一种简易大鼠固定装置的制作和使用方法

目的制作和使用一种简易大鼠固定装置。方法用深色布、木板等制作简易实用的大鼠固定装置;方便对鼠尾进行恰当的处理,如:使鼠尾处于最低位、采用40℃左右的水浴等。结果大鼠得到了良好的固定;给药、采血快捷便利。结论该装置适合SPF环境的特点,用于大鼠尾静脉采血与注射,制作简单、使用方便,可减少对鼠的损伤,减少鼠的应激反应,使实验结果准确可靠。     

大鼠尾静脉取血方法介绍

大鼠作为实验室较为常用的实验动物,常被用作多种实验。但大鼠的形体比较小,因此在实验过程中不伤害大鼠顺利采取一定量的血液是大家关注和探讨的问题。目前,对大鼠取血的方法虽然较多,但多数都会对大鼠造成严重的伤害,甚至导致其死亡。     

紫蓝素静脉注射的急性毒性实验

目的观察紫蓝素静脉注射对大鼠产生的急性中毒反应,以评价其安全性。方法 60只大鼠随机分为紫蓝素组(700 mg.kg-1.d-1)、3%碳酸氢钠溶液组、0.9%氯化钠溶液组,各20只。记录每只大鼠毒性反应的症状及开始和消失时间,连续观察14 d。结果①紫蓝素组给药2 h后大鼠全身皮肤呈紫色,大便呈紫蓝色,尿液呈黄褐色,第5天恢复正常。整个实验过程无大鼠死亡。②紫蓝素组大鼠体质量显著低于另外两组。③第1天紫蓝素组大鼠摄食量明显低于另外两组。④紫蓝素组大鼠肾脏脏器系数显著高于另外两组。⑤紫蓝素可引起部分大鼠肾脏髓质区域不同程度增大,皮质和髓质交界区域部分肾小管扩张;个别大鼠肾盂扩张,肾小管内有大量紫蓝色沉着。结论紫蓝素大鼠静脉注射给药的最大耐受量>700 mg.kg-1.d-1,主要表现为肾脏毒性。     

外源性rIL-10基因质粒静脉注射及其在大鼠体内表达

目的建立大鼠体内质粒DNA尾静脉快速大容量注射法,使外源性rIL-10在肝组织中高表达,为探索肝脏疾病的基因治疗提供动物试验手段。方法以rIL-10为报告基因,将含不同体积及不同质粒浓度的质粒DNA溶液经大鼠尾静脉快速注射,在注射后的不同时间内分别收集血浆及肝、肾、肺、脾和心组织,使用RT-PCR、ELISA和免疫组化法检测rIL-10在体内的表达情况。结果尾静脉快速大容量注射rIL-10DNA溶液可使rIL-10基因在大鼠肝脏有较明显转录及表达。血浆中rIL-10浓度可通过质粒的重复注射使其保持在一个稳态。结论尾静脉快速大容量注射法是一种简单、方便和有效的大鼠体内基因转移及基因表达的方法,为进一步探讨rIL-10基因在肝脏疾病的基因治疗打下基础。     

早期糖尿病大鼠肾组织尾加压素Ⅱ表达的实验研究

目的：探讨早期糖尿病大鼠肾组织中尾加压素Ⅱ（urotensin Ⅱ,UⅡ）的表达及其意义。方法：用链脲佐菌素（STZ）诱导糖尿病大鼠模型,将实验动物分为正常对照组（C组）、糖尿病组（D组）和胰岛素干预组（Y组）。5周后收集肾组织,观察各组肾脏病理情况及UⅡ在肾组织中的表达。结果：处理5周后,与C、Y组比较,D组肾小球肥大、肾小球表面积显著增大,小管扩张,上皮细胞肿胀;D组肾小管上皮细胞UⅡ表达明显升高（与C组比较,P〈0.05）;Y组肾小管上皮细胞UⅡ表达有不同程度的下降（与D组比较,P〈0.05）。结论：STZ诱导的早期糖尿病大鼠肾小管上皮细胞UⅡ表达明显上调;应用胰岛素严格控制血糖可部分下调肾组织UⅡ的表达。UⅡ在STZ诱导的早期糖尿病大鼠肾脏病变的发展过程中可能起一定作用。     

静脉注射三乙醇胺对SD大鼠的病理性损伤作用

目的观察静脉注射三乙醇胺后SD大鼠的组织病理学改变及其可逆性。方法 60只SD大鼠,随机分为对照组和300mg/kg剂量组,连续30d给药和恢复4周,分别进行大体解剖和组织病理学检查。结果连续给药30d,SD大鼠肝细胞嗜酸性变,肾髓质肾小管上皮细胞变性,脾小体生发中心增大,白髓边缘带增宽,淋巴结内淋巴滤泡数量增多,生发中心增大;恢复4周,肝脏、脾脏和淋巴结病变恢复不明显。结论静脉注射一定剂量的三乙醇胺,对SD大鼠肝脏、肾脏、脾脏和淋巴结有一定的损伤作用,其中,肾脏的损伤可逆,脾脏、淋巴结和肝脏的损伤有一定程度的恢复。     

小鼠尾静脉注射法

小鼠尾静脉注射是药理、毒理实验中常用的注射方法,有些实验要求注射时速快、准确.我们在长期的动物实验技能操作中,总结出一种新的小鼠尾静脉注射方法,具体方法介绍如下.     

两种静脉注射穿刺方法的观察

静脉注射是临床护理工作中最常用的一项基本操作，如何减少穿刺的疼痛，减轻病人的痛苦，提高成功率，是值得探讨的问题。笔者自2000-06~2001-06对280例静脉注射(包括输液)病人进行了直刺法和斜刺法的对比，现报道如下。 1 资料与方法 静脉注射治疗病人280例，男150例，女130例，年龄14~60岁，将280例病人随机分为二组，采用7号头皮针。直刺法在穿刺 两组穿刺成功率比较P<0.01 3 讨论 ①结果表明，直刺法对组织产生的刺激明显小于斜刺法，因为针头对局部组织是一种刺激，直刺法针头刺入皮下后直接快速的进入静脉，减少了针头对组织的…     

静脉注射PHPB对大鼠脑缺血再灌注损伤的脑保护作用研究

目的：通过大鼠脑缺血再灌注损伤后长期生存实验观察静脉注射PHPB对MCAO大鼠的脑保护作用。方法：将wistar大鼠随机分为假手术组、模型组、MK801阳性组（0．5mg／kg）、PHPB给药组（1．3、3.9、12．9mg／kg）等6组。各组n=10～17只。除假手术组只断颈外动脉外，其他各组行大脑中动脉阻断术（MCAO），缺血后5min静脉注射给药，缺血后120min再灌注，以再灌后存活动物进行统计。术后连续14天观察动物的体重、神经行为学评分及死亡率变化，在14天后观察存活动物的脑梗死体积。结果：术后14天，各给药组体重与模型对照组比较均有所改善。术后24小时模型组、MK801组、PHPB给药组（1．3、3．9、12．9mg／kg）死亡率分别为29％、23％、0％、15％、6％。14天后死亡率和平均生存时间显示各组与模型组（53％，8．24天）比较均有改善，其中PHPBl．3mg／kg组死亡率只有（17％），其平均生存时间与模型组比较延长了62％，具有显著性差异。神经行为学评价显示各给药组与模型组比较均有不同程度的改善，在14天后存活动物脑梗死体积测定方面显示PHPB3．9mg／kg组（16．6％±4．9％）与模型组（39．4％±5．7％）比较具有显著的改善作用。结论：PHPB静脉注射后、可以改善MCAO大鼠急性脑损伤，提高平均生存时间，减少死亡率。在脑缺血治疗有很好的开发前景，值得进一步研究。     

小儿静脉注射方法浅谈

笔者从护２０余年，在多年的临床实践中对静脉注射特别是小儿静脉注射的方法积累了一些经验与体会，在此做以简要介绍，以便与同行们相互探讨，共同提高。１选择血管 按照人体解剖学理论，手背、足背的浅表静脉血管均适合于静脉注射，然而由于年龄、病情和治疗目的的不同，选择穿刺部位也不尽相同。新生儿至３岁的小儿宜选用头皮静脉；４－１２岁的儿童宜选用四肢静脉：慢性疾病宜从距心脏较远的部位开始选择：危重病人抢救时应选择肘静脉和桡静脉；一般治疗宜选头皮静脉和肢端静脉；静脉推注钙剂、５０％葡萄糖等高渗透刺激性药物宜选肘静…     

Sensitivity to noradrenaline and electrical stimulation decreases with age in the rat tail artery

Summary We have studied vasoconstrictor responses to noradrenaline and electrical field stimulation in the isolated perfused/superfused tail arteries of rats of 6–7, 16–17 and 30–31 months of age. Maximal vasoconstrictor responses to noradrenaline were the same at all three ages. Sensitivity to noradrenaline and to electrical stimulation were reduced in the 16–17 and 30–31 month old rats. The noradrenaline content of the arteries of the two latter age groups was reduced. We conclude that ageing in this resistance vessel is accompanied by a decrease in the arterial noradrenaline content and in the sensitivity of the artery to noradrenaline.     

正交设计法优选骨肽注射液纯化参数的研究

目的:探讨优选骨肽注射液提取的工艺条件。方法:采用正交设计法,骨肽注射液多肽含量及操作可行性为考察指标,对骨肽注射液提取过程中乙醇沉淀浓度、酸沉淀(pH 2.0～4.0)、碱沉淀(pH 6.8～7.2)3个因素进行筛选。结果:对于选定的三因素三水平,骨肽注射液最佳纯化参数组合为乙醇沉淀浓度70%、酸沉淀pH 4.0,碱沉淀pH 8.0,结果具有较显著的统计学意义。结论:根据骨肽注射液最佳提取条件对猪骨进行骨多肽提取,提取效率高,成本低。     

An experimental design approach to the optimisation of a flow injection analysis method for glycine

A flow injection analysis method for the determination of glycine, based on the reaction with ortho-phtalaldehyde and N-acetylcysteine in a basic buffer, was optimised. In the first step screening of the variables, to select the most important ones, was performed using: (i) a half-fraction factorial design and (ii) a quarter-fraction factorial design, for five factors at two levels. The effects of the factors on the peak height were calculated from both screening designs and compared. For the half-fraction factorial design (resolution IV), the significance of the factor effects on the peak height was checked by: (i) comparing them with a critical effect, calculated from two-factor interactions and based on a t-test, (ii) using a non parametric approach and (iii) drawing a normal probability plot. For the quarter-fraction factorial design (resolution III) the significance of the effects of the factors on the peak height was checked using: (i) a randomization test method, (ii) the non parametric method and (iii) a normal probability plot. In the second step, the factor found to be of importance was optimised using the uniplex method.     

苦碟子注射液对非缺血型视网膜静脉阻塞的临床疗效及对血液流变学的影响

目的观察苦碟子注射液(清热解毒中药)对非缺血型视网膜静脉阻塞患者的临床疗效。方法 92例非缺血型视网膜静脉阻塞患者,随机分为对照组(44例44眼)与治疗组(48例48眼)。对照组进行常规治疗;治疗组在常规治疗基础上,加用苦碟子注射液。每个疗程后,记录并分析所有病人临床疗效和血液流变学变化。结果总有效率和总显效率、低切和高切全血比黏度、血浆黏度、纤维蛋白原量及血小板黏附率,治疗组与对照组比较差异均有显著统计学意义(P<0.05)。结论苦碟子注射液能改善非缺血型视网膜静脉阻塞患者血液流变学的各项指标,改善临床治疗效果。     

Pharmacological characterization of neurotensin receptors in the rat isolated portal vein using analogues and fragments of neurotensin

The contractile effects of the tridecapeptide neurotensin (NT) and several NT fragments and analogues were evaluated and compared in the rat isolated portal vein. The removal of the sequence pGlu1-Leu2-Tyr3-Glu4-Asn5-Lys6-Pro7 produced practically no change in the myotropic activity of NT while the deletion of Leu13 or the last 3 C-terminal amino acids (e.g. Tyr11, Ile12 and Leu13) gave compounds with very low agonist activity (NT(1-12)) or devoid completely of affinity and intrinsic activity (NT(1-10)). Replacing Tyr11 with Ala, Leu, D-Tyr or D-Phe markedly decreased the stimulant effect of NT but did not confer to the molecule antagonistic properties. On the other hand, the substitution of Try11 with D-Trp or Tyr(Me) gave NT analogues which behave as specific and competitive antagonist of the contractile effect of NT in the portal vein. pA2 values of [D-Trp11]-NT and [Tyr(Me)11]-NT measured in the venous preparation were similar to those found in the coronary vasculature of the rat. Taken all together, these results suggest that: (1) the minimum structure required for the full expression of the myotropic activity of NT in the rat portal vein is -Arg9-Pro10-Tyr11-Ile12-Leu13-OH; (2) Tyr11 appears to be closely involved in the process of NT receptor activation since its replacement with D-Trp or Tyr(Me) produced specific and competitive antagonist of NT; (3) the receptors mediating the contractile effect of NT in the rat portal vein appear to be pharmacologically similar to those found in the coronary vessels of the rat. The possibility for the existence of different types of NT receptor in other tissues is discussed.     

葛根注射液抗心肌缺血的药理作用研究

目的 考察葛根注射液的抗心肌缺血作用.方法 考察葛根注射液高中低剂量组对大鼠离体心脏左室峰压(LVSP)、冠脉流量(CF)及大鼠离体心脏缺血再灌注后的LVSP、左室舒张期末压(LVEDP)、心率(HR)、CF的影响.结果 葛根注射液可升高大鼠离体心脏心肌收缩力及冠脉流量;对离体心脏缺血再灌注导致的LVSP和LVEDP的升高、心率及冠脉流量的降低均有对抗作用.结论 葛根注射液具有抗心肌缺血的作用.     

Repeated tail pinch leads to desensitization of postsynaptic α2-adrenoceptors which modulate the jaw-opening reflex in the rat

There are few in vivo studies which have investigated the modulation of central postsynaptic α ₂-adrenoceptors functionality provoked by stress. We assessed in the rat the effects of either single or repeated tail pinch on clonidine-induced inhibition of the jaw-opening reflex (JOR) via activation of postsynaptic central α ₂-adrenoceptors. At the end of each experimental period, the progressive inhibition of the digastric electromyographic responses elicited by orofacial electrical stimulation after the IV administration of cumulative doses (× 3.3) of clonidine (0.1–10 000 μg/kg) was recorded. Single tail pinch did not significantly modify the ability of the agonist to inhibit the JOR, although there was a tendency to decrease the basal amplitude of the reflex (a 40% reduction) immediately after exposure to the single stressor. However, the dose-response curve for clonidine-induced inhibition of the JOR was clearly shifted to the right in rats exposed to repeated tail pinch (ED₅₀ was increased by 152%, P < 0.0001) when compared with the unstressed control group, without affecting the slope of the inhibitory function and the estimated maximum effect for the agonist. These results show that repeated stress leads to a subsensitivity of the α ₂-adrenoceptors which modulate the JOR, suggesting the development of adaptive mechanisms in postsynaptic α ₂-adrenoceptors in response to stress. Received: 21 October 1997/Final version: 22 December 1997     

The actions of angiotensin II on the isolated portal vein of the rat

Isolated rat portal vein suspended in Krebs bicarbonate medium showed regular rhythmic activity and contracted in response to angiotensin II, noradrenaline, adrenaline, tyramine, acetylcholine, serotonin and histamine. Angiotensin II was 3–10 times as potent as noradrenaline on a weight basis. Responses to angiotensin II were unchanged in the presence of antagonists to these drugs, excepting high concentrations of phentolamine. Electrical stimulation or noradrenaline did not potentiate responses to angiotensin II; angiotensin II did not potentiate responses to noradrenaline. Angiotensin II acts directly on the smooth muscle of rat portal vein; its action is independent of noradrenaline. Spontaneous contractions and responses to angiotensin II and noradrenaline were transiently depressed and then potentiated in media made hyperosmolar by addition of NaCl, sucrose or urea. Responses were depressed in hypo-osmolar low NaCl solution but unaffected by isosmolar low NaCl. An increase of intracellular potassium concentration would not alone account for the entire effect of increased osmolarity.     

Characterization of the angiotensin II-receptor subtype in the longitudinal smooth muscle of the rat portal vein

Summary The purpose of the present study was to identify the angiotensin II-receptor subtype involved in the enhancement of the amplitude of the phasic contractions by angiotensin II in the isolated rat portal vein preparation.At an extracellular Ca²⁺ concentration of 0.9 mmol/l and a K⁺ concentration of 4 mmol/l, angiotensin II induced concentration-dependent increases in the amplitude of the phasic contractions. The enhancement of phasic contraction amplitude caused by angiotensin II was not significantly altered by pretreatment of the rat portal vein with indomethacin 10^–5 mol/l or nitro-L-arginine 10^–4 mol/l, indicating that neither prostaglandins nor the endothelium derived-relaxing factor (NO) are involved. Losartan (DuP 753), a nonpeptide selective AT₁-receptor antagonist, concentration-dependently shifted the concentration-response curve for the effect of angiotensin II on the amplitude of the contractions to the right, without reducing the maximal response (pA₂ = 8.6, slope = 0.98), thus suggesting competitive antagonism at the level of AT₁-receptors. By contrast, PD 123177, a nonpeptide selective AT₂-receptor antagonist, even at 10^–5 mol/l, caused no significant change of the phasic myogenic response to angiotensin II, indicating the absence of AT₂-receptor involvement. Dithiothreitol, a disulfide-reducing agent which is known to inactivate AT₁-receptors in various tissues, markedly inhibited (3 mmol/l) or even abolished (5 mmol/l) the contractile response of the rat portal vein to angiotensin II, supporting the conclusion that these receptors can be classified as AT₁-receptors.In conclusion, the receptor subtype mediating the angiotensin II-induced potentiation of the spontaneous phasic contractions in the rat portal vein appears to belong to the AT₁-receptor subtype.Preliminary data were presented at the Spring Meeting of the German Pharmacological Society, Mainz, 1992Correspondence to J. S. Zhang at the above address     

红花注射液预处理对鼠肺缺血再灌注损伤的保护性研究

目的探讨红花注射液预处理对鼠肺缺血再灌注损伤的保护作用。方法健康wistar大鼠36只,随机分为3组,每组12只。Ⅰ组：未行缺血再灌注处理;Ⅱ组：行左肺缺血再灌注处理;Ⅲ组：红花预处理与行左肺缺血再灌注处理。结果Ⅱ组再灌注1、2、3h动脉血PaO2显著降低而PaCO2显著升高,各时点血浆MDA、髓过氧化物酶（MPO）和左肺组织W/D均显著升高（与Ⅰ组比较）;电镜显示Ⅱ组有明显的肺超微结构损伤,Ⅲ组红花注射液预处理后可明显改善上述指标变化。结论红花注射液预处理对肺缺血/再灌注损伤有明显的保护作用。