血压病患者病程愈长冠状动脉造影病变程度及范围愈重。     

Ⅱ型糖尿病患者血脂水平分析

目的通过对Ⅱ型糖尿病患者血脂水平分析,有效地控制糖尿病并发症的发生。方法用7170A生化分析仪检测72例Ⅱ型糖尿病患者和83例健康体检者血清中的TG、TC、HDL-C、LDL-C。结果Ⅱ型糖尿病患者血清中的TG、TC、LDL-C均比健康对照组高,HDL-C比健康对照组低。结论Ⅱ型糖尿病患者均有脂类代谢异常。     

Cytotoxicity and mitochondrial dysfunction of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in isolated rat hepatocytes

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that induces hepatic and extrahepatic oxidative stress and the mechanisms of TCDD-induced reactive oxygen species are not fully investigated. Moreover, the potential toxicity of TCDD in isolated rat hepatocytes is not fully explored. The aim of the current study was to explore the possible cytotoxic effect of TCDD on primary rat hepatocytes and to explore the impact of mitochondria in TCDD-induced toxicity. Hepatocytes were isolated from adult rat liver and incubated with 0, 5, 10 or 15 nM of TCDD for 24, 48 and 72 h. Cell viability, lactate dehydrogenase (LDH) leakage into media along with reactive oxygen species (ROS) generation and hydrogen peroxide (H₂O₂) production, mitochondrial membrane potential (Δψ_m), superoxide dismutase (SOD), catalse (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), total thiol contents, hepatic aryl hydrocarbon hydroxylase (AHH), and ethoxyresorufin O-deethylase (EROD) were performed in hepatocytes. In addition, superoxide anion generation, lipid peroxidation (LPO), mitochondrial protein carbonyl content and respiratory chain complexes II and IV were assayed in hepatocyte mitochondria. Cell viability was significantly decreased while LDH leakage into media was significantly increased in a dose and time related manner. ROS generation and H₂O₂ production along with EROD and AHH activities were significantly increased in hepatocytes in the same pattern. The antioxidant enzymes SOD, CAT, GPx and GR and the non-enzymatic protein thiols, in addition to Δψ_m were significantly decreased in hepatocytes in a concentration and time dependent pattern. On the other side, mitochondrial superoxide anion along with LPO and mitochondrial protein carbonyl content were significantly increased while the respiratory chain complexes II and IV activities were significantly decreased in hepatocyte mitochondria. This effect may lead to disruption in the functional integrity of hepatocytes and hepatocyte mitochondria. In conclusion, our data clearly show that TCDD induces hepatocyte toxicity and mitochondrial dysfunction by a mechanism involving generation of ROS. Mitochondria might be the primary source of (or at least contribute to) the oxidative stress response and resulting toxicological outcomes elicited by TCDD.     

肺癌患者脂质过氧化物代谢及保护酶类的研究

目的综合研究分析肺癌患者体内过氧化物代谢及抗氧化酶类的存在状态和相关性。方法采用紫外光度法及生物化学方法测定了肺癌患者、肺良性疾患患者和健康人血清GST、GSH-Px、CAT活性及LPO水平。结果肺癌组血清GST活性显著高于健康组和良性组(P<0.01)。健康组和良性组血清GST活性差异无显著性(P>0.05)。GSH-Px活性各組间均有显著性差异(P<0.05),健康组和肺癌组相比有极显著差异(P<0.01);各组间CAT活性无显著差异(P>0.05);LPO水平随病变进展明显升高,组间有极显著差异(P<0.01)。LPO/GSH-Px值随病变进展显著升高,组间有极显著性差异(P<0.01)。结论血GST和GSH-Px活性及LPO水平与疾病发生和发展之间可能存在量的关系。肺癌的发病或易感性可能与GSH-Px活性下降、GST活性和LPO水平显著升高有关。     

脂肪乳对局麻药中毒大鼠的作用研究

目的 研究布比卡因诱导的大鼠心跳骤停的模型中,脂肪乳复合肾上腺素心肺复苏的效果.方法 40只SD大鼠,随机分为两组,每组20只,A组:肾上腺素对照组,L组:肾上腺素联合脂肪乳组.将大鼠麻醉后静脉注射布比卡因20 mg/kg,心跳停搏后行心肺复苏(CPR).A组开始CPR时注入肾上腺素10 μg/kg,共3次,之后每5分钟注入肾上腺素10 μg/kg.同时注入0.9%氯化钠注射液5 ml/kg,然后0.9%氯化钠注射液1 ml·kg-1·min-1;L组肾上腺素的应用与A组相同,并且在注入肾上腺素后注入20%脂肪乳5 ml/kg,接着注入脂肪乳0.25 ml·kg-1·min-1.监测心率、血压和体温.在麻醉后、心肺复苏成功5 min、30 min测量动脉血气.记录大鼠CPR成功的时间、数量,肾上腺素的用量.结果 A组心肺复苏成功11只, 成功率为55%,L组复苏成功16只,成功率为80%,脂肪乳组成功率高(P<0.05).A组用的肾上腺素剂量比L组小(P<0.05).两组大鼠复苏后5 min、30 min心率正常.复苏后30 min,两组的收缩压均在正常范围,L组的收缩压比A组高.L组的PaO2比A组高(P<0.05).结论 布比卡因中毒心跳骤停的大鼠用脂肪乳联合肾上腺素比单纯肾上腺素心肺复苏效果好.     

Effect of pentoxifylline on veno-occlusive priapism-induced corporeal tissule lipid peroxidation in a rat model

Objective: To investigate whether pentoxifylline could play a role in attenuation of the hazardous effects of ischemia/reperfusion on corporeal tissue in a rat model of veno-occlusive priapism (VOP). Materials and methods: Placebo and pentoxifylline were given to eight groups of rats prior to priapism being induced by a vacuum constrictive device for durations of 6 and 12 h, respectively. Half of the groups of rats that underwent the same duration of priapism (ischemic) were subjected to 1 h of detumescence after band removal (reperfusion). One group underwent no manipulation and no drug administration and served as a baseline determination (control). Corporeal homogenates were examined for lipid peroxidation (LP) derived malondialdehyde (MDA) accumulation via thiobarbituric acid assay. Results: MDA concentration differed significantly between VOP rats and controls (P < 0.001) but did not differ significantly between ischemic-only groups and reperfused groups (P > 0.05). In the pentoxifyllinepretreated groups, although MDA accumulation tended to be slightly lower than in the placebo groups, the difference was not statistically significant (P > 0.05) either in the 6- or 12-h duration priapic groups. Conclusions: LP, an indicator of radical oxygen metabolite (ROM) induced injury, occurs in rat corporeal tissue during and after abolishment of VOP. Single-dose pentoxifylline pretreatment failed to exert a protective effect on corporeal tissue in a rat model of VOP in terms of attenuation of LP.     

地奥心血康对心肌缺血再灌犬心肌细胞膜Na~＋，K~＋—ATP酶活性与LPO含量

１６只成年杂种犬复制心肌缺血再灌模型。分为地奥心血康治疗组（ＤＡＸＸＫＧ）和生理盐水对照组（ＮＳＣＧ）。差速离心分离心肌细胞质膜，无机磷法测定心肌细胞膜Ｎａ￣＋，Ｋ￣＋－ＡＴＰ酶活性，荧光法测定心肌细胞膜与血清脂质过氧化物（ＬＰＯ）含量。结果表明：（１）ＤＡＸＸＫＧＮａ￣＋，Ｋ￣＋－ＡＴＰ酶活性明显高于ＮＳＣＧ（Ｐ＜０．０１）；（２）血清ＬＰＯ含量，随着再灌时间延长，ＮＳＣＧ呈上升趋势，ＤＡＸＸＫＧ略下降，再灌２４０ｍｉｎ两组比较差异显著（Ｐ＜０．０１）；心肌细胞膜ＬＰＯ含量，ＤＡＸＸＫＧ低于ＮＳＣＧ（Ｐ＜０．０５）；（３）心肌细胞膜Ｎａ￣＋，Ｋ￣＋－ＡＴＰ酶活性与ＬＰＯ含量呈明显负相关（ｒ＝－０．８３，Ｐ＜０．０１）。这些结果提示ＤＡＸＸＫ可通过抗脂质过氧化而实现其保护心肌细胞膜的效应。     

比较异丙酚和依托咪酯对心脏瓣膜置换术患者过氧化脂质和超氧化物歧化酶的影响

目的:观察异丙酚对心脏瓣膜置换术患者过氧化脂质和超氧化物歧化酶的影响。方法:20例瓣膜置换术患者分为异丙酚组和依托咪酯组。分别在心肌缺血再灌注前后取血做过氧化脂质和超氧化物歧化酶测定,同时记录心电图和平均动脉压。结果:过氧化脂质在异丙酚组主动脉插管时下降,主动脉开放后升高,均有显著差异(P<0.05,P<0.01)。依托咪酯组主动脉开放后明显升高,亦高于异丙酚组同时值,差异均显著(P<0.01)。超氧化物歧化酶主动脉开放后两组均下降(P<0.05,P<0.01),两组间无差异。主动脉开放后心律失常、心肌缺血、电击复跳例数异丙酚组少于依托咪酯组。结论:异丙酚可明显降低心肌缺血再灌注后过氧化脂质含量,减少心律失常和心肌缺血现象。     

五项衰老生化指标的探讨

本文观察了2月、10月和24月龄大鼠红细胞膜Na~ -K~ -ATP酶、全血谷胱甘肽过氧化物酶(GSH-PX),红细胞超氧化物歧化酶(SOD)活性及红细胞膜和血浆脂质过氧化物(LP0)水平,结果显示10月龄与2月龄组相比,Na~ -K~ -ATP酶活性增高24.16%.GSH-PX活性增高4o.07%.红细胞膜LPO增高44.44%,血浆LPO增高了102.72%;24月龄与10月龄组相比,Na~ -K~ -ATP酶活性下降45.16%,GSH-PX活性下降了22.3%,SOD活性下降12.32%,而红细胞膜LPO升高30.0%.由此认为上述5项指标可用于评估机体衰老情况     

阿霉素对心肌过氧化代谢和功能的影响

采用在体、离体心脏灌流和体外心肌细胞培养的方法,观察阿霉素引起的心肌代谢和功能损伤。体内实验表明,阿霉素一次给药(20mg/kg,ip)可引起心肌GSH水平下降,多次给药(5mg/kg/次隔日,共7次)可引起小鼠心肌MDA升高,GSH下降。在Langendorf灌流实验中,10~(-6)mol/L阿霉素可引起大鼠心肌收缩力下降,冠脉血流量减少。在培养心肌细胞中,1mmol/L阿霉素可引起培养基中LDH升高及细胞中MDA含量增加。结果表明阿霉素对心肌有直接损伤作用。这种作用可能与内源性氧化-抗氧化系统失衡有关。