血浆内源性阿片肽升高与实验性肝硬化高动力循环状态及腹水形 …

目的：通过检测实验性肝经各阶段３种内源性阿片肽（ＥＯＰ）血浆浓度变化，探讨基佤肝硬化高动力循环状态及腹水形成的关系，方法；应用放射免疫法测定了卤氯化碳诱发大鼠肝硬化过程中血浆３种ＥＰＯ的含量变化。结果显示：肝硬化腹水组及肝经无腹水组血浆亮啡肽（Ｌ－ＥＮＫ）、强啡肽的含量均显著高于正常对照组，而且升高的水平与肝功能损害的程度呈显著正相关，但血浆β内啡肽的含量在３缚中无显著差异。提示肝脏灭活功能受损志     

血浆内源性阿片肽升高与实验性肝硬化高动力循环状态及腹水形成的关系

目的:通过检测实验性肝硬化各阶段3种内源性阿片肽(EOP)血浆浓度变化,探讨其与肝硬化高动力循环状态及腹水形成的关系.方法:应用放射免疫法测定了四氯化碳(CCl_4)诱发大鼠肝硬化过程中血浆3种EOP的含量变化.结果显示:肝硬化腹水组及肝硬化无腹水组血浆亮啡肽(L-ENK)、强啡肽(Dyn Al-13)的含量均显著高于正常对照组(P<0.01,P<0.05),而且升高的水平与肝功能损害的程度呈显著正相关,但血浆β内啡肽(β-EP)的含量在3组中无显著差异(P>0.05).提示肝脏灭活功能受损导致大鼠血浆小分子阿片肽含量升高,后者又是引起实验性肝硬化高动力循环状态及腹水形成的原因之一.     

血浆内源性阿片肽升高与肝硬化外周动脉扩张及腹水形成的关系

目的：探讨血浆三种内源性阿片肽浓度变化，以了解它与肝硬化外周动脉扩张及腹水形成的关系。方法：用放免法检测了20例正常人，20例非肝病及50例肝硬化患者的血浆强啡肽（DynA1－13），亮啡肽（L－ENK）和β-内啡肽（β-EP）。结果：肝硬化无腹水组和有腹水组血浆DynA1－13和L-ENK浓度均明显高于正常对照组和非肝病对照组（P均＜0．01）；随病情加重，DynA1－13和L－ENK均呈上升趋势，肝硬化有腹水组的L－ENK亦明显高于无腹水组（P＜0．01）。相关分析表明：DynA1－13与A／G比值、L－ENK与A／G比值之间均呈显著负相关；血浆DynA1－13与L－ENK之间呈显著正相关。二组肝硬化患者血浆β－EP浓度与正常组和非肝病对照组比较，差异无显著性。结论：DynA1－13和L-ENK反映肝硬化的严重程度，并且在肝硬化外周动脉扩张及钠水潴因导致腹水形成中起重要作用β-EP不起主要作用。     

内源性神经肽与肝硬化腹水的形成

目的:探讨肝硬化患者血浆亮啡肽(LENK)、神经肽Y(NPY)的变化规律及其在腹水形成中的意义。方法:用放射免疫法检测19例有腹水、18例无腹水的肝硬化患者血浆LENK、NPY含量,并以18例慢性肝炎,14例急性肝炎和10名健康者为对照。结果:肝硬化患者血浆LENK含量显著高于正常人和急、慢性肝炎(P <0.01),有腹水者显著高于无腹水者(P<0、01),而血浆NPY水平肝硬化患者明显下降(P<0.01),有腹水者下降更明显(P<0.01)。结论:肝硬化患者血浆LENK、NPY等内源性神经肽水平明显变化,且以有腹水者为甚,提示这种神经肽可能参与了肝硬化患者的高动力状态循环异常,并与腹水形成有关。     

血浆内源性阿片肽与实验性肝硬变及腹水形成的作用

目的探讨血浆内源性阿片肽(Eop)在实验性肝硬变及腹水形成过程中的变化的意义.方法应用放射免疫法测定正常对照组及CCl4诱发大鼠肝硬变(n=37)及形成腹水(n=17)过程中血浆3种Eop的含量变化.结果肝硬变腹水组及肝硬变组血浆亮氨酸脑啡肽(L-ENK)含量均显著高于正常对照组(P均＜0.01),且都与血清清蛋白浓度呈显著负相关(r=-0.69,P＜0.01; r=-0.56,P＜0.01);与凝血酶原时间(PT)呈显著正相关(r=0.68,P＜0.01; r=0.69,P＜0.01). 同样两肝硬变组血浆强啡肽(DynA1-13)含量均显著高于正常对照组(P均＜0.01). 且与血清清蛋白浓度呈显著负相关(r=-0.64,P＜0.01; r=-0.59,P＜0.01),与PT呈显著正相关(r=0.65,P＜0.01; r=0.67,P＜0.01). 但两肝硬变组血浆L-ENK,DynA1-13与血ALT不相关. β-内啡肽(β-EP)的血浆含量在两肝硬变组及正常对照组中无显著差异.结论肝脏灭活功能受损是血浆小分子阿片肽(L-ENK与DynA1-13)含量升高的重要原因,后者又是实验性肝硬变腹水形成的主要原因之一. 而在β-EP体内灭活过程中,肝脏不起主要作用.     

肝硬化患者血浆亮啡肽,神经肽Y含量的变化及临床意义

目的　探讨肝硬化患者血浆亮啡肽（ＬＥＮＫ）、神经肽Ｙ（ＮＰＹ）含量的变化规律及其临床意义。方法用放射免疫法检测４９例肝硬化患者血浆ＬＥＮＫ、 ＮＰＹ含量，并以１８例慢性肝炎、１４例急性肝炎和１０名健康者作对照。结果　肝硬化患者血浆ＬＥＮＫ含量显著高于正常人和急、慢性肝炎（Ｐ＜０．０５），有腹水、肝性脑病者分别显著高于无腹水和无肝性脑病者（Ｐ＜０．０５）；而血浆ＮＰＹ水平肝硬化患者明显下降（Ｐ＜０．０５），有腹水或肝性脑病者下降更明显（Ｐ＜０．０５）。结论肝硬化患者血浆ＬＥＮＫ、ＮＰＹ等内源性神经肽水平明显变化，且以有腹水、肝性脑病等严重并发症者更为明显，提示这些神经肽可能参与了肝硬化患者的高动力状态循环异常，并与腹水及肝性脑病形成有关。     

糖尿病患者血浆β—内啡肽,亮啡肽和强啡肽A1—13的变化与病程及病情 …

测定７５例糖尿病患者血浆阿片肽的改变。方法，用放射免疫测定β－是肽，亮啡肽及强啡肽Ａ１－１３。结果３种阿片肽均随病程的延长而下降，尤以强啡肽Ａ１－１３为明显。结论糖尿病患者强啡肽Ａ１－１３下降与病程及并发症的关系最密切。     

病毒性肝炎患者血浆亮啡肽的变化及其意义

目的 探讨病毒性肝炎患者血浆亮啡肽(LENK)的变化规律及意义。方法 用放射免疫法(RIA)检测了67例各型肝炎病人及10例正常人LENK含量变化,并观察其与机体免疫学指标的关系。结果 LENK含量在各型肝炎显著高于正常对照(P<0.05),且慢重肝和慢性肝炎重度显著高于其它各型肝炎(P<0.05);在慢性肝炎中,LENK与血清总胆红素呈正相关,与白蛋白和凝血酶原活动度呈负相关。结论 病毒性肝炎时LENK显著升高,并与肝损害程度基本一致,它可能参与了病毒性肝炎的病理损害过程,并与某些临床症状有关,可作为评价肝功能的一项辅助指标。     

糖尿病患者血浆β-内啡肽、亮啡肽和强啡肽A_(1-13)的变化与病程及病情的关系

目的测定７５例糖尿病患者血浆阿片肽的改变。方法用放射免疫法测定β内啡肽、亮啡肽及强啡肽Ａ１１３。结果３种阿片肽均随病程的延长而下降，尤以强啡肽Ａ１１３为明显。血糖较高者及并发神经病变和高血压者降低更明显。结论糖尿病患者强啡肽Ａ１１３下降与病程及并发症的关系最密切     

Progestins increase endogenous opioid peptide activity in postmenopausal women

To determine the effect of administration of a progestin alone on endogenous opioid peptide activity, we infused naloxone (2 mg/h for 4 h) into seven estrogen-deficient postmenopausal women before and after oral medroxyprogesterone acetate (Provera; 20 mg) daily for 30 days. Baseline serum LH levels were significantly decreased by the Provera therapy [70.3 +/- 6.6 (+/- SE) vs. 27.5 +/- 1.7 mIU/ml; P less than 0.001]. Naloxone infusion before Provera treatment had no effect on serum LH levels. In contrast, after Provera therapy, a significant (P less than 0.001) increase in LH levels toward the pre-Provera baseline occurred with naloxone infusion. These findings suggest that progestins exert their negative feedback effects on LH at least in part through an opioid peptide-mediated mechanism and that progestin treatment alone can reestablish opiatergic control of LH.     

犬肝硬化形成过程中生长抑素和前列腺素E2含量的动态变化

目的观察犬在形成肝纤维化过程中血浆生长抑素（ＳＳ）和前列腺素 Ｅ２（ＰＧＥ２）含量的变化。方法杂种犬１０只,４０％以四氯化碳造模,用放免法检测造模前和造模后３０天、６０天、９０天、１２０天血浆ＳＳ和ＰＧＥ２含量。结果造模３０天后ＳＳ和ＰＧＥ２含量的下降,造模前与造模后各时间段血浆ＳＳ和ＰＧＥ２含量下降水平比较,均有显著差异性（Ｐ＜０．０５或０．０１）。结论犬在形成肝硬化过程中血浆ＳＳ和ＰＧＥ２含量均降低。推测这可能是参与肝硬化并发门脉高压性胃肠病和消化性溃疡的重要因素。     

肝硬化患者血浆前脑利钠肽水平变化及其临床意义

目的探讨血浆前脑利钠肽（proBNP）对肝硬化心肌病的判断价值。方法对38例肝硬化患者（LC组）和20名健康体检者（CG组），用ELISA法测定血浆proBNP水平，并行心电图检查。比较两组proBNP水平及心电图改变（QTc、QTd、QTcd和Pd）的差异；对肝硬化患者，分析心电图改变与CTP积分、MELD评分、proBNP的关系。结果Lc组proBNP水平为（228．0±83．4）fmol／ml，显著高于CG组（127．4±21．1）fmol／ml。LC组QTc、QTd、QTcd、Pd分别为（446．9±28．0）ms1/2、（36．4±6．6）ms、（40．6±9．0）ms1/2、（22．8±4．8）ms，均显著长于CG组（417．2±21．5）ms1/2、（29．6±4．9）ms、（31．1±4．9）ms1/2、（19．0±4．1）ms，且与CTP、MELD、proBNP水平呈正相关。结论肝硬化患者存在心肌受损，血浆proBNP可较好地反映肝硬化心肌病病情。     

多发性骨髓瘤患者血浆左旋肉碱含量变化及临床意义

目的探讨多发性骨髓瘤(multiple myeloma,MM)患者治疗前后血浆左旋肉碱含量及临床意义。方法选取10名正常人及36例MM患者(初诊21例,复发15例)。所有患者均接受含或不含蒽环类的方案化疗,采用高效液相色谱法检测患者及正常人的血浆左旋肉碱水平。结果无论初诊或复发患者的血浆左旋肉碱水平均低于正常人,化疗前复发患者组血浆左旋肉碱水平低于初治患者组,差异均具有统计学意义(P0.05);化疗后1 d及1周患者的血浆左旋肉碱水平均低于治疗前,含有蒽环类药物的方案可明显降低血浆左旋肉碱的水平,差异有统计学意义(P0.05)。结论化疗可导致MM患者的血浆左旋肉碱水平低下,化疗过程中补充左旋肉碱具有重要的意义。     

Adaptative changes of metabolic zonation during the development of cirrhosis in growing rats

To evaluate changes in liver metabolic zonation during development of juvenile cirrhosis, zonal activities of succinate dehydrogenase, glutamate dehydrogenase, glucose-6-phosphatase, and nicotinamide adenine dinucleotide phosphate (NADPH) dehydrogenase were measured by quantitative cytochemistry in the liver of developing rats intoxicated with carbon tetrachloride and phenobarbitone. During treatment, activities were most decreased in perivenular zones and subsequently at the periphery of the cirrhotic nodules for succinate dehydrogenase and glucose-6-phosphatase, whereas glutamate dehydrogenase and NADPH dehydrogenase were less affected. In the periportal zones, enzyme activities decreased less. After stopping intoxication, the rats remained cirrhotic, but enzyme activities returned to control perivenular levels at the periphery of the cirrhotic nodule and to control periportal levels at its center. It is concluded that a metabolic zonation persists in carbontetrachloride/phenobarbitone-induced juvenile cirrhosis and that enzyme activities can recover despite persisting cirrhosis. In this model, afferent vessels seem to be located at the center of the cirrhotic nodules, and efferent vessels, at their periphery. A different metabolic zonation may exist in other human and animal liver cirrhosis that could be related to the site of initial liver damage.     

Declining plasma progesterone levels eliminate endogenous opioid peptide suppression of LH pulse frequency on day 22 of gestation in the rat

Endogenous opioid peptides (EOPs) suppress pulsatile LH release during pregnancy in the rat, but the stimulatory effect of the EOP receptor antagonist naloxone on LH pulse frequency is reduced or eliminated on day 22 of gestation. Plasma progesterone (P) levels are elevated through day 20 and fall by day 22. The aim of this study was to determine whether the decline in plasma P levels underlies the loss of EOP suppression of LH pulse frequency on day 22. Rats were bled on day 20 of pregnancy while being infused with 0.9% saline (0.5 ml/h) for 3 h, or implanted with empty or P-filled silastic capsules on day 20 and bled on day 22 while being infused first with saline for 3 h and then naloxone (0.5 mg/kg/h) for 3 h. Plasma P levels in the P-capsule group did not differ significantly from day 20 values, whereas P values in the empty capsule group were markedly decreased compared to day 20 levels and to values in the P-capsule group. Plasma estradiol values did not vary significantly between the two capsule-implanted groups. Mean blood LH levels increased between day 20 and day 22 due to an increase in LH pulse frequency and a small but significant increase in LH pulse amplitude. On day 22, mean blood LH levels, pulse amplitude and pulse frequency values during the saline infusion period in the P-capsule group were less than in the empty capsule group, and did not differ from values in the day 20 group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Liver plasma membrane-associated fibroblast growth: stimulatory and inhibitory activities during experimental cirrhosis.

During experimental CCl4 cirrhosis, an increase of membrane-associated factor stimulating 3T3 cell proliferation in vitro was observed. This stimulator is a 150-kD protein similar to one previously described. In situ perfusion released growth stimulatory activity, suggesting a peripheral plasma membrane protein localizing on basolateral surfaces. The activity increased with increasing number of CCl4 treatments, reaching a maximum at the 14th intoxication. It was faster than the proliferation of connective tissues determined histologically. Cessation of treatment caused a decrease in activity to that of the level of untreated liver, although the number of fibroblastlike cells remained large. This data, taken with the results of experiments with enriched hepatocyte fraction, may serve as an evidence in favor of hepatocyte origin of the factor. A factor inhibiting fibroblast proliferation was measured in detergent extracts from membranes, suggesting an integral membrane protein. The activity of the inhibitory factor increased in acute liver lesions, but at the stage of maximal fibrogenesis this factor is reduced to levels comparable to those of the intact liver. Therefore it is unlikely that this factor is involved in CCl4-induced fibrogenesis at the final stages. These factors may be common controls for various hepatic lesions causing fibrosis, both in clinical and experimental modeling.