口服色苷酸钠治疗应激性肠综合征对101名腹泻型患者的研究

口服色苷酸钠(DSCG)治疗食物引起的全身不良反应曾有不少报道,但DSCG对胃肠道症状的作用研究较少。应激性肠综合     

利多卡因后处理对急性心肌缺血再灌注大鼠感觉神经肽P物质水平的影响

目的通过观察利多卡因后处理对急性心肌缺血再灌注大鼠感觉神经肽P物质(SP)水平的影响,探讨利多卡因对缺血再灌注心肌保护作用的可能机制。方法健康成年雄性SD大鼠24只,采用随机数字表法分为3组,假手术组、缺血再灌注组和利多卡因后处理组(每组8只)。采用酶联免疫吸附试验(ELISA)的方法观察心肌组织和血中SP的表达水平。结果心肌组织中利多卡因后处理组表达SP水平较缺血再灌注组及假手术组均明显增加(P=0.013、P=0.000);与缺血再灌注组和假手术组比较,利多卡因后处理组术后血中SP浓度较术前明显增加(P=0.000)。结论利多卡因后处理可诱发心肌组织和血中表达SP增加,提示利多卡因通过上调心肌感觉神经肽水平发挥保护缺血再灌注损伤心肌的作用。     

1,3-双(2-羧基色酮-7氧基)2-羟基丙烷二钠盐(78012)的简易合成方法

78012(本研究编号)是色甘酸钠(disodium cromoglycate,简称DSCG)的一个异构体,其结构为1,3-双(2-羧基色酮-7-氧基)2-羟基丙烷二钠盐(Ⅳ)。1972年Cairns等报道此化合物对被动皮肤过敏(PCA)实验有保护作用,吴若鉥等进一步将它与DSCG的抗过敏作用进行了比较,其作用强度相似,目前临床试用于过敏性鼻炎,过敏性哮喘等疾病,初步观察,具有一定的疗效。     

2013-2017 年我院化脓性链球菌儿童株耐药模式及其感染特点分析

目的 了解化脓性链球菌(Streptococcus pyogenes, SP) 在儿童中的致病谱及其耐药特点。方法 回顾性分析我院 2013-2017 年细菌培养为SP 的患儿的临床特点。结果 分离到SP 的患儿514 例，其中6 例同时在咽拭子和阴道分泌物中培养 出SP。407 株(79.2%) 来自阴道分泌物，91 株(17.7%) 来自呼吸道标本，无菌标本10 株(1.9%)，其他标本12 株(2.3%)。患儿年龄 (7.02±2.26) 岁。侵袭性感染10 例。所有菌株对青霉素、头孢曲松和万古霉素敏感，青霉素MIC50和MIC90分别为0.023 和0.048μg/ mL；98.4% 的菌株对左氧氟沙星敏感，对红霉素、克林霉素耐药率分别为94.6% 和93%。2 例化脓性脑膜炎患儿发生脑梗塞、 脑瘫后遗症。结论 SP 主要引起儿童呼吸道和外阴阴道感染，青霉素和头孢曲松可作为该菌感染的首选用药，局部使用左氧氟 沙星可作为SP 外阴阴道炎的基础治疗。     

呼吸道定植菌对人类偏肺病毒感染患儿喘息的影响

目的探讨呼吸道定植菌对人类偏肺病毒(hMPV)感染患儿喘息的影响。方法收集531例hMPV感染患儿鼻咽分泌物,RT-PCR检测hMPV,普通痰培养法检测细菌,观察肺炎链球菌(SP)、流感嗜血杆菌(HI)、卡他莫拉菌(MC)和金黄色葡萄球菌(SA)定植情况。分析四种定植菌与hMPV感染患儿临床表现的关系。结果 hMPV感染患儿中,SP、HI、MC和SA定植主要见于3岁以下患儿,无明显性别差异。定植菌阳性组喘息发生率高于定植菌阴性组(73.6%vs.49.1%)(P<0.05)。细菌(主要是SP、HI和MC)定植与hMPV感染患儿喘息症状相关(OR=3.27,P<0.01)。结论鼻咽部定植菌,尤其是SP、HI、MC,对hMPV感染患儿的喘息症状有重要影响。     

老年慢性阻塞性肺疾病并发自发性气胸23例临床分析

目的:探讨23例老年慢性阻塞性肺疾病(COPD)并发自发性气胸(SP)的临床特点。方法:对2000年—2010年住院治疗的23例老年COPD并发SP患者(老年组)与同期16例非老年COPD并发SP患者(非老年组)的临床资料进行回顾性分析和比较。结果:老年组诱发因素以近期呼吸道感染为首位,临床表现为基础疾病多、体征不明显、病情较重、误诊率高、治疗时间长、死亡率高;非老年组诱发因素以剧烈咳嗽为首位,临床表现为发病急、基础疾病少、治疗时间相对较短。结论:老年性COPD并发SP与非老年性COPD并发SP在临床上有很大差别,临床医生要掌握老年COPD并发SP的临床特点,以免延误治疗。     

几个有关哮喘治疗的问题

我补充谈几个有关哮喘治疗的问题: 一、肥大细胞膜稳定剂肥大细胞膜稳定剂应算是一类病因治疗性药物,色甘酸二纳(DSCG)是这类药物中最早问世的品种,通常需以其干粉或2%水悬液喷雾吸入。我省金坛县制药厂生产的敏喘宁(丙氧苯氮嘌呤酮、M&B22948)作用强于DSCG,且口服可以取效,甚为方便。国外尚有硫蒽四唑(Doxantra-zole)和噻哌酮(甲哌噻庚酮、Ketotifen)等口服药品,特别是噻哌酮颇受重视,它的作用比DSCG和敏喘宁都强得多,成人剂量1～2mg/日”它不仅能稳定肥大细胞、抑制介质释放和抑制磷酸二酯酶的活性,兼能降低支气管的高反应性,直接拮抗组胺和慢反应物质促使支气管平滑肌收缩的效应,据报导总有效率达85%(其中显效率65%)。它对运动性哮喘、药物性     

促进离子化水溶性药物的透皮吸收

本文用硫氮(艹卓)酮(DIL)和色甘酸二钠(DSCG)作为阳离子和阴离子水溶性模型药物,研究促进离子化水溶性药物透皮吸收方法。膜制备方法A:将DIL 0.6g溶解于80％乙醇40ml中,再加入羧乙烯聚合物(CVP)0.6g,羟丙基纤维素(HPL-H)0.6g和各种附加剂0.1g,匀化后涂膜,经45～55℃干燥约15小时,制成膜厚50～60μm,面积7.0×7.0cm~2,內含DIL90～100mg。以同样方法制得每张含70～80mg DSCG的膜。     

展枝马尾藻硫酸多糖对呼吸道合胞病毒的抗病毒活性及其机理研究

目的研究从褐藻展枝马尾藻Sargassumpatens中分离到的一种硫酸多糖SP2的抗病毒活性及抗病毒作用机理。方法通过细胞致病效应实验、MTT测定和空斑形成抑制实验对该多糖的抗病毒活性、细胞毒性和可能的抗病毒机理进行测定。结果通过空斑形成抑制实验测定结果显示,该多糖对呼吸道合胞病毒有好的抗病毒活性,其EC50值为1.1但没有抗流感病毒A和B、副流感病毒的活性。多糖的CC50高达3000μg.mL-1。其对呼吸道合胞病毒的抗病毒选择性指数被估计大于2727。用SP2预处理宿主细胞,不显示任何对病毒感染的保护作用。SP2对呼吸道合胞病毒有一定的杀病毒活性,其EC50值超过100μg.mL-1。时间加入实验证明,只有在37℃呼吸道合胞病毒吸附时期加入SP2才能完全抑制病毒的复制。结论SP2可能是一种有潜力的抗呼吸道合胞病毒感染的多糖。其对呼吸道合胞病毒的抗病毒作用机制与抑制病毒的吸附有关。     

抗过敏药Pemirolast Potassium

异名 Alegysal 化学名 9-甲基-3-(1H-四唑-5-基)-4H-吡啶并[1,2-a]嘧啶-4-酮钾盐药效分类抗过敏药开发单位 (美)勃列斯多·迈耶公司上市厂商 (日)东京田边药厂于1991年上市 1967年Altounyan率先开发了一种肥大细胞脱颗粒抑制剂即色甘酸钠(DSCG)作为抗变态反应药,此后又有几个口服抗变态反应药物被开发以抑制化学介质的释放,但在临床上不如DSCG。本品是具有独特化学     

Inhibition of the excitatory non-adrenergic, non-cholinergic neurotransmission in the guinea pig tracheo-bronchial tree mediated by alpha 2-adrenoceptors

Guinea pig main bronchi were studied in vitro for the presence of motor innervation. Field stimulation of the main bronchi revealed that besides the excitatory cholinergic component a slow and atropine resistant contraction similar to that previously found in the hilus bronchi (Grundstr?m et al. 1981a) was present also at this level of the airways. This slow contraction was blocked by tetrodotoxin whereas it was left unaffected by a number of conventional antagonists (i.e. atropine, guanethidine, propranolol, yohimbine and prazosin) suggesting that it was due to activation of non-adrenergic, non-cholinergic neurones. In the presence of a beta-adrenoceptor blocking drug, noradrenaline inhibited the slow contractions induced by field stimulation in both the main and hilus bronchi. By contrast, contractions elicited by histamine were left unaffected by noradrenaline. In order to characterize the receptor for noradrenaline the effects of alpha1-and alpha2-adrenoceptor blockers were evaluated. The results indicate that in the guinea pig bronchi noradrenaline inhibits non-adrenergic, non-cholinergic neurotransmission by acting on prejunctional alpha 2-adrenoceptors.     

Inhibition of the Excitatory Non-adrenergic,Non-cholinergic Neurotransmission in the Guinea Pig Tracheo-bronehial Tree Mediated by α2-Adrenoceptors

Abstract: Guinea pig main bronchi were studied in vitro for the presence of motor innervation. Field stimulation of the main bronchi revealed that besides the excitatory cholinergic component a slow and atropine resistant contraction similar to that previously found in the hilus bronchi (Grundström et al. 198 la) was present also at this level of the airways. This slow contraction was blocked by tetrodotoxin whereas it was left unaffected by a number of conventional antagonists (i.e. atropine, guanethidine, propranolol, yohimbine and prazosin) suggesting that it was due to activation of non-adrenergic, non-cholinergic neurones. In the presence of a β-adrenoceptor blocking drug, noradrenaline inhibited the slow contractions induced by field stimulation in both the main and hilus bronchi. By contrast, contractions elicited by histamine were left unaffected by noradrenaline. In order to characterize the receptor for noradrenaline the effects of α₁- and α₂-adrenoceptor blockers were evaluated. The results indicate that in the guinea pig bronchi noradrenaline inhibits nonadrenergic, non-cholinergic neurotransmission by acting on prejunctional α₁-adrenoceptors.     

Pharmacological Characterization of the Autonomous Innervation of the Guinea Pig Tracheobronchial Smooth Muscle

Abstract: From the trachea, main bronchi and hilus bronchi of guinea pigs, preparations were isolated for registration of mechanical tension on electrical field stimulation and drugs. The trachea contracted on short trains of electrical stimulation. Usually these contractions were followed by a relaxant response. The contractions were abolished while the relaxations were potentiated by atropine. In the main bronchi field stimulation induced a contractile response which was abolished by atropine. In the latter preparation relaxant responses were never observed, even not after atropine. In the trachea and main bronchi neither the α₁ blocker prazosin nor the α₂ blocker yohimbine affected the contractile or relaxant responses when used in α-blocking concentrations. The relaxant response in trachea was neither affected by the “P1 blocker” theophylline nor by the “P2 blocker” quinidine but it was partially inhibited by guanethidine or β-blocking agents. The hilus bronchi contracted on field stimulation as well as by histamine. The contractile response on electrical stimulation was only slightly inhibited by atropine or guanethidine. In all three preparations responses on field stimulation were abolished by tetrodotoxin. It is suggested that in both trachea and main bronchi excitatory cholinergic innervation is present. Further, the trachea but not the main bronchi is innervated by both adrenergic and nonadrenergic inhibitory nerves. The hilus bronchi contains a non-adrenergic non-cholinergic excitatory nervous system.     

Participation of neuropeptides in antigen-induced contraction of guinea pig bronchi via NK(2) but not NK(1) receptor stimulation

We evaluated the contribution of neuropeptides to antigen-induced contractions of isolated bronchi and tracheae of passively sensitized guinea pigs using CP-96345 and SR 48968, specific antagonists of NK(1) and NK(2) receptors, respectively, in combination with treatment by an antihistaminic and a cysteinyl leukotriene antagonist. SR-48968 but not CP-96345, significantly inhibited the late phase of the bronchial contraction. Phosphoramidon, a neutral endopeptidase inhibitor, tended to potentiate bronchial contraction. Posttreatment with SR-48968 decreased the enhanced contraction induced by the inhibitor as well as the nonenhanced contraction to similar levels of tension. On the other hand, antigen-induced tracheal contraction was not altered by either neuropeptide antagonist. These results suggest that neuropeptides mediate the antigen-induced contractile response of the guinea pig bronchus partly through NK(2) receptor stimulation.     

Pharmacological actions of oxatomide (KW-4354). 3. Actions on experimental asthma and Schultz-Dale reaction

The present experiment was carried out to elucidate the effectiveness of oxatomide for prophylaxis in the bronchial anaphylaxis and Schultz-Dale response. 1) Oxatomide administered i.v. was found to be as active as disodium cromoglycate (DSCG) in inhibiting IgE-mediated active anaphylactic bronchoconstrictions in rats. In contrast to DSCG, oxatomide was effective when administered p.o. 2) Passive anaphylactic broncho-constrictions in guinea pigs mediated IgG-like rabbit antibody against egg albumin was also prevented dose-dependently by treatment with oxatomide given p.o. and i.v., but not by DSCG. 3) Oxatomide and DSCG inhibited passive anaphylactic bronchoconstrictions in guinea pigs mediated by IgE-like antibody against BPO X BGG. 4) The anaphylactic reaction of the isolated guinea pig ileum, the so-called Schultz-Dale reaction, showed a bi-phasic response: a short, rapid contraction followed by a partial relaxation and a slow contractile response. Oxatomide significantly depressed both the rapid first contraction and the slow sustained one. 5) Oxatomide administered after the development of antigen-induced contraction of isolated guinea pig trachea resulted in relaxation. These results suggest that oxatomide may be effective for the treatment of allergic bronchial asthma.     

Further studies on the effects of disodium cromoglycate on guinea pig ileum

Transmural electrical stimulation was carried out on innervated strips of the longitudinal muscle of guinea pig ileum. Disodium cromoglycate (DSCG) inhibited the electrically induced contractions. Five minutes later, prostaglandin E2 (2.5 ng/ml) was added to the bath and it reversed the action of DSCG. Furthermore, DSCG inhibits significantly the guinea pig ileum contractions induced by nicotine and also those induced by histamine and acetylcholine on ileum denervated by cooling. These results suggest that DSCG effects on guinea pig ileum contraction are mediated by membrane-stabilizing properties of this drug on smooth muscle fibres as well as on myenteric plexus.     

Inhibition of cholinergic and non-adrenergic, non-cholinergic bronchoconstriction in the guinea pig mediated by neuropeptide Y and alpha 2-adrenoceptors and opiate receptors

The mechanisms underlying the regulatory influence of neuropeptide Y (NPY) and of alpha 2-adrenoceptor and opiate receptor activation on cholinergic and excitatory non-adrenergic, non-cholinergic (e-NANC) neurotransmission were studied in guinea pig hilus bronchi in vitro. NPY inhibited both the cholinergic and e-NANC bronchial contractions evoked by field stimulation. The NPY attenuation of the e-NANC contraction could not be antagonized by the alpha 2-antagonist, idazoxan, or naloxone. UK 14,304 a specific alpha 2-agonist, also reduced the two nervous components of bronchial contraction and this action was inhibited by idazoxan. NPY and UK 14,304 exerted a minor influence on the bronchial smooth muscle tone per se or on contractions evoked by acetylcholine or neurokinin A. This suggested that the inhibitory responses were caused by a prejunctional action reducing the release of transmitter substances from sensory and cholinergic nerve endings. Furthermore NPY (10(-7) M) seemed to be more potent to inhibit both contractile components than noradrenaline (10(-6) M) in the presence of propranolol (3 X 10(-6) M). Morphine was able to reduce the e-NANC response via a naloxone-sensitive mechanism. The capsaicin-evoked bronchoconstriction and the bronchodilator NANC effect evoked by field stimulation were, however, not influenced by UK 14,304. It is concluded that NPY, alpha 2-receptor and opiate receptor activation inhibit the release of sensory transmitters evoked by field stimulation but not by capsaicin.     

Significant role of peptide leukotrienes (p-LTs) in the antigen-induced contractions of human and guinea pig lung parenchymas and bronchi or tracheas in vitro.

Chemical mediators responsible for the antigen-induced contractions of isolated, passively sensitized human and guinea pig lung parenchymas and bronchi or tracheas were evaluated by several antagonists and enzyme inhibitors, with emphasis on the effects of the potent and selective peptide leukotriene (p-LT) antagonist MCI-826. All of these preparations showed long-lasting contractions in response to an antigen challenge which lasted for more than 60 min. In either the human lung parenchyma and brochus or guinea pig lung parenchyma, pretreatment with 10(6) g/ml (2.4 x 10)-6) M) MCI-826 significantly inhibited the late phase at 10 to 60 min after the challenge of the contraction following slight suppression of the early phase. The early phase contractions of these preparations were moderately antagonized by 10(-6) g/ml mepyramine, but the late phases were not influenced or even rather enhanced. The combination treatment of MCI-826 with mepyramine additionally and markedly inhibited both phases of these preparations. On the other hand, although mepyramine apparently inhibited the early phase of the guinea pig tracheal contraction but not the late phase, no synergistic inhibitions of the contraction were observed when it was combined with MCI-826. The p-LT antagonist FPL 55712, atropine and indomethacin at 10(-6) g/ml either slightly inhibited or enhanced the contractions of human lung parenchymas, guinea pig tracheas and lung parenchymas, but the effects were not significant. From these results, it should be emphasized that p-LTs largely contribute to induction of the anaphylactic contractions of human lung parenchymas as well as human bronchi and guinea pig lung parenchymas but not guinea pig tracheas.     

Cooperation of ATP and norepinephrine in inducing contractile responses in guinea pig vas deferens

Stimulation of the hypogastric nerve to the guinea pig vas deferens induced biphasic contraction consisting of a rapid transient phase (mediated by ATP) and a delayed tonic phase (mediated by norepinephrine, NE), whereas stimulations in the presence of selective antagonists caused each contractile phase separately. Stimulation in the absence of antagonist induced a larger rapid transient contraction than that induced by stimulation in the presence of alpha 1-antagonist. Results obtained in separate or simultaneous additions of exogenous ATP and NE showed synergism in the rapid transient contraction. These findings indicate that NE assisted ATP in inducing the hypogastric nerve-mediated contractile response in guinea pig vas deferens, but not vice versa.     

Effects of nitric oxide on slow waves and spontaneous contraction of guinea pig gastric antral circular muscle

We examined the effects of nitric oxide (NO) donors, S-nitroso-L-cysteine (Cys-NO) and 3-morpholinosydnonimine hydrochloride (SIN-1), on slow waves and contractile activity in the circular muscle of guinea pig gastric antrum. In the presence of atropine and guanethidine, electrical field stimulation (EFS) reduced the amplitude of phasic contraction. The effect of EFS was significantly inhibited by both the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester and a soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Cys-NO and SIN-1 mimicked the effect of EFS on phasic contraction and reduced the amplitude of slow waves in a concentration-dependent manner, with no effect on frequency and resting membrane potential. Phasic contraction was more sensitive to NO donors than slow waves. The inhibitory effects of NO donors were antagonized by ODQ and mimicked by a membrane permeable cGMP analogue 8-bromo-cGMP. Several K(+) channel blockers such as apamin, iberiotoxin, and glibenclamide had no effect on the inhibitory action of SIN-1. These results suggest that NO inhibits the phasic contraction and slow waves through cGMP-dependent mechanisms in guinea pig gastric antrum. The effect of NO is unlikely to be mediated by the activation of Ca(2+)-activated or ATP-sensitive K(+) channels.