血浆丙二醛及红细胞超氧化物歧化酶测定与呼吸系统疾病的关系

对呼吸系统疾病患者的血浆丙二醛（Ｐ－ＭＤＡ）含量及红细胞超氧化物歧化酶活性（ＲＢＣ－ＳＯＤＡ），进行了测定，并与对照组比较。结果显示：肺心病急性加重期与重度肺结核患者Ｐ－ＭＤＡ含量高于对照组（Ｐ〈０．０１），ＲＢＣ－ＤＯＳＡ明显低于对照组（Ｐ〈０．０１）；肺癌与轻、中度肺结核患者Ｐ－ＭＤＡ含量及ＲＢＣ－ＳＯＤＡ与对照组比较差异无显著意义（Ｐ〉０．０５）。表明肺心病急性加重期与重度肺结核患者自由基的     

老年慢性阻塞性肺疾病患者肾上腺皮质功能的变化

目的：观察老年慢性阻塞性肺疾病患者（ＣＯＰＤ）垂体—肾上腺皮质功能的变化。方法：将１００例老年ＣＯＰＤ分为稳定期、Ⅰ型呼吸衰竭、Ⅱ型呼吸衰竭３个组，并设立３２例同龄对照组，行血气分析，用放免法测定血浆皮质醇及动态ＡＣＴＨ浓度。结果：老年ＣＯＰＤ患者血浆皮质醇浓度升高；ＰａＯ２越低，其皮质醇及ＡＣＴＨ浓度就越高；ＰａＣＯ２越高，则二者浓度就越低。结论：缺氧刺激ＡＣＴＨ及皮质醇的分泌，二氧化碳潴留，使Ⅱ型呼吸衰竭病人的应激能力低于Ⅰ型呼吸衰竭病人。     

大剂量胸腺肽治疗恶性淋巴瘤对免疫指标的影响

将４０例不断发展恶性淋巴患者随机机分为治疗组，用胸腺肽１００ｍｇ／ｄ静滴，合并使用常规化疗方案（包括ＣＨＯＰ ＥＡＣＯＰ方案），对照组仅使用常规化疗方案。结果：治疗组有效率７０％，对照组有效率６０％（Ｐ〉０．０５）。治疗组治疗组后ＩｇＧ、ＣＤ４、ＣＤ４、ＣＤ４／ＣＤ８，ＮＫ细胞活性均明显高于治疗前（Ｐ〈０．０５）。说明：胸腺肽可调节Ｔ淋巴细胞功能，提高ＩｇＧ水平、ＣＤ３＋、ＣＤ４＋细胞数及ＮＫ细胞     

住院慢性阻塞性肺疾病患者人体测量分析

通过对住院ＣＯＰＤ患者人体测量分析，结果显示，ＣＯＰＤ患者营养不良普遍存在，表现在ＡＣ、ＡＭＣ、ＴＳＰ和ＩＢＷ％，均较３为低，而且肺气肿病人和肺心病病间营养状况也存在着一定判别说明病情对营养状态也有一定影响，为临床ＣＯＰＤ营养支持提供了依据。     

脂质过氧化与血管内皮的关系及培哚普利的影响

研究脂质过氧化在血管内皮损伤中的意义及培哚普利对内皮影响的机理。方法采用ＳａｔｏｈＴＢＡ比色法测定ＬＰＯ,采用Ｐｙｒｏｇａｌｌｏｌ－ＮＢＴ比色法测定ＳＯＤ以及循环内皮细胞计数和验正。结果高血压病组培哚普利治疗前ＣＥＣ、ＬＰＯ、ＭＡＰ、ＳＢＰ、ＤＢＰ明显高于对照组;治疗后ＣＥＣ、ＬＰＯ、ＭＡＰ、ＳＢＰ、ＤＢＰ显著低于治疗前;ＳＯＤ三组间无统计学判别且高血压病组干预前,后ＣＥＣ与ＬＰＯ成正相关,相关系     

冠心病高危室性心律失常的心率变异性分析

本文对２６例冠心病合并ＬｏｗｎⅡ－Ⅳ级室性心律失常患者（Ａ组）及３０例合并ＬｏｗｎＯ－Ｉ级室性心律失常患者（Ｂ组）进行心率变异性分析。结果显示：１．Ａ组ＳＤＮＮ和ＳＤＡＮＮ明显低于Ｂ组（Ｐ〈０．００１）。２．Ａ组ＨＦ明显低于而ＬＦ／ＨＦ明显高于Ｂ组（Ｐ〈０．０１），表明Ａ组迷走神经张力明显低于而交感神经张力明显高于Ｂ组。Ａ组中，室速１３例（Ａ１组），成对室早１０例（Ａ２组），Ａ１和Ａ２两组间ＨＲＶ     

普罗布考对冠心病高脂血症降脂抗氧化作用的研究

目的：探讨普罗布考对冠心病高脂血症患者的降脂疗效及对氧化修饰低密度脂蛋白（ＯＸ－ＬＤＬ）的影响。方法：８０例冠心病合并高脂血症患者随机分为治疗组（普罗布考５００ｍｇ／次,ｂｉｄ）和对照组,服药前及服药后４周测定总胆固醇（ＴＣ）、低密度脂蛋白（ＬＤＬ－Ｃ）、甘油三酯（ＴＧ）,载脂蛋白Ａ１（ＡｐｏＡ１）、载脂蛋白Ｂ１００（ＡｐｏＢ１００）及血浆氧化修饰低密度脂蛋白（ＯＸ－ＬＤＬ）浓度。结果：治疗组服药     

吸烟对慢性阻塞性肺疾病脂质过氧化系统及α1—抗胰蛋白酶的影响

吸烟对慢性阻塞性肺疾病（ＣＯＰＤ）患者体内自由基水平和α１－抗胰蛋白酶的影响。采用硫代巴比妥法、放射免疫法和酶标法对３５例吸烟和２５例非吸烟ＣＯＰＤ患者血清脂质过氧化物（ＬＰＯ）、超氧化物歧化酶ＳＯＤ）、α１－ＡＴ和α１－酸性糖蛋白（α１－ＡＧ）进行测定。结果显示：吸烟ＣＯＰＤ组血中ＬＰＯ、α１－ＡＧ明显高于非吸烟组，ＳＯＤ、α１０－ＡＴ明显低于非吸烟组；吸烟组ＬＰＯ和α１－ＡＴ呈负相关，ＳＯＤ和     

慢性阻塞性肺疾病合并呼吸衰竭患者血清、红细胞锌含量测定及临床意义

２９例ＣＯＰＤ合并呼吸衰竭的患者血清、红细胞锌含量进行测定。发现病人血清及红细胞锌含量均明显降低（Ｐ＜０．０１），而且Ⅱ型呼衰组低于Ⅰ型呼衰组（Ｐ＜０．０５）。血气分析发现，红细胞内锌含量与ＰａＯ_２呈正相关（ｒ＝０．３６９ ８，Ｐ＜０．０５），与ＰａＣＯ_２呈负相关（ｒ＝－０．５２２ ２，Ｐ＜０．０５）。检查免疫功能显示，ＣＯＰＤ呼衰病人免疫功能指标明显减低（Ｐ＜０．０５或Ｐ＜０．０１）。对照研究发现，补锌后免疫功能指标明显恢复。提示ＣＯＰＤ呼衰患者存在锌缺乏，Ⅱ型呼衰患者较Ⅰ型呼衰者更为严重。表明缺锌可通过影响机体的免疫功能及气体交换参与ＣＤＰＤ及呼吸衰竭的发病机制。     

肺心病时自由基代谢变化的临床意义

为进一步探明肺心病时自由基代谢变化的规律，寻求肺心病治疗的新方案，以３０例健康人作对照，对２９例肺心病人的超氧化物歧化酶（ＳＯＤ）总量（Ｔ－ＳＯＤ）、锰ＳＯＤ（Ｍｎ－ＳＯＤ）活力、还原型谷胱甘肽（ＧＳＨ）、丙二醛（ＭＤＡ）过氧化氢酶（ＣＡＴ）和总抗氧化能力（Ｔ－ＡＣＯ）等八项自由基指标进行了检测，结果肺心病时Ｔ－ＳＯＤ、Ｍｎ－ＳＯＤ、铜锌ＳＯＤ（ＣｕＺｎ－ＳＯＤ）、ＣＡＴ、ＧＳＨ五项指标均显著低于正常对照组（Ｐ＜０．０１），肺心病急性期Ｍｎ－ＳＯＤ和ＧＳＨ显著低于缓解期（Ｐ＜０．０５），而Ｔ－ＡＣＯ及ＭＤＡ则高于正常人（Ｐ＜０．０１或Ｐ＜０．０５），Ｍｎ－ＳＯＤ／Ｔ－ＳＯＤ之比在肺心病时也有所升高但无统计学差异，ＭＤＡ在急性期的增高程度与缓解期无显著差别（Ｐ＞０．０５）。初步认为肺心病患者的自由基代谢变化。主要表现为自由基的形成与清除失衡，应用抗氧化剂是治疗过程中的一项有效措施。     

Degraded and undegraded carrageenans and experimental gastric and duodenal ulceration

The prevention of histamine-induced gastric and duodenal ulceration in the guinea-pig has been examined using a series of undegraded and degraded carrageenans. Undegraded carrageenans were active at lower doses than degraded carrageenans. The high viscosity of the undegraded carrageenans in solution prevented their use in larger doses. Degradation of carrageenan without serious loss of sulphate, gives a product which allows the dose to be increased to an extent that its effect more than offsets the slight loss in activity caused by the degradation. No single feature of carrageenan structure can be related to anti-ulcer activity although degradation, and hence reduction of molecular size, generally reduces activity. Sulphate contents over 30% have little apparent effect on activity; κ-carrageenans were not consistently different in anti-ulcer activity from Λ-carrageenans. This contrasts with the antipeptic activity of carrageenans where κ-carrageenans are less active than their Λ-counter-parts. As with antipeptic activity, the degree of anti-ulcer activity is probably determined by a combination of structural features which includes molecular size and polyanionic properties.     

Affective and Anxiety Disorders and Alcohol and Drug Dependence:

Depression and anxiety frequently coexist in patients with substance use disorders. This clinically-oriented article examiens the relationship between these conditions and emphasizes data showing that substances of abuse can cause signs and symptoms of both depression and anxiety. These substance-related syndromes appear to have a different course and prognosis than uncomplicated, independent anxiety and major depressive disorders, and clinicians should consider the role of alcohol and other drugs in all patients presenting with these complaints. The authors will also outline an approach for diagnosing and managing patients with the combination of a substance use and depressive or anxiety disorder.     

Alcohol and Substance Use and Abuse in Women and Children

No abstract available for this article.     

Excretion and biotransformation of alfentanil and sufentanil in rats and dogs

The excretion and biotransformation of alfentanil (ALF) and sufentanil (SUF), two recent analogues of the synthetic opioid fentanyl, were studied after single iv administration of the tritium-labeled drugs in male rats and dogs. The drugs were almost completely metabolized in the two species, which resulted in a large number of metabolites. The excretion of the metabolites was rapid and exceeded 95% within 4 days, except for that of ALF metabolites in dogs (about 85%). For ALF, excretion of the radioactivity with the urine (73% in rats, about 76% in dogs) exceeded that with the feces. For SUF, excretion of the radioactivity with the urine amounted to 38 and 60% and that with the feces to 62 and 40%, in rats and dogs, respectively. Bile-cannulated rats excreted 68% with the bile within 24 hr after SUF dosing, and about 22% of this biliary radioactivity was subjected to enterohepatic circulation. After an ALF dose, the biliary excretion amounted to 24%, and the enterohepatic circulation was minimal. The main metabolic pathways of the two drugs were the oxidative N-dealkylation at the piperidine nitrogen and at the amide nitrogen, oxidative O-demethylation, aromatic hydroxylation, and the formation of ether glucuronides. N-[4-(Hydroxymethyl)-4-piperidinyl]-N-phenylpropanamide (M6) was the main metabolite of both ALF and SUF in rats. In dogs, the glucuronide of N-(4-hydroxyphenyl)propanamide (M5) was the main metabolite of ALF. After SUF dosing in dogs, N-[4-(methoxymethyl)-4-piperidinyl]-N-phenylpropanamide was more abundant than M5.