Brain natriuretic peptide enhances the endothelium-independent cAMP and vasorelaxant responses of calcitonin gene-related peptide in rat aorta

Calcitonin gene-related peptide (CGRP) causes vasorelaxation in rat aorta involving endothelium/nitric oxide (NO)-dependent elevations of both cAMP and cGMP levels. When endothelium is removed, preincubation with exogenous NO uncovers and potentiates direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP. This enhancing effect of NO potentially involves elevation of cGMP and inhibition of Type III (cGMPinhibitable) phosphodiesterase, causing accumulation of cAMP. However, NO may have other actions. The aim of the present study was to determine if brain natriuretic peptide (BNP), which elevates cGMP levels independent of NO, could enhance cAMP accumulations and vasorelaxations induced by CGRP in rat aortic rings denuded of endothelium. When added separately, neither CGRP (100 nM) nor BNP (10 nM) altered cAMP levels. When added in combination, CGRP (100 nM) and BNP (10 nM) significantly elevated cAMP levels (from control of 0.95 ± 0.08 to 1.53 ± 0.09 pmol/mg protein) at 2 min. BNP (10 nM) elevated cGMP levels 10-fold at 2 min and this response was not altered by co-administration of CGRP (100 nM).Pretreatment with BNP at concentrations as low as 1 nM in endothelium-denuded aortic rings greatly enhanced the direct vasorelaxant effects of CGRP (100 nM) (from control of 0% to 57.6 ± 6.8% relaxation of phenylephrineprecontractions). Our findings indicate that BNP enhances direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP in rat aorta, thus supporting the concept that cGMP inhibits cAMP metabolism and enhances CGRP-induced responses in aortic smooth muscle cells.     

Behavioral, biochemical and neurotoxicological actions of the alpha-ethyl homologue of p-chloroamphetamine

The present set of experiments was designed to examine the effects of extension of the alpha-methyl of p-chloroamphetamine (PCA) to an alpha-ethyl. Therefore, the alpha-ethyl homologue of PCA, 1-(4-chlorophenyl)-2-aminobutane (CAB), was compared to PCA in a number of pharmacological assays. CAB was 2-fold less potent than PCA at inhibiting synaptosomal uptake of [3H]5-hydroxytryptamine ([3H]5-HT), and 5-fold less potent at inhibiting uptake of [3H]dopamine ([3H]DA). In drug discrimination assays, CAB was approximately 3-fold less potent than PCA in animals trained to discriminate 3,4-methylenedioxymethamphetamine (MDMA) or its alpha-ethyl homologue, S-(+)-N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine (S-(+)-MBDB), from saline. Monitoring with in vivo microdialysis, 10 mg/kg of PCA caused a large increase in extracellular DA and a significant decrease in 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum. In contrast, 11 mg/kg CAB caused no increase and 22 mg/kg CAB caused only a slight increase in extracellular DA. Both doses of CAB caused a decrease in extracellular DOPAC. The potential 5-HT neurotoxicity of CAB was examined by measuring monoamine and metabolite levels and [3H]paroxetine binding at one week following acute doses. A 10 mg/kg dose of PCA caused an 80% decrease in cortical and hippocampal serotonergic markers, while an equimolar dose of CAB decreased only hippocampal 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels. However, 22 mg/kg of CAB produced a 20-40% decrease in all serotonergic markers. Thus, extension of the alpha-alkyl significantly decreases the dopaminergic effects of PCA. The similar decrease in relative 5-HT neurotoxicity and the decreased ability to alter dopaminergic systems in vivo and in vitro supports the involvement of DA in the neurotoxicity of PCA.     

增产菊胺酯对雄性小鼠生殖激素的影响

为了探讨增产菊胺酯引起小鼠精了生成障碍的可能机理，本文研究了增产菊胺酯对雄性小鼠卵泡刺激素（ＦＳＨ）、黄体生成素（ＬＨ）及睾酮（Ｔ）的影响。小鼠经口染毒，隔天一次，连续１０次，第３５天处死。检验因清ＦＳＨ、ＬＨ没有明显变化，而睾丸组织睾酮含量出现剂理依赖性降低，高剂量组与对照组比较有显著性差异（Ｐ〈０．０５），结果表明，增产菊胺酯不影响ＦＳＨ、ＬＨ，而影响Ｔ的合成和分泌。这可能是增产菊胺酯对小鼠精     

钙拮抗剂TMB-8抑制BHQ,NE和KCl引起的培养乳牛基底动脉单个平滑肌细胞内游离钙的升高

用AR CM MIC阳离子测定系统,测量单个细胞内游离钙浓度([Ca²⁺]i),研究8-(N,N-二乙胺)-n-辛基 3,4,5-三甲氧基苯甲酸酯(TMB-8)对培养乳牛基底动脉平滑肌[Ca²⁺]i的作用。在细胞外钙浓度为1.3mmol·L^-1时,TMB-8(30μmol·L^-1)可明显抑制BHQ,NE及KCl引起[Ca²⁺]i的升高。在细胞外钙为零+EGTA 0.1mmol·L^-1时,TMB-8(10,30及100μmol·L^-1)可浓度依赖性地降低静息[Ca²⁺]i,TMB-8(30μmol·L^-1)可几乎完全阻断BHQ及NE引起[Ca²⁺]i的增加。研究表明TMB-8降低培养乳牛基底动脉平滑肌[Ca²⁺]i的机制,主要是抑制肌浆网Ca²⁺的释放,或增加肌浆网对Ca²⁺的摄入,并由此间接地抑制细胞外钙的内流。     

多发性肌炎的动物模型及雷公藤多甙对其疗效的研究

目的　寻找一种多发性肌炎的良好动物模型及其有效的治疗药物。　　方法　给动物注射同种大鼠的肌匀浆 ,观察其活动状态 ;通过肌肉组织染色及ELISA法 ,研究肌肉的病理学变化 ,同时给动物喂服雷公藤多甙观察药物疗效。　　结果　部分动物表现肌无力和肌萎缩 ,大多数肌肉组织学检查示肌纤维炎性变 ;免疫组化检查可见肌膜、肌内膜和肌束膜中有IgG沉积。动物服雷公藤多甙后肌肉病变明显减轻 ,其疗效与强的松相似。　　结论　用同种大鼠肌匀浆免疫动物可诱导出多发性肌炎的动物模型 ;雷公藤多甙能有效地治疗多发性肌炎。     

胎骨移植治疗骨肿瘤缺损：附10例报告

近3年来，用制备的胎骨充填良性骨肿瘤及病样病变术后骨缺损，经观察10例效果良好。胎骨因其自身组织学和生理学特点，具有抗原性小、诱导成骨活性高，利于“爬行各代”等优点。而且来源丰富、采制简单、储存容易、费用低度，是一种良好的植骨材料，特别适于儿童及年老体弱患者自身取骨困难的骨缺损植骨需要。但其为异体骨，有一定免疫原性，抗支撑强度略差，应注意严格无菌操作、消除免疫原性、配合使用内、外固定等措施。     

纤维支气管镜胸膜腔检查对原因不明胸腔积液的诊断价值

为评价纤维支所管镜行胸膜检查在诊断原因不明胸腔积液中的价值，用纤维支气管镜对１０例原因不明的胸腔积液患者进行胸腔检查。结果９例２检查后明确了病因，且无并发症，提示该法对于不明胸腔积液的诊断是一种阳性率高、安全、简便的检查方法。