膀胱过度活动症的新进展

<正>排尿功能障碍最常见的临床表现之一:膀胱过度活动症(Overactive bladder,OAB);主要症状为尿频、尿急、尿失禁,常伴有夜尿[1]。包括不稳定膀胱及逼尿肌反射亢进,在神经性膀胱称为逼尿肌反射亢进,在非神经性膀胱则称为逼尿肌不稳定[2],其发病原因则是多方面的。目前OAB的病因尚不完全清楚,目前的研究提示与     

血浆肠肽和生长抑素含量变化的临床意义研究

血浆肠肽和生长抑素含量变化的临床意义研究山西省放射免疫中心（０３０００１）高桂珠，武玲梅山西医学院第二附属医院张辉，杨波本文测定了１２５例消化系统良、恶性疾病患者的血浆生长抑素（ＳＳＴ）和肠血管活性肽（ＶＩＰ），并与正常人进行了对比分析，现报道如下。...     

膀胱功能的非肾上腺素能非胆碱能(NANC)神经调节研究进展

膀胱功能为周期性储尿和排尿。储尿期 ,在达到最大膀胱容量以前膀胱内压较低并维持相对稳定 ,无逼尿肌收缩 ;排尿期 ,逼尿肌收缩 ,尿道内、外括约肌协调性松弛 ,排空膀胱。传统观念认为副交感 (胆碱能 )神经和交感 (肾上腺素能 )神经是调节膀胱尿道功能的主要神经 ,但近 10余年来 ,非肾上腺素能非胆碱能 (ｎｏｎａｄｒｅｎｅｒｇｉｃｎｏｎｃｈｏｌｉｎｅｒｇｉｃ,ＮＡＮＣ)神经的作用受到重视。1　血管活性肠肽 (ＶＩＰ)ＶＩＰ是 1970年在猪的小肠中纯化促胰液素时被首次分离出来的 ,4年后其氨基酸序列被确定 ,并被人工合成。ＩＶＰ是由2 8…     

实验性哮喘豚鼠血浆及肺组织血管活性肠肽含量的研究

目的:探讨非肾上腺素能非胆碱能阻抑神经与哮喘的关系。方法:采用放射免疫方法,测定实验性哮喘豚鼠血浆及肺组织血管活性肠肽的含量。结果:试验组血浆及肺组织血管活性肠肽含量较对照组显著降低。结论:血管活性肠肽含量的变化与哮喘的发作密切相关。     

神经原性膀胱患者B型超声的声像图特点及其诊断价值

神经原性膀胱患者Ｂ型超声的声像图特点及其诊断价值０５００８１中国人民解放军第４６７医院外科孙军，任红，常广，蔡发堂，王学民神经原性膀胱临床上常见为逼尿肌反射亢进和逼尿肌无反射两大类型，关于其Ｂ型超声声像特点国内外报告极少．以往用于明确该病诊断的检查，...     

鸡肠中血管活性肠肽的提取与测定

目的研究鸡肠不同部位血管活性肠肽的含量及其不同提取方法对血管活性肠肽含量的影响。方法分别取新鲜鸡的十二指肠、空肠、和回肠段,除去油脂及污物,用水冲洗干净,甩干水分,分别称取20.0g,采用不同方法提取,用酶联免疫吸附法测定血管活性肠肽的含量。结果鸡的十二指肠、空肠和回肠部位血管活性肠肽含量分别为25.53,25.01和23.27ng/g;热水提取含量较高,在酸性条件下加热容易破坏。结论鸡的全肠均含丰富的血管活性肠肽。     

血管活性肠肽在中枢神经系统疾患作用的研究

对３０例急性脑炎脑病患儿的血浆和脑脊液（ＣＳＦ）血管活性肠肽（ＶＩＰ）含量进行了放免测定，并对其中１１例ＣＳＦ ＶＩＰ进行了复查。结果表明，急性期血浆和脑脊液ＶＩＰ水平均明显高于对照组（Ｐ〈０．００１），随着病情好转ＣＳＦ ＶＩＰ仍在较高水平维持２￣３周。死亡患儿临终前ＣＳＦ ＶＩＰ水平多呈低值，提示ＶＩＰ水平可作为病情严重程度的参考指标。     

肠易激综合征患者血清血管活性肠肽,一氧化氮浓度变化及意义

目的：探讨血管活性肠肽（ＶＩＰ）和一氧化氮（ＮＯ）在肠易激综合征（ＩＢＳ）发病中的变化及意义，方法：分别采用酶标法和放射免疫分析法对３２例ＩＢＳ（便秘型１２型，腹泻型２０例）和１６例健康对照者血浆ＶＩＰ和ＮＯ浓度进行测定，观察正常时和不同类型的ＩＢＳ患者血ＶＩＰ和ＮＯ水平的变化。结果：ＩＢＳ组血ＮＯ水平较健康对照组显著增高（Ｐ〈０．０５），且以便秘型ＩＢＳ增调理我明显（Ｐ〈０．０１），ＶＩＰ水平在     

胃肠激素与肠易激综合征的相关性

目的：研究血管活性肠肽（VIP）,P物质（SP）和酷神经肽（NPY）在肠易激综合征（IBS）患者血浆和乙状结肠粘膜中的变化及临床意义。方法：用放射免疫法分别检测IBS患者（40例）和正常对照组（15例）血浆和乙状结肠粘膜中以上三种激素的含量。结果：IBS患者血浆和乙 状结肠粘膜中NPY含量明显低于对照组（P＜0．05）,而IP和SP在血浆中含量与正常对照组无显著差异（P＞0．015）,在乙状结肠粘膜中含量明显高于对照组（P＜0．01）,结论：P乙状结肠粘膜中三种胃肠激素的变化在IBS的腹痛,腹泻发病中有一定作用。     

补中益气丸对膀胱出口梗阻大鼠膀胱逼尿肌的影响

目的观察补中益气丸对膀胱出口梗阻大鼠离体膀胱逼尿肌收缩功能的影响。方法建立膀胱出口梗阻大鼠模型。给予高中低剂量的补中益气丸4周;制备离体膀胱逼尿肌标本,采用离体膀胱条张力实验观察药物对逼尿肌收缩功能的影响。结果模型组和小剂量组大鼠膀胱湿重明显大于假手术组（P＜0．05）,其他各组膀胱湿重与假手术组差异无统计学意义（P＞0．05）。与假手术组相比,模型组、小剂量组标本收缩反应明显减弱（P＜0．05或＜0．01）,Emax值增小,EC50值变大;与模型组相比,补中益气丸大、中剂量组逼尿肌收缩反应Emax值增大,EC50值变小（P＜0．05或＜0．01）,与假手术组比较差异无统计学意义（P＞0．05）。结论补中益气丸大中剂量组能明显改善膀胱出口梗阻大鼠膀胱逼尿肌收缩功能。     

肽能神经递质在犬脊髓损伤后神经源性膀胱中的表达及意义

目的 探讨犬不同脊髓平面损伤后神经源性膀胱时肽能神经递质血管活性肠肽(VIP)、P物质(SP)、降钙素相关基因肽( CGR P)在膀胱中表达的变化规律及意义.方法 健康成年雌性家犬14只,分为4组,应用脊髓横断的方法建立犬神经源性膀胱动物模型.A组,胸8～9平面横断脊髓;B组,腰1～2平面横断脊髓;C组,腰7骶1平面横...     

Antidipsogenic action of vasoactive intestinal peptide in the rat

The effect of vasoactive intestinal peptide (VIP) on the intake of water was studied in the rat. Intracerebroventricular administration of vasoactive intestinal peptide strongly inhibited drinking in rats deprived of water, but peripheral administration had no effect, indicating that the site of action was central. Drinking induced by angiotensin II was also markedly blocked by simultaneous administration of vasoactive intestinal peptide. The results indicate that in the rat, vasoactive intestinal peptide may play a role in the control of intake of water as a neuropeptide thirst inhibitor.     

盐酸戊乙奎醚对小鼠血浆血管活性肠肽的影响

目的观察盐酸戊乙奎醚对小鼠胃肠动力及血浆血管活性肠肽的影响。方法健康昆明小鼠30只,体重18～24g,雌雄不限,随机分为对照组、阿托品组和盐酸戊乙奎醚组,每组10只。阿托品组腹腔注射阿托品0.3mg/kg,盐酸戊乙奎醚组腹腔注射盐酸戊乙奎醚0.3mg/kg,对照组给予等容量0.9%氯化钠溶液。3组给药15min后以营养性半固体糊0.8ml/只灌胃,30min后处死小鼠,采用放免法测定血管活性肠肽水平,计算胃内残留率。结果与对照组比较,阿托品组血管活性肠肽水平升高(P<0.05),盐酸戊乙奎醚组血管活性肠肽水平差异无统计学意义(P>0.05);与阿托品组比较,盐酸戊乙奎醚组血管活性肠肽水平下降(P<0.05)。与对照组比较,阿托品组胃内残留率升高,盐酸戊乙奎醚组胃内残留率差异无统计学意义(P>0.05);与阿托品组比较,盐酸戊乙奎醚组胃内残留率降低(P<0.05)。结论与阿托品比较,盐酸戊乙奎醚不抑制胃肠运动,其对血管活性肠肽的分泌无影响。     

Elcatonin Raises Levels of Vasoactive Intestinal Peptide in Human Plasma

Elcatonin, used for treatment of hypercalcaemia, Paget's disease and osteoporosis, causes flushing of the face and hands. To determine whether this was because of increased levels of vasoactive intestinal peptide, which is known to induce vasodilation, the effect of elcatonin on the plasma levels of vasoactive intestinal peptide was studied in five healthy volunteers. After a single intramuscular administration of elcatonin (20 int. units), peak plasma elcatonin levels (approx. 30 pg mL^?1) were achieved 30 min after injection. Plasma vasoactive intestinal peptide concentrations rose similarly with peak levels of about 17 pg mL^?1 after 30 min. Side-effects such as cutaneous flushing (most obvious in the face and hands) occurred to an extent dependent on the amount of elcatonin administered, and declined over 45 min in parallel with the fate of plasma vasoactive intestinal peptide. The side-effects of elcatonin, especially cutaneous flushing, seem to be closely connected with vasoactive intestinal peptide.     

The role of cyclic AMP in the inhibition of leukotriene biosynthesis by neuropeptides

Certain neuropeptides, including vasoactive intestinal peptide, inhibit peptidoleukotriene release from platelet activating factor-stimulated rat lung. We have now shown that vasoactive intestinal peptide will also inhibit peptidoleukotriene release from platelet activating factor-stimulated or ovalbumin-challenged guinea pig lung, but not from calcium ionophore-stimulated rat or guinea pig lung. In rat lung a pre-incubation with the peptide prior to addition of platelet activating factor was required for the effect to be maximal. When vasoactive intestinal peptide was substituted with cyclic AMP, the inhibitory effect was reproduced. In addition, pre-incubation with MDL 12330A, an inhibitor of adenylate cyclase, reduced the inhibitory effect of vasoactive intestinal peptide on platelet activating factor-stimulated leukotriene C4 biosynthesis. We suggest that the inhibition of platelet activating factor-stimulated peptidoleukotriene release in rat lung by vasoactive intestinal peptide involves the events prior to phospholipase A2 activation and requires cyclic AMP as a mediator.     

Inhibition of intestinal secretion without reduction of cyclic AMP levels

Net water transport by the jejunum of anaesthetized rats was measured together with jejunal cyclic AMP content. Vasoactive intestinal peptide stimulated secretion and elevated the cyclic AMP level. Morphine (10 mg/kg s.c.) inhibited the stimulated secretion but failed to depress the cyclic AMP accumulation. It is suggested that cyclic AMP may not be the mediator of intestinal fluid secretion. Alternatively, morphine may block the secretory effect of cyclic AMP elevated by vasoactive intestinal peptide.     

Impairment by lovastatin of neural relaxation of the rabbit sphincter of Oddi.

We sought whether inhibition of cholesterol biosynthesis by lovastatin influenced the nitrergic relaxation response of the sphincter of Oddi. Rabbit sphincters of Oddi rings were tested for changes in isometric tension in response to field stimulation in the presence of 4 microM guanethidine and 1 microM atropine. Tissue samples were then analyzed for cAMP and cGMP content by radioimmunoassay for nitric oxide concentration by electron spin resonance and for vasoactive intestinal peptide and calcitonin gene-related peptide (CGRP) release by radioimmunoassay. Membrane G(salpha) protein was determined by Western blot analysis. Field stimulation relaxed the preparations with an increase in nitric oxide, cAMP and cGMP concentrations at increased calcitonin gene-related peptide and vasoactive intestinal polypeptide (VIP) release. Preparations from rabbits pre-treated with lovastatin (5 mg/kg/day intragastrically, over 5 days) contracted under the same conditions with an attenuated cGMP-increase at preserved increase in NO content and neuropeptide release. The relaxation was recaptured combining lovastatin with farnesol (1 mg/kg intravenously, twice a day for 5 days). The field stimulation-induced increase in cyclic nucleotides was also restored. Lovastatin decreased membrane G(salpha) protein content, which was re-normalized by farnesol. Farnesol treatment reinstates neurogenic relaxation of the sphincter of Oddi deteriorated by lovastatin possibly by normalizing G-protein coupling.     

Effects of vasoactive intestinal peptide on transmission from excitatory and inhibitory nerves to smooth muscle cells in chicken rectum

The effects of vasoactive intestinal peptide on electrical membrane properties and neuromuscular transmission, which is resistant to atropine and guanethidine, were investigated in isolated circular muscle strips from chicken rectum. Intracellular microelectrodes were used to record changes in membrane potential. Vasoactive intestinal peptide (0.2-1.0 microM) hyperpolarized the membrane of cells of the muscle strip. The mean maximal hyperpolarization produced by 1 microM vasoactive intestinal peptide was 5.3 +/- 0.4 mV. Electrotonic potentials were unchanged in amplitude and the slopes of the current-voltage curves were similar before and after application of the peptide, indicating no change in membrane resistance in the presence of the peptide. The hyperpolarizing effect was preserved in the presence of apamin. These properties of the peptide-induced hyperpolarization were shared by the inhibitory junction potential. In addition, vasoactive intestinal peptide (0.5 or 1.0 microM) markedly inhibited or abolished the inhibitory junction potential but had little effect on the excitatory junction potential. The present results suggest a possible physiological implication of this peptide as a neurotransmitter of the inhibitory neurone in chicken rectum.     

Use of immunoblockade to study the involvement of peptidergic afferent nerves in the intestinal vasodilatory response to capsaicin in the dog

Capsaicin evokes intestinal vasodilatation when given by close arterial injection probably by acting on primary sensory neurons. Several peptides known to occur in primary afferents also have vasodilator effects. We have used immunoblockade to test the hypothesis that the vasodilator effect of capsaicin was mediated by release of these peptides. Antisera to substance P, cholecystokinin, vasoactive intestinal peptide and somatostatin inhibited specifically and dose dependently the effect of each of these peptides given alone. Graded doses of the antisera to substance P, cholecystokinin and vasoactive intestinal peptide also produced a dose dependent inhibition of the vasodilator response to capsaicin. In contrast, administration of somatostatin antiserum enhanced the vasodilator action of capsaicin. Prior administration of antibodies to substance P, cholecystokinin and vasoactive intestinal peptide produced an 80% inhibition of the response to capsaicin. In the presence of these antibodies, and of atropine, the response to capsaicin was reduced by more than 90%. The results suggest that capsaicin increases mesenteric blood flow due to release of substance P, cholecystokinin and vasoactive intestinal peptide. The precise cellular origins of these peptides is unknown, but they may well be released from the peripheral endings of primary afferent neurons.