糖皮质激素在孤束核内对去甲肾上腺素/神经肽Y引起的心血管效应的影响及其机制

本研究观察了糖皮质激素自身在孤束核（ＮＴＳ）内的心血管效应,以及它在ＮＴＳ内对ＮＡＮＰＹ诱导的心血管活动变化的影响及机制。结果发现,大剂量地塞米松（Ｄｅｘ）在大鼠ＮＴＳ内能很快导致血压下降,血清中ＮＯ浓度升高。小剂量Ｄｅｘ在ＮＴＳ内能很快抑制ＮＡＮＰＹ在ＮＴＳ内诱导的心血管效应,并维持较长时间。表明Ｄｅｘ对ＮＡＮＰＹ在ＮＴＳ诱导的心血管效应的抑制作用可能有基因和非基因两种途径参与。进一步分析它的非基因机制发现这种快速抑制作用与胞内糖皮质激素受体无关,而是通过兴奋ＧＡＢＡＡ受体,降低减压反射;或者降低α２受体的敏感性,抑制ＮＯ的形成;或者直接作用于细胞膜上的离子通道以影响它们对ＮＡＮＰＹ的反应;从而抑制ＮＡＮＰＹ在ＮＴＳ内诱导的降压和心率减慢的效应     

地塞米松、去甲肾上腺素及神经肽Y对急性分离的孤束核神经元延时外向钾电流的影响

孤束核（ＮＴＳ）是中枢心血管活动调节的第一个重要中继站，去甲肾上腺素（ＮＡ）及神经肽Ｙ（ＮＰＹ）在ＮＴＳ内对心血管活动具有重要的调节作用。我们的前期工作发现地塞米松（Ｄｅｘ）可通过非基因调控途径快速消除ＮＡ／ＮＰＹ在ＮＴＳ引起的心血管效应。这种作用是...     

地塞米松对大鼠孤束核压力感受性神经元微电泳NA/NPY所致反应的影响

实验采用多管微电泳记录神经元胞外放电技术,观察地塞米松（Ｄｅｘ）、去甲肾上腺素（ＮＡ）及神经肽Ｙ（ＮＰＹ）对孤束核（ＮＴＳ）压力感受反射性神经元的作用,以及将这些神经元用Ｄｅｘ预处理后对ＮＡ／ＮＰＹ反应的变化。向ＮＴＳ内３８个压力感受神经元微电泳Ｄｅｘ后,压力感受兴奋性神经元主要表现为抑制（８／１９）,压力感受抑制性神经元则主要表现为兴奋（９／１９）。而电泳ＮＡ或ＮＰＹ,压力感受兴奋性神经性元以兴     

一氧化氮对去甲肾上腺素在大鼠孤束核内引起的心血管效应的影响

一氧化氮(ＮＯ)是Ｌ精氨酸(ＬＡｒｇ)在Ｎｏ合酶作用下的合成产物。许多资料表明,Ｎｏ在孤束核(ＮＴＳ)内参与心血管活动的调节;ＮＴＳ在心血管活动调节中具有重要作用。ＮＴＳ内注射去甲肾上腺素(ＮＡ)产生由α2肾上腺素能受体介导的降压效应。硝酸甘油(ＮＯ供体)在ＮＴＳ后也能产生类似作用,用α2受体拮抗剂预处理可消除该药在ＮＴＳ内引起的降压效应。由此推测ＮＯ与ＮＡ两系统在ＮＴＳ的心血管活动调节中可能存在相互作用。为此我们观察了ＬＡｒｇ和Ｎω硝基Ｌ精氨酸(ＬＮＮＡ,ＮＯ合酶的抑制剂)对ＮＡ在ＮＴＳ引起的心血管效应的影响,…     

神经肽Y和去甲肾上腺素在杏仁内侧核内影响血压和心率中的相互作用

分别向杏仁内侧核（ＭＡＮ）内微量注射去甲肾上腺素（ＮＡ）或神经肽Ｙ（ＮＰＹ）。ＮＡ引起血压升高,心率加快;而ＮＰＹ引起血压降低,心率减慢。如果注入不能改变血压的小剂量ＮＰＹ,则可抑制ＮＡ引起的升压作用,反映ＮＰＹ与ＮＡ共同参与心血管活动的中枢性调节过程。向ＭＡＮ中注射ＮＰＹ后血中ＮＡ的含量也相应降低,表明在ＭＡＮ中注射ＮＰＹ引起的血压、心率反应是通过降低血浆中ＮＡ含量而实现的。     

神经肽Y和去甲肾上腺素在杏仁内侧核内影响血压和心率中…

分别向杏仁内侧核（ＭＡＮ）内微量注射去甲肾上腺素（ＮＡ）或神经肽Ｙ（ＮＰＹ）。ＮＡ引起血压长高,心率加快;而ＮＰＹ引起血压降低,心率减慢。如果注入不能改变血压的小剂量ＮＰＹ,则可抑制ＮＡ引起的升压作用,反映ＮＰＹ与ＮＡ共同参与心血管活动的中枢性调节过程。向ＭＡＮ中注射ＮＰＹ后血中ＮＡ的含量也相应降低,表明在ＭＡＮ中注射ＮＰＹ引起的血压、心率反应是通过降低血浆中ＮＡ含量而实现的。     

地塞米松、噻庚啶和山莨菪碱对LPS诱导大鼠肝脏TNFα表达的影响

地塞米松（Ｄｅｘ）、噻庚啶（Ｃｙｐ） 和山莨菪碱（Ａｎｉ） 对脂多糖（ＬＰＳ） 诱导的大鼠肝脏ＴＮＦα表达的影响。Ｗｉｓｔａｒ大鼠４０ 只, 静脉注射ＬＰＳ（ＥｃｏｌｉＯ１１１Ｂ４ ５ｍ ｇ／ｋｇ） 后, 立即静脉给予Ｄｅｘ ５ｍ ｇ／ｋｇ、Ｃｙｐ５ｍ ｇ／ｋｇ 或Ａｍ ｉ１０ｍ ｇ／ｋｇ,于ＬＰＳ攻击后２ｈ 取动物的肝脏,ＡＰＡＡＰ法进行ＴＮＦα免疫组织化学研究,Ｎｏｒｔｈ－ｅｒｎ 杂交分析ＴＮＦαｍ ＲＮＡ 表达水平。结果发现ＬＰＳ攻击后２ｈ, 肝脏ＴＮＦαｍ ＲＮＡ 表达水平显著增高, 肝脏枯否氏细胞胞浆内有大量的ＴＮＦα红染颗粒。Ｄｅｘ、Ｃｙｐ 或Ａｎｉ均能显著降低大鼠肝脏ＴＮＦαｍ ＲＮＡ 水平和ＴＮＦα含量。结果表明Ｄｅｘ、Ｃｙｐ 和Ａｎｉ均显著抑制ＬＰＳ诱导的ＴＮＦα基因表达, 可能有抗感染性休克作用。     

披针叶胡颓子果实营养成分的测定

披针叶胡颓子果实营养成分的测定毛学文（天水师范高等专科学校,天水７４１０００）ＤＥＴＥＲＭＩＮＡＴＩＯＮＯＦＮＵＴＲＩＥＮＴＣＯＮＳＴＩＴＵＥＮＴＳＩＮＳＥＥＤＳＯＦＥＬＡＥＡＧＮＵＳＬＡＮＣＥＯＬＡＴＡＭａｏＸｕｅ－ｗｅｎ（ＴｉａｎＳｈｕｉＴｅａｃ...     

地塞米松诱导红系细胞凋亡的观察(英文)

正常机体内,红细胞生成素（ＥＰＯ）诱导红系细胞分化,并阻止其凋亡,使其维持机体所需足够的数量。本文采用诱发贫血病毒（ＦＶＡ）诱导ＢＡＬＢ／ｃ小鼠脾细胞所形成的红细胞为实验系统,研究了外界因子？？地塞米松（Ｄｅｘ）对ＥＰＯ作用的影响。取６８周雌性ＢＡＬＢ／ｃ小鼠,尾部静脉注射含ＦＶＡ的小鼠血清。１５天后,断颈处死。取脾于ＩＭＤＭ中漂洗、剪碎、过滤、离心、制成单细胞悬液,在ＥＰＯ存在下,于平皿中培养至不同的时期后,进行不同浓度、不同时间的Ｄｅｘ处理。取细胞进行：（１）台盼蓝染色计数死细胞数;（２）观察ＤＮＡ电泳图谱;（３）电镜检察细胞学变化。Ｆｉｇ．１表明：随着Ｄｅｘ处理浓度和时间的增加,细胞死亡率也增加。Ｆｉｇ．２表明：１０－４浓度Ｄｅｘ处理,即可使早（１２ｈ）、中（２４ｈ）幼期红细胞凋亡,ＤＮＡ断裂成多聚核小体,产生明显ＤＮＡ梯形带。Ｆｉｇ．３表明：高浓度Ｄｅｘ可以使早幼期红细胞凋亡。电镜观察表明：与对照（Ｆｉｇ．４）比较,Ｄｅｘ处理后,细胞核固缩,染色质沿核膜内面周边凝聚,核周间隙扩张,胞质内出现空泡（Ｆｉｇ．５）;随后细胞破碎,出现大量凋亡小体（Ｆｉｇ．６）。Ｄｅｘ拮抗ＥＰＯ,诱导红系细胞凋亡的现象此     

种子萌发和幼苗生长的抗逆能力与乙烯产生及组织对乙烯敏感性的变化

种子萌发和幼苗生长的抗逆能力与乙烯产生及组织对乙烯敏感性的变化黄学林（中山大学生物学系,广州５１０２７５）ＳＥＥＤＧＥＲＭＩＮＡＴＩＯＮ,ＳＥＥＤＬＩＮＧＧＮＯＷＴＨＡＮＤＥＴＨＹＬＥＮＥＰＲＯＤＵＥＴＩＯＮＯＦＰＬＡＮＴＳＡＮＤＴＨＥＩＲＳＥＮＳＩ...     

Y2 receptors for neuropeptide Y in the nucleus of the solitary tract mediate depressor responses.

In anesthetized, spontaneously breathing rats, microinjections of selective agonists of neuropeptide Y (NPY) receptor subtypes were made into the medial region of the caudal nucleus of the solitary tract (NTS) at the level of the area postrema. This region of the rat NTS exhibits very high densities of NPY binding sites. Microinjections of the long C-terminal NPY fragment, NPY(13-36), a selective agonist at Y2 receptors, into the caudal NTS elicited pronounced, dose-related reductions in blood pressure and respiratory minute volume. Moreover, the specific pattern of cardiorespiratory responses elicited by NPY(13-36) was remarkably similar, over approximately the same dosage range, with the cardiorespiratory response pattern elicited by intact NPY. In contrast to the potent NTS-mediated responses evoked by NPY(13-36), similar microinjections conducted with either NPY(26-36), an inactive C-terminal NPY fragment, or [Leu31,Pro34]NPY, a NPY analog with specific agonist properties at Y1 receptors, into the same caudal NTS sites did not appreciably affect cardiorespiratory parameters even at 10-20-fold higher dosages. The present results with selective agonists for NPY receptor subtypes suggest that the depressor responses and reductions in minute volume elicited by microinjections of intact NPY and NPY(13-36) were mediated by Y2 receptors in the caudal NTS, likely distributed at presynaptic sites in the medial region of the subpostremal NTS.     

Nitric oxide mediates depressor responses by activation of N-methyl-D-aspartate receptors in the nucleus tractus solitarius of cat

Nitric oxide (NO) is involved in cardiovascular regulation and sympathetic nerve activity of the central nervous system (CNS). The nucleus tractus solitarius (NTS) is important to cardiovascular regulation. However, the physiological role of NO in cardiovascular regulation effecting through the NTS remains unclear. The purpose of this study is to investigate the effect of NO measured by in vivo voltammetry on the cardiovascular responses in NTS induced by N-methyl-D-aspartate (NMDA) in anesthetized cats. Extracellular NO concentration was monitored through a Nafion- and porphyrin-coated carbon fiber electrode, which has previously been demonstrated sensitive and selective to NO responses. Microinjection of NMDA into NTS elicited a dose-dependent decrease in cardiovascular responses associated with NO release. Following the dose-response curve, a dose of 3 nmol of NMDA was selected. Microinjection of NMDA into NTS produced depressor responses and NO release. These responses in NTS to NMDA were attenuated by pretreatment with a competitive antagonist, 2-amino-5-phosphonopentanoat (AP-5, 1 nmol), and methylene blue (MB, 1 nmol), an inhibitor of guanylate cyclase. These results suggest that NO is formed from NMDA activation in NTS and that NO diffuses out of neurons into the nearby target neurons to produce depressor response and NO release through cyclic guanosine monophosphate (cGMP) formation. In conclusion, NO mediates depressor response consequent to activation of NMDA receptors in neurons of NTS.     

Cardiovascular effects of neuropeptide Y in the nucleus tractus solitarius of rats: relationship with noradrenaline and vasopressin

The central haemodynamic effects of neuropeptide Y (NPY), both alone and together with either noradrenaline (NA) or vasopressin (AVP), have been investigated by microinjecting synthetic peptide into the nucleus tractus solitarius (NTS) of anaesthetized rats. NPY alone elicited dose-dependent changes in blood pressure (BP) and heart rate (HR); 470 fmol inducing a pressor response, and 4.7 pmol a fall in BP. The hypotensive response to 20 nmol NA was significantly modified by both simultaneous and prior injection of an ineffective dose (47 fmol) of NPY. Prior injection of a similar dose of NPY also modified the NTS pressor effect of 10 ng AVP. A relationship between the action of AVP and NPY in the NTS was further indicated by the finding that prior injection of an ineffective dose of AVP (1 ng) reduced the hypotensive response to 4.7 pmol NPY, and by the demonstration of contrasting effects of 4.7 pmol NPY in AVP-deficient Brattleboro rats compared to parent strain LE rats. These results, taken together with the recent localization of NPY-like immunoreactivity in the NTS, suggest a role for NPY in central cardiovascular control. In addition, NPY has been shown to exhibit functional interactions with both an amine neurotransmitter and a neuropeptide present in the NTS of rats.     

Neuropeptide Y modulation of interleukin-1{beta} (IL-1{beta})-induced nitric oxide production in microglia

Given the modulatory role of neuropeptide Y (NPY) in the immune system, we investigated the effect of NPY on the production of NO and IL-1β in microglia. Upon LPS stimulation, NPY treatment inhibited NO production as well as the expression of inducible nitric-oxide synthase (iNOS). Pharmacological studies with a selective Y(1) receptor agonist and selective antagonists for Y(1), Y(2), and Y(5) receptors demonstrated that inhibition of NO production and iNOS expression was mediated exclusively through Y(1) receptor activation. Microglial cells stimulated with LPS and ATP responded with a massive release of IL-1β, as measured by ELISA. NPY inhibited this effect, suggesting that it can strongly impair the release of IL-1β. Furthermore, we observed that IL-1β stimulation induced NO production and that the use of a selective IL-1 receptor antagonist prevented NO production upon LPS stimulation. Moreover, NPY acting through Y(1) receptor inhibited LPS-stimulated release of IL-1β, inhibiting NO synthesis. IL-1β activation of NF-κB was inhibited by NPY treatment, as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-κB p65 subunit, leading to the decrease of NO synthesis. Our results showed that upon LPS challenge, microglial cells release IL-1β, promoting the production of NO through a NF-κB-dependent pathway. Also, NPY was able to strongly inhibit NO synthesis through Y(1) receptor activation, which prevents IL-1β release and thus inhibits nuclear translocation of NF-κB. The role of NPY in key inflammatory events may contribute to unravel novel gateways to modulate inflammation associated with brain pathology.     

Effect of glucocorticoids on the development of suppressive activity in human lymphocyte response to a polysaccharide purified from Candida albicans

The action of glucocorticoids on the proliferative response of human lymphocytes stimulated in vitro by MPPS has been investigated. The effect of Dex was dependent on the time of steroid addition to the cultures. Dex added at the beginning of the culture period inhibited, cell proliferation and IL 1/IL 2 synthesis, although not completely. However, a delayed addition of 24 to 48 hr resulted in an enhancing effect on cell proliferative responses that was maximal at day 4. The effect of Dex on T suppressor cell activity was then investigated. Dex added 1 day before the appearance of suppressor cells resulted in a marked decrease or disappearance of the suppressive activity. Moreover, primed T lymphocytes treated with Dex in the presence of exogenous IL 2 enhanced the proliferative responses of fresh autologous PBMC stimulated by MPPS. Taken together, our data suggest that glucocorticoids inhibit the differentiation of T suppressor cells and that IL 2 is unable to reverse this inhibitory effect.     

Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo

Nitric oxide (NO) in the nucleus tractus solitarii (NTS) plays an important role in regulating sympathetic nerve activity. The aims of this study were to determine whether the activation of N-methyl-D-aspartate (NMDA) receptors in the NTS facilitates the release of L-glutamate (Glu) via NO production, and, if so, to determine whether this mechanism is involved in the depressor and bradycardic responses evoked by NMDA. We measured the production of NO in the NTS as NO2- and NO3- (NO(x)) or Glu levels by in vivo microdialysis before, during, and after infusion of NMDA in anesthetized rats. We also examined effects of N(omega)-nitro-L-arginine methyl ester (L-NAME) on the changes in these levels. NMDA elicited depressor and bradycardic responses and increased the levels of NO(x) and Glu. L-NAME abolished the increases in the levels of NO(x) and Glu and attenuated cardiovascular responses evoked by NMDA. These results suggest that NMDA receptor activation in the NTS induces Glu release through NO synthesis and that Glu released via NO enhances depressor and bradycardic responses.     

Role of alpha adrenoceptors and nitric oxide on cardiovascular responses in acute and chronic hypertension

The contribution of α-adrenoceptors and nitric oxide (NO) on the alterations of sympathetically mediated cardiovascular responses after acute (AcH) and chronic (ChH) hypertension was evaluated in pithed aortic coarcted hypertensive rats. Pressor and tachycardia response produced by electrical stimulation of preganglionic sympathetic fibers or exogenous noradrenaline (NA) were recorded in the absence and presence of prazosin (α₁-antagonist), rauwolscine (α₂-antagonist), or N ^G-nitro-l-arginine methyl ester (l-NAME; an inhibitor of NO synthase). Compared with age-matched sham-operated rats (Nt), the pressor response produced by electrical stimulation or NA was smaller in AcH rats and larger in ChH rats. Prazosin caused a decrease of pressor response elicited by electrical stimulation or NA in all groups. However, this effect was higher in ChH. Rauwolscine produced a similar increase of sympathetically mediated pressor response in Nt and AcH rats. Nevertheless, this antagonist did not affect the sympathetically mediated pressor response in ChH rats. In addition, rauwolscine did not affect the NA-induced pressor response in all groups. The pressor response elicited by l-NAME was larger in all groups compared without l-NAME and in presence of l-arginine. Moreover, l-NAME in the presence of NA increased sympathetically mediated pressor response is in all groups, compared without it or in the presence of l-arginine. Compared with Nt, basally produced NO in aortic rings was increased in AcH but decreased in ChH. Collectively, our data suggest that decreased cardiovascular reactivity in AcH is due to an increase in basally produced NO. In ChH, enhanced cardiovascular response appears to be associated with a decrease in produced NO and an increase in released NA from sympathetic nerves.     

颈动脉注射辣椒素对脑干心血管相关核团一氧化氮合酶和Fos表达的影响

实验采用NADPH－d组化技术和Fos蛋白免疫组化技术相结合的方法,观察了颈动脉注射辣椒不时,大鼠脑干心血管相关核团内NOS和Fos蛋白的分布以及两者的共存关系。结果显示：（1）颈动脉注射辣椒不可诱发脑干中最后区（AP）、孤束核（NTS）、巨细胞旁外侧核（PGL）和蓝斑（LC）等多个部位Fos样免疫反应（FLI)神经元显著增加 中脑中央灰质（PAG）和中缝核群（RN）的FLI神经元无明显改变。（2）PGL和NTS内NO合成神经元以及PGL内双标神经元数量也明显增加,而AG和RN中NO合成神经元无明显变化,在LC和AP仅偶见或未见NO合成神经元。（3）预先应用辣椒素受体阻断剂钌红或NMDA受体阻断剂MK－801,则明显减弱辣椒素的上述效应,以上结果表明,颈动脉注射辣椒素可兴奋脑干心血管活动相关核团神经元,NO在脑干核团对辣椒素的反应中发挥间接的调制作用,辣椒素的效应由香草酸受体（辣椒素受体）介导并有谷氨酸参与。