烧伤大鼠肠道组织内Ca2+-ATPase、CGRP含量对胃肠动力功能的影响

目的研究烫伤大鼠早期肠道组织内Ca2+-ATPase、降钙素基因相关肽(calcitonin gene rdatedpeptide,CGRP)的变化,探讨该Ca2+-ATPase、CGRP含量变化与肠道推进功能的关系,进一步阐明烧伤后胃肠功能障碍的发生机制.方法选用清洁大鼠30只,采用30%烫伤大鼠模型,随机分为烫伤组、内毒素组及对照组测定烫伤后1 h大鼠胃肠推进距离及肠道组织中Ca2+-ATPase和CGRP的含量.结果烫伤及内毒素腹腔注射1 h后大鼠肠道碳素墨水推进距离为(53.00±8.88)cm和(91.00±10.22)cm,对照组为(142.00±11.11)cm,两两比较肠道碳素墨水推进距离,烫伤组和内毒素组明显缩短,差异有显著性(P＜0.001).肠道组织内Ca2+-ATPase分别为(263.8±58.30)、(244.4±105.5)和(380.5±116.7)mol/s,烫伤组及内毒素组肠道组织中Ca2+-ATPase与对照组比较,均有不同程度的降低(P＜0.05),CGRP的含量分别为(52.38±39.23)ng/mL,(20.48±23.11)ng/mL及(0.75±1.96)ng/mL,烫伤组及内毒素组肠道组织中CGRP含量均有不同程度的增高,两两比较差异有显著性(P＜0.01,P＜0.05).结论烫伤早期肠道组织CA2+-ATPase活性下降及CGRP含量的增高与肠道动力功能的减弱有着十分密切的关系.     

谈中医术语“气”的英译

谈中医术语“气”的英译江苏省海门卫校（江苏２２６１００）袁洪仁中医术语“气”的内涵较多，在中医及中西医结合等文献中有多种英译：（互）ｏ，（２）Ｖｉｔａｌｅｎｅｒｇｙ，（３）Ｖｉｔａｌ－Ｑｉ，（４）ｈ。ｌｔｈｔｅｎｅｒｓｓ，（５）ｈ。ｌｔｈｓＱｉ等。按...     

超大分子F1—ATP酶空间晶体生长预实验

ＡＴＰ合成酶是氧化磷酸化过程中催化ＡＴＰ合成的关键酶。具有催化活性的Ｆ１－ＡＴＰ酶部分高分辨率三维结构的解析，对阐明氧化磷酸化的机理具有重要意义。     

The reactivation of the proscillaridin-inhibited membrane ATPase by specific antibodies

Summary The action of proscillaridin (p.) on a partially purified Na⁺–K⁺-ATPase preparation was studied, using a linked optical enzyme assay. A half maximal ATPase inhibition was obtained with 6.3×10^–7 M p. Testing 5 additional glycosides and genins we observed a maximal suppression of the enzyme activity of up to 80%. Following the immunization of rabbits against a p.-human serum albumin complex, the antibody was shown to prevent and rapidly reverse the inhibition of the enzyme in a linear dose-dependent fashion.Supported by the Deutsche Forschungsgemeinschaft.     

Cardiac glycosides: Correlations among Na+, K+-ATPase,sodium pump and contractility in the guinea pig heart

Summary Relationships among positive inotropic response to cardiac glycosides, Na⁺,K⁺-ATPase inhibition and monovalent cation pump activities were studied using paced Langendorff preparations of guinea-pig heart. Na⁺,K⁺-ATPase activity was estimated from the initial velocity of (³H)-ouabain binding in ventricular homogenates, and cation pump activity from ouabain-sensitive ⁸⁶Rb uptake of ventricular slices. These parameters were assayed in control, ouabain- or digitoxintreated hearts either at the time of inotropic response to the cardiac glycosides or during the course of drug washout. Development and loss of the inotropic response during ouabain or digitoxin perfusion and washout was accompanied by reduction and subsequent recovery of the initial ouabain binding velocity, respectively. If homogenates from glycoside-treated hearts were incubated at 37°C for 10 min during ouabain-binding studies, the levels of binding were not different from those of control hearts, indicating a rapid dissociation of the glycosides from cardiac Na⁺,K⁺-ATPase in this species. Despite differences in the time course of the loss of inotropic responses produced by ouabain or digitoxin, the relationship between Na⁺,K⁺-ATPase inhibition and inotropic responses were similar. Inotropic responses to digitoxin during perfusion, and subsequent los during washout, also were accompanied by a reduction and subsequent recovery of ⁸⁶Rb uptake. A correlation between inhibition of cation pump activity and positive inotropy has hitherto not been demonstrated. Thus, it appears that with cardiac glycosides, a relationship exists among contractility, cardiac Na⁺,K⁺-ATPase and monovalent cation pump activities.     

Nanomolar level of ouabain increases intracellular calcium to produce nitric oxide in rat aortic endothelial cells

Changes in [Ca(2+)](i) across the cell membrane and/or the sarcoplasmic reticulum regulate endothelial nitric oxide (NO) synthase activity. In the present study, we investigated the effect of ouabain, a specific inhibitor of Na(+)/K(+)-ATPase, on NO release and [Ca(2+)](i) movements in cultured rat aortic endothelial cells (RAEC) by monitoring NO production continuously using an NO-specific real-time sensor and by measuring the change in [Ca(2+)](i) using a fluorescence microscopic imaging technique with high-speed wavelength switching. The t((1/2)) (half-time of the decline of [Ca(2+)](i) to basal levels after stimulation with 10 micro mol/L bradykinin) was used as an index of [Ca(2+)](i) extrusion. A very low concentration of ouabain (10 nmol/L) did not increase the peak of NO production, but decreased the decay of NO release and, accordingly, increased integral NO production by the maximal dose-response concentration induced by bradykinin. The same dose of ouabain affected [Ca(2+)](i) movements across the cell membrane and/or sarcoplasmic reticulum induced by bradykinin with a time-course similar to that of NO release. Moreover, the t((1/2)) was significantly increased. Pretreatment of RAEC with Na(+)-free solution, an inhibitor of the Na(+)/Ca(2+) exchanger, and nickel chloride hexahydrate prevented the effects induced by bradykinin and ouabain. These observations using real-time recording indicate that a small amount of ouabain contributes to the bradykinin-stimulated increase of NO production through inhibition of plasma membrane Na(+)/K(+)-ATPase activity and an increase in intracellular Na(+) concentrations. The membrane was then depolarized, leading to a decline in the bradykinin-stimulated increase in [Ca(2+)](i) by forward mode Na(+)/Ca(2+) exchange to prolong the Ca(2+) signal time. From these results, we suggest that nanomolar levels of ouabain modulate [Ca(2+)](i) movements and NO production in RAEC.     

Environmental boron exposure and activity of delta-aminolevulinic acid dehydratase (ALA-D) in a newborn population.

Following boron intake, multiple effects have been observed in animal experiments. However, human data is lacking, and no data is available on the ability of boron to accumulate in fetal tissues. Positive responses in animal species suggest that developmental toxicity may be an area of concern in humans, following exposure to boron. Two hypotheses have seemed to account for the multiple effects described in scientific findings. One hypothesis is that boron is a negative regulator that influences a number of metabolic pathways by competitively inhibiting some key enzyme reactions. The other hypothesis is that boron has a role in ionic membrane transport regulations. To better understand boron potential toxicity, the present study examined the relationship between boron exposure and some key enzymes, well-known for their affinity for mineral elements, such as delta-aminolevulinic acid dehydratase (ALA-D), and two fundamental enzymes having a role in ionic membrane transport regulations (Ca-pump and Na(+)K(+)-ATPase). We investigated the potential effects of an environmental boron exposure on the activity of these enzymes in an urban population of 197 "normal" newborns. Environmental boron exposure was assessed in placental tissue. Because of the well-known inhibiting effect of lead on these enzymes, cord blood and placental lead were also analyzed. After adjustment for potential confounders, including lead, placental boron levels were negatively significantly correlated to ALA-D activity while Ca-pump and Na(+)K(+)-ATPase activities did not seem to be affected by the level of boron exposure. Given boron's ability, as a Lewis acid, to complex with hydroxyl groups, we suggest that such a mechanism would explain the inhibiting effect of boron on ALA-D.     

Glutamate receptors communicate with Na+/K+-ATPase in rat cerebellum granule cells

Two glutamate receptor agonists, NMDA (N-methyl-d-aspartic acid) and ACPD (cis-(1S/3R)-1-aminocyclopentane-1,3-dicarboxylic acid), induce the reactive oxygen species (ROS) production in rat cerebellum granule cells, whereas the third one, 3-HPG (3-hydroxyphenylglycine), decreases this parameter. The simultaneous presence of 3-HPG, together with NMDA or ACPD, prevents the generation of ROS by neuronal cells. A similar effect of these ligands on Na⁺/K⁺-ATPase can be demonstrated: NMDA and ACPD inhibited the enzyme activity, but 3-HPG activated Na⁺/K⁺-ATPase and prevented its inhibition by NMDA or ACPD. In terms of current classification, NMDA is an agonist of ionotropic glutamate receptors of the so-called NMDA class, whereas ACPD and 3-HPG belong to metabotropic agonists, the former primarily being an activator of metabotropic glutamate receptors (mGluRs) of groups 2 and 3, and the latter, that of mGluRs of groups 1 and 5. Thus, the data presented illustrate the existence of diverse mechanisms of the cross talk between Na⁺/K⁺-ATPase and different glutamate receptors, as well as that between glutamate receptors of different classes.     

Microglial ecto-Ca(2+)-ATPase activity in a rat model of focal homologous blood clot embolic cerebral ischemia: an enzyme histochemical study

Post-ischemic changes in ecto-Ca(2+)-ATPase activity in microglia and the infarcted tissue were studied in a rat model of focal embolic cerebral ischemia using an enzyme histochemical method. Ecto-Ca(2+)-ATPase activity was observed in whole brains in non-operated and sham-operated control animals. In addition, this enzyme activity was determined to be localized in ramified microglia. At 30 min after ischemia, non-microglial ecto-Ca(2+)-ATPase activity in the infarcted tissue slightly decreased and continued to decrease thereafter. The ecto-Ca(2+)-ATPase activity in microglia did not appear changed at this time. The decrease of enzyme activity in the infarcted tissue made it much easier to clearly observe ecto-Ca(2+)-ATPase-positive microglia. The enzyme activity of microglia in the ischemic area began to decrease 2 or 4h after embolization and remarkably decreased, except in the perinuclear cytoplasm, apical parts of the processes, and several parts along the processes, 8h after ischemia. By 12h after onset of embolization, the enzyme activity of microglia and infarcted tissue had almost completely disappeared. Ecto-Ca(2+)-ATPase of microglia is likely to play an important role in the metabolism of extracellular nucleotides in the ischemic area immediately after the onset of embolization by means of ecto-enzymes. Thus, the findings of the present study suggest that microglia might serve to protect the infarcted tissue in the ischemic brain.     

糖尿病发病过程中大鼠主动脉血管平滑肌细胞钙泵活性以及血流动力学变化的研究

目的探讨糖尿病发病过程中大鼠主动脉平滑肌细胞钙泵活性变化与血流动力学变化之间的联系以及对糖尿病大血管病变产生和发展的影响。方法用链脲佐菌素(STZ)诱导糖尿病模型,第4、8、12、16周用彩色多普勒对各组主动脉进行血流参数测量。然后处死各组动物取其主动脉并分离得到肌浆网蛋白和胞膜蛋白,分别测定SERCA和PMCA的活性。结果4wk开始随着病程延长糖尿病组大鼠腹主动脉峰值血流速度、平均血流速度较对照组明显降低(P<0.05),而搏动指数和阻力指数则明显增高(P<0.05);12wk开始血管内径逐渐减小(P<0.05),16wk时内膜中膜厚度明显增加(P<0.05);PMCA的活性在早期(4wk)轻度增高,从12wk开始明显降低(P<0.05);SERCA活性在8wk起较对照组明显降低(P<0.05)。结论随着糖尿病病程逐渐延长,糖尿病大鼠主动脉血管结构发生改变,功能损坏;PMCA和SERCA活性改变导致的胞内钙离子调控紊乱参与了糖尿病大血管病变的发生和发展。