大鼠对注射巴马亭的类过敏反应

巴马亭(Palmatine)是一种生物碱,其化学结构与延胡索乙素及小蘖碱相似.作者在研究巴马亭等药物对大鼠ACTH分泌活动的影响时,观察到大鼠于皮下注射巴马亭约半小时后,动物的嘴鼻部及四肢出现明显的浮肿.为了解巴马亭的致浮肿作用及此作用的性质,我们作了下列的研究.结果与讨论所用动物为体重100-150克的雄性大鼠.用微分卡尺量大鼠的一侧后爪的厚度.以给药前与给药后后爪厚度相差的毫米数,作为判定浮肿形成的程度的指标.(一)大鼠对注射巴马亭的类过敏反应     

巴马亭的合成

巴马亭(又称黄藤素、非洲防已碱,palmatine,1),化学名为5,60-二氢-2,3,9,10-四甲氧基二苯并[a,g]喹嗪内鎓盐,具有广谱抗菌作者,临床上可用于治疗妇科炎症、菌痢、肠炎、呼吸道和泌尿道感染、外科感染及结膜炎等.     

小蘖碱、巴马亭及四氢巴马亭(延胡索乙素)对大鼠促皮质素释放的影响

我们曾报告延胡索乙素有刺激大鼠促皮质素(ACTH)释放的作用,本文报告在化学结构上与延胡索乙素相似的两种药物——小蘗碱及巴马亭(Palmatine)对大鼠垂体——肾上腺皮质功能的影响,以及延胡索乙素对ACTH释放的抑制作用。小蘗碱5或10毫克/公斤,巴马亭25或50毫克/公斤皮下注射一次,都能引起大鼠肾上腺内维生素C含量明显降低,对去垂体大鼠肾上腺的维生素C则无影响,戊巴比妥钠麻醉可明显抑制小蘗碱的降低肾上腺维生素C作用,唯对巴马亭的这种作用却无影响,在戊巴比妥钠麻醉的基础上,吗啡能完全抑制巴马亭的降低肾上腺维生素C作用。每日给大鼠注射延胡索乙素1次(70毫克/公斤),连续6次后,对低温(8℃或4℃1小时)刺激引起的ACTH释放有明显抑制作用。总括我们的结果,延胡索乙素、小蘗碱及巴马亭这三种化学结构相似的药物,都能刺激大鼠ACTH的释放,但其作用机制或部位可能彼此不同,此外,延胡索乙素的多次注射还可抑制ACTH的释放,这些作用的不同可能与上述三药的化学结构特别是第3环的饱和与否有关系。     

小蘖碱、巴马亭及四氢巴马亭(延胡索乙素)对大鼠促皮质素释放的影响

我们曾报告延胡索乙素有刺激大鼠促皮质素(ACTH)释放的作用,本文报告在化学结构上与延胡索乙素相似的两种药物——小蘗碱及巴马亭(Palmatine)对大鼠垂体——肾上腺皮质功能的影响,以及延胡索乙素对ACTH释放的抑制作用。小蘗碱5或10毫克/公斤,巴马亭25或50毫克/公斤皮下注射一次,都能引起大鼠肾上腺内维生素C含量明显降低,对去垂体大鼠肾上腺的维生素C则无影响,戊巴比妥钠麻醉可明显抑制小蘗碱的降低肾上腺维生素C作用,唯对巴马亭的这种作用却无影响,在戊巴比妥钠麻醉的基础上,吗啡能完全抑制巴马亭的降低肾上腺维生素C作用。每日给大鼠注射延胡索乙素1次(70毫克/公斤),连续6次后,对低温(8℃或4℃ 1小时)刺激引起的ACTH释放有明显抑制作用。总括我们的结果,延胡索乙素、小蘗碱及巴马亭这三种化学结构相似的药物,都能刺激大鼠ACTH的释放,但其作用机制或部位可能彼此不同,此外,延胡索乙素的多次注射还可抑制ACTH的释放,这些作用的不同可能与上述三药的化学结构特别是第3环的饱和与否有关系。     

类过敏反应的研究进展

目的对类过敏反应的症状特点、发生机理、评价方法及存在的问题进行了综述和分析,为类过敏反应的深入研究提供文献依据。方法对近年来有关类过敏反应的国内外文献进行了整理与归纳。结果虽然类过敏反应的症状表现与过敏反应相似,但两者发生机制并不相同,其无需提前致敏、抗体介导,首次接触即可发生,危害严重。目前,类过敏反应的临床前评价方法主要有动物实验和细胞实验,检测指标有组胺、IgE等,其诊断需结合症状特点及生物指标综合判断。结论亟待建立可行的有关类过敏反应的临床前评价方法。     

药用注射辅料聚山梨酯80诱发类过敏反应的细胞研究

目的:观察聚山梨酯80诱导大鼠嗜碱性粒细胞白血病细胞株RBL-2 H3细胞脱颗粒现象,探讨其诱发类过敏反应的可能机制。方法:聚山梨酯80与RBL-2 H3细胞共同孵育60 min后,透射电镜观察细胞发生脱颗粒反应的形态学变化,荧光显微镜下观察细胞膜磷脂酰丝氨酸与Annexin V结合变化,分光光度法测定细胞上清液β-氨基己糖苷酶释放百分率,并通过阿利新蓝染色试验进行定性观察。结果:不同浓度聚山梨酯80可诱导细胞发生典型的脱颗粒反应形态学变化,与阴性对照组相比脱颗粒率及组胺释放率显著升高,且具有浓度依赖性。结论:聚山梨酯80单次、首次给药即可诱导RBL-2 H3细胞脱颗粒,释放组胺,诱发类过敏反应,这可能是其临床首次用药即引起严重不良反应的机制之一。     

注射β-内酰胺类抗菌素致迟缓型过敏反应的护理体会

注射β－内酰胺类抗菌素致迟缓型过敏反应的护理体会福建医科大学附属第一医院华侨病房江姿芳近年来，β－内酰胺类抗菌素（包括青霉素类和头孢菌素类）由于其抗菌性强、疗效好，临床应用药居首位。但是其药物的半抗原特性仍旧不能忽视。虽然，临床上应用时均有进行严格的...     

Compound 48/80诱导BN大鼠类过敏反应的蛋白组学研究

目的探讨Compound 48/80诱导BN大鼠类过敏反应的发生机制,采用iTRAQ蛋白组学技术对类过敏的发生过程进行研究,并鉴定候选标志物。方法将BN大鼠按体质量随机分为对照1组、2组和Compound 48/80 1组、2组,每组各6只。对照组iv生理盐水5 mL/kg,Compound 48/80组分别iv Compound 48/80 2.5 mL/kg,取血浆样品经蛋白提取、电泳和质谱分析,确定类过敏反应差异蛋白。结果通过蛋白组学研究共鉴定10585个肽段,总共鉴定1987个蛋白质。提取7个与类过敏反应相关的差异蛋白。与对照组比较,Ica、Galectin-1上调;Hpse HEP、Mpo、MMP8、Hprt1、MMP9下调。结论Hpse HEP、Mpo、MMP8、Hprt1、Ica、MMP9、Galectin-1均可以作为类过敏反应的候选生物标志物。     

尿道内注射利多卡因致过敏反应

[病例] 男,19岁.因尿道骑跨伤急诊入院.患者既往体健,否认药物过敏史.入院后2 h主管医生为患者行导尿术,尿道内注入2%利多卡因5 ml+生理盐水5 ml.注入5 min后患者突然出现寒战、胸闷、呼吸困难、面色苍白、出冷汗,脉搏120/min,呼吸30/min,血压90/60 mmHg.遵医嘱立即给予氧气吸入,地塞米松5 mg肌内注射,20 min后上述症状缓解,生命体征正常.     

注射环丙沙星引起过敏反应8例

环丙沙星是近年来广泛应用于临床的一种新型抗生素 ,具有良好的抗菌效果。但随着药物的广泛应用 ,随之带来的副作用也相应增多 ,现将 8例过敏反应报告如下。1　临床资料8例中男 3例 ,女 5例 ,年龄 2 8～ 70岁 ,原发病 :慢性支气管炎急性发作 4例 ,肺间质纤维化合并肺部感染 1例 ,急性肺炎 2例 ,慢性肾盂肾炎 1例。注射环丙沙星后约 3～ 10 m in8例患者均出现注射部位红色丘疹 ,沿静脉走向逐渐增多 ,皮肤瘙痒明显 ,其中 3例合并胸闷、憋气 ,即刻停止用药并注射抗过敏药物后逐渐好转 ,典型病例介绍如下。例 1,男 ,65岁。患慢性喘息性支气管炎…     

Pellagri氏反应的改进及其在吗啡类化合物比色定量上的应用

本文对Pellagri氏反应作了較全面的探討与改进,得出: 1.最合适的脱水剂是HCl-H₂SO₄(1ml:2滴),加酸后在水浴上蒸發半小时脫水,然后用KH₂PO₄-NaOH緩冲溶液及NaHCO₃溶液中和到PH7左右时所得結果最好,氧化剂以碘酸溶液为最佳。2.反应产物可用有机溶剂抽出,其中正丁醇的抽出力最强,使反应的鑑识限度提高为1γ嗎啡鹽基. 3.依照本文条件試驗,反应产物的水溶液,正丁醇抽出液及苯抽出液都符合Beor氏定律(圖2),可用作嗎啡类化合物的比色定量(表1)。     

THE USE OF A RAT ISOLATED ILEAL PREPARATION TO INVESTIGATE THE RELEASE OF NEUROTENSIN

1. An isolated and perfused preparation of rat ileum was used to investigate the effects of cholinergic, adrenergic and bombesin stimuli on neurotensin release into the vascular compartment. 2. A vigorous release of neurotensin like immunoreactivity (NTLI) to 200% above basal values in response to intraluminal infusions of emulsified soybean oil (Intralipid) demonstrated the physiological responsiveness of the preparation. 3. Carbachol significantly stimulated the release of both NTLI and bombesin like immunoreactivity (BLI), with maximal responses at 5 times 10^-9 mol/l carbachol of 100% and 400% above basal values for NTLI and BLI, respectively. 4. Noradrenaline at 10^-6 and 10^-4 mol/l caused no significant release of NTLI but markedly inhibited spontaneous BLI release. 5. Synthetic amphibian bombesin caused a marked release of NTLI to 81% and 100% above basal at infusion concentrations of 5 times 10^-11 and 5 times 10^-10 mol/l respectively. 6. These results suggest that there is either a direct effect of cholinergic agents on the N cells bringing about NTLI release, or an indirect effect via the release of bombesin like peptides from intrinsic gut neurones. This preparation provides a useful model to study the complex neural, paracrine and endocrine interactions in the gastrointestinal tract.     

MECHANISMS OF THE PRESSOR RESPONSE TO INTRAVENOUS THYROTROPIN-RELEASING HORMONE IN THE RAT

1. The purpose of this study was to examine the contribution of the sympatho-adrenomedullary system to the blood pressure response to an intravenous bolus of thyrotropin-releasing hormone (TRH) in conscious medullectomized and sham-operated rats. 2. The peak pressor effect of 0.5 mg TRH was significantly increased in rats having no adrenal medulla (+ 24.2 ± 1.6 mmHg, mean ± s.e.m., P<0.01) as compared to sham-operated animals (+12.2 ± 3.0 mmHg). 3. Blockade of alpha-adrenergic receptors with phentolamine abolished the pressor effect of TRH in control rats (+ 2.1 ± 1.9 mmHg) but did not attenuate the blood pressure response of medullectomized rats (+ 21.5 ± 4.7 mmHg). In contrast, beta-blockade with propranolol blunted the blood pressure responsiveness of rats subjected to adrenal medullectomy (+ 12.4 ± 2.6 mmHg) but did not modify the effect of TRH in sham-operated controls (+ 10.9 ± 2.9 mmHg). 4. The direct in vitro effect of TRH on isolated mesenteric rat arteries was also evaluated. TRH did not induce contractions of isolated arteries. 5. These results suggest that in rats with intact adrenals, the pressor effect of intravenous TRH is mediated primarily by a stimulation of alpha-adrenergic receptors. Adrenal medullectomy appears to enhance the blood pressure response to intravenous TRH. Activation of cardiac beta-adrenocep-tors seems to contribute to the blood pressure increasing effect of intravenous TRH in medullectomized animals.     

THE NATURE OF THE PRESSOR RESPONSE TO CAROTID ARTERY OCCLUSION IN THE HEXAMETHONIUM-TREATED RAT

1. The blood pressure monitored from the cannulated right carotid artery and heart rate responses to occlusion of the intact left carotid artery were investigated in rats. 2. Hexamethonium abolished the response to ganglion stimulants but not that to carotid occlusion, although the time course and nature of the response were altered. 3. The pressor response to carotid occlusion in the presence of hexamethonium was not abolished by carotid sinus denervation, vagal section, tubocurarine, atropine, ethyl alcohol or an angiotensin II antagonist, but it was abolished by high doses of phenoxybenzamine. In six out of eight experiments the response was not abolished by cervical cord section. 4. It was concluded that the pressor response to carotid occlusion in the presence of hexamethonium in the rat involves an adrenergic mechanism which is at least in part independent of the autonomic ganglia, and which is mediated by an agent liberated from the brain, possibly under conditions of cerebral ischaemia.     

REGIONAL VARIATION IN THE RESPONSE OF THE RAT VAS DEFERENS TO FIELD STIMULATION, TO NORADRENALINE AND TO TYRAMINE

SUMMARY 1. Experiments were performed with preparations obtained by medial transection of the rat vas deferens providing urethral and testicular segments, to determine whether the smooth muscle of this organ responds uniformly along its length to field excitation of sympathetic nerve terminals and to sympathomimetic amines. 2. Both preparations responded to pulses applied at 0.1 Hz with twitches which were blocked by guanethidine (1–10 μM) indicating that sympathetic nerve terminals were being stimulated. Xylazine (0.01–1 μM) also blocked the twitches. 3. In response to stimulation at 0.1 Hz the twitches of the urethral segment were larger but briefer than those of the testicular segment. However, the increase in tension with increase in stimulation frequency over the range 0.01–10 Hz was greater in the testicular than in the urethral segment. After a train of pulses at 1 Hz or above, the first few twitches of the testicular segment evoked by pulses applied at 0.1 Hz were facilitated, whereas twitches of the urethral segment were inhibited. 4. Noradrenaline (1–100 μM) and tyramine (1–100 μM) regularly enhanced twitches in response to stimulation at 0.1 Hz in the testicular segment but often reduced those in the urethral segment. Contractions in response to these amines occurred more regularly and were stronger in the testicular than in the urethral segment. The α-adrenoreceptor antagonists phenoxybenzamine (0.01 μM), phentolamine (10 μM) and thymoxamine (10 μM) blocked contractions and blocked or reversed the twitch enhancement produced by noradrenaline and tyramine. These observations indicate that the density of excitatory α-adrenoreceptors is greater at the testicular end of the tissue. 6. Twitch inhibition evoked by noradrenaline or by tyramine in urethral segments was resistant to blockade by phenoxybenzamine (0.01 μM), phentolamine 10 μM), thymoxamine (10μM) and propranolol (10 μM). 7. A histological comparison of the two ends of the vas deferens indicated that at the urethral end there was more circularly arranged muscle and that this interrupted bundles of longitudinally arranged muscle. The testicular end was thinner but had the higher proportion of longitudinally arranged fibres. 8. The differences between the two ends of the vas deferens in the arrangement of muscle layers and in the response to sympathetic nerve stimulation and to drugs may be of physiological significance in relation to the transport of sperm from the epididymis to the urethra.     

OPIATES INHIBIT THE DOPAMINERGIC ENHANCEMENT OF THE RENAL RESPONSE TO ALDOSTERONE IN THE RAT

1. Both naloxone, an opiate antagonist, and levorphanol, an opiate agonist, inhibit the enhanced renal response to aldosterone produced by both ?-dopa pretreatment and a high K⁺ diet. 2. This supports the evidence for a common mechanism of action for the enhancement of the renal response to aldosterone produced by ?-dopa and a high K⁺ diet. Whether this mechanism is dopaminergic or opiate is uncertain. 3. The inhibition of the enhanced response, produced by ?-dopa, by opiates is consistent with previous findings of displacement of ³H-dopamine from renal homo-genates by opiates and supports the hypothesis that the binding sites relate to the renal response to aldosterone.     

VASOCONSTRICTOR RESPONSES TO COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM IN CYCLOSPORIN-INDUCED HYPERTENSION IN THE RAT

1. Since plasma renin activity is increased in cyclosporin A (CsA)-induced hypertension in the rat, the role of the vascular renin-angiotensin system (RAS) in CsA-induced hypertension was investigated in rat mesenteric resistance vessels. 2. Female Wistar rats received CsA (10 mg/kg per day, s.c.) or vehicle for 30 days. CsA treatment increased tail-cuff systolic blood pressure (CsA treated 135 ± 3 mmHg vs control 125 ± 1 mmHg, P<0.0001). 3. Mesenteric resistance arteries (200–300 μm) were isolated and mounted in a microvessel myograph. Concentration-response curves to tetradecapeptide renin substrate (10-¹¹-10^?6 mol/L), angiotensin I (10-^l1-10^?6 mol/L) and angiotensin II (10-¹²-10^?6 mol/L) showed no differences between CsA-treated and control groups. 4. Mesenteric vascular angiotensin-converting enzyme (ACE) characteristics were determined by radioligand binding. There were no differences in the content or affinity of ACE between CsA-treated and control rats. 5. These results suggest that the mesenteric vascular RAS does not play a major role in CsA-induced hypertension in the rat.     

ATTENUATION OF PRESSOR RESPONSES TO SYMPATHETIC STIMULI IN THE RAT BY ENALAPRIL

Intravenous administration to pithed Wistar rats of the angiotensin converting enzyme inhibitor enalapril (0.1-1.0 mg/kg) lowered the diastolic blood pressure and reduced pressor responses occurring during electrical stimulation (1-30 Hz) of the spinal sympathetic outflow. These doses of enalapril given intravenously also attenuated pressor responses to intravenous injection of the muscarinic ganglion stimulant McNeil-A-343 (50, 100, 150 micrograms/kg) and noradrenaline (0.1-5.0 micrograms/kg). Enalapril (1.0 mg/kg, i.v.) reduced pressor responses to the nicotinic ganglion stimulant 1,1-dimethyl-4-phenyl-piperazinium (300 micrograms/kg, i.v.). These results confirmed that the actions of enalapril resemble those of captopril in the pithed rat, by causing reductions in both blood pressure and pressor responses to sympathetic stimuli.