脉冲式电磁辐射对大鼠血脑屏障影响的量效关系

目的 研究脉冲式电磁辐射(EMR)对大鼠血脑屏障(BBB)影响的量效关系。方法 采用伊思蓝静脉注射，荧光显微镜下观察不同脉冲次数的EMR辐照对大鼠BBB开放的影响。结果 伊思蓝在EMR诱发的大鼠BBB开放局部呈现荧光斑；随着EMR脉冲次数(0～200次)的增加，荧光斑数量增加、面积增大；荧光斑在EMR组全脑的分布，以皮质、丘脑、下丘脑、小脑、尾壳核和延髓较多。结论 不同脉冲次数EMR诱发大鼠BBB开放程度不同，随脉冲次数增加，血管通透性增强，200次时达开放高峰，皮质区BBB开放最明显。     

Renal interstitial pressure and tubuloglomerular feedback control in rats during infusion of atrial natriuretic peptide (ANP)

Atrial natriuretic peptide (ANP), injected at physiological concentrations, is known to induce both natriuresis and diuresis. It has been suggested by some investigators that these changes result from an increasing glomerular filtration rate (GFR), but others have been unable to demonstrate an increased GFR. The tubuloglomerular feedback (TGF) mechanism is an important regulator of GFR, and the sensitivity of TGF is decreased during ANP administration. Furthermore, resetting of TGF is, in most instances, related to changes in renal interstitial hydrostatic and oncotic pressures. It is also known that ANP may increase capillary permeability which may change renal interstitial pressure. The present study was performed to examine renal interstitial pressures and the TGF mechanism during ANP infusion. In accordance with previous studies, TGF sensitivity was found to be decreased. The tubular flow rate which elicited half the maximal drop in stop-flow pressure (P_sf) was increased from 18.5 to 25.7 nl min^-1. In contrast, ANP infusion resulted in a decreased interstitial hydrostatic pressure and an increased interstitial oncotic pressure. From previous experiments, such changes in interstitial pressures would be expected to increase TGF sensitivity. The changes in interstitial pressure cannot, therefore, directly explain the resetting of the feedback mechanism. In conclusion, the present paper shows a decreased renal net interstial pressure after intravenous administration of ANP.     

决明子对营养性肥胖大鼠的影响

目的:观察大鼠自由饮用决明子水煎剂对营养性肥胖的影响,并初步探讨其作用机制.方法:用高营养饲料制备肥胖大鼠模型,让大鼠在生理状态下自由饮用不同浓度的决明子水煎剂,观察其对大鼠体质量和糖、脂代谢及抗脂质过氧化作用等的影响.结果:60g/L浓度的决明子水煎剂可明显降低营养性肥胖大鼠的体质量[(336.0±22.1)g→(299.5±20.3)g,P＜0.01],Lee's指数[(358.6±8.6)→(341.8±7.3),P＜0.05]、空腹血清甘油三酯[(1.4±1.3)→(0.8±0.4)mmol/L,P＜0.05]、胰岛素[(35.6±13.4)→(22.8±9.5)mU/L,P＜0.01]和丙二醛[(4.6±0.7)→(2.9±0.3)nmol/L,P＜0.01]含量,游离脂肪酸(339±88)μmol/L→(283±64)μmol/L含量也有下降趋势,总抗氧化能力(10.7±1.4)kU/L→(11.7±1.0)kU/L水平有升高趋势.结论:决明子水煎剂能明显抑制营养性肥胖大鼠体质量的增加,可能改善或纠正胰岛素抵抗,增强抗脂质过氧化作用,其作用机制可能与其调节葡萄糖及脂肪代谢等有关.     

大鼠脑多梗死性栓塞痴呆模型的建立

 目的建立大鼠脑多梗死性痴呆(MID)模型及观察指标,评价药物对该模型的作用。方法采用从颈外动脉逆行注入微血栓颗粒的方法,制备MID模型,通过对术后大鼠的苏醒时间测定、倾斜板实验、神经症状评分3个方面评价动物的一般状态;采用大鼠穿梭箱实验、水迷宫实验检测各组大鼠学习记忆能力;并测定脑中丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的活性,考察MID大鼠的行为学异常以及其作用机制。结果MID大鼠与正常组、假手术组比较,苏醒时间明显延长,在倾斜板上停留的时间显著变短,神经症状评分有显著差异;穿梭箱实验中电击时间明显延长,水迷宫实验学习记忆潜伏期延长;同时脑组织中MDA含量明显升高,SOD活力显著降低。给予药物氢化麦角碱(商品名:喜得镇)治疗后症状有所改善。结论该造模方法能显著造成大鼠脑多梗死性痴呆的多项体征,符合临床病理过程,为进一步判定一些药物是否具有治疗MID的前景打下基础。     

平喘合剂治疗小儿哮喘发作期的临床研究

认为哮喘是外因作用于内因的结果 ,痰瘀伏肺为其宿根 ,外邪引触伏痰、痰瘀胶结、阻塞气道、痰阻气逆为其病机 ,寒热夹杂为其病性。具有宣肺化痰、降气平喘、清热活血功效的中药平喘合剂可明显改善哮喘发作期患儿的肺通气功能 ,明显降低患儿血浆中sICAM 1、IgE水平 ,与对照组比较有显著性差异 (P <0 .0 1,P <0 .0 5 ) ,推测其作用机制可能与减轻气道阻塞、调节免疫反应及抑制气道炎症等多个环节有关     

家兔化学裸露心肌标本制备及其张力-pCa关系

家兔右室乳头肌在含3mM EDTA、5mM Na_2ATP、10mM Tris、140 mM KCl的溶液中浸浴150min,其Ca~(2+)通透性显著增高。Ca~(2+)浓度为10~(-7)M时,便可产生张力,10~(-4.6)M时,张力达到最大。相对张力-pCa(Ca~(2+)浓度的负对数)关系近似一S形曲线,产生50％最大张力的Ca~(2+)(pCa_(50))约为10~(-6.6)M。同法制备的大鼠乳头肌Ca~(2+)通透性未见增高。     

青少年型帕金森病的临床特征

目的　探讨青少年型帕金森病 (PD)的临床特征。方法　对 2 8例青少年型PD患者的临床资料进行回顾性分析。结果　 2 8例中 5例有家族史 ,呈常染色体隐性遗传 (AR JP) ;症状轻、病程长 ,症状常左右不对称 ,腱反射活跃和症状波动较常见 ;头部CT或MRI检查一般正常 ;对多巴制剂反应良好 ,但其所诱发的症状波动出现早。与散发性PD患者相比 ,AR JP患者发病年龄更早 ,为 (2 0 6± 5 6 8)岁 ,病程更长 ,为 (9 5±5 77)年 ,而病情较轻、症状波动和腱反射活跃更多见 ,多巴制剂不良反应更常见。结论　青少年型PD具有独特的临床特征 ,可能是一个独立的疾病实体。AR JP与散发性青少年型PD临床特征不同 ,提示二者可能具有不同的发病机制。     

Effects of vitamin D3 and cyclosporin A on HgCl2-induced autoimmunity in Brown Norway rats

BACKGROUND.: Mercuric chloride (HgCl₂ induces a lymphoproliferative disorderand autoimmune glomerulonephritis in Brown Norway (BN) rats.This syndrome is the consequence of T cell-dependent polyclonalB cell activation and autoantibody production. We have previouslyshown that HgCl₂-induced autoimmune perturbations can be preventedin BN rats by the administration of cyclosporin A (CsA). Themost potent vitamin D₃ metabolite 1,25(OH)₂ D₃ (Vit D₃) sharescertain immunomodulatory properties with CsA. We therefore choseto compare the effects of Vit D₃ to those of CsA in BN ratstreated with HgCl₂ in order to establish whether Vit D₃ eitheralone or in combination with CsA can attenuate an autoimmunesyndrome in vivo. METHODS.: BN rats were treated with HgCl₂ according to a standard protocol.Subgroups of rats were also given CsA alone, Vit D₃ or syntheticanalogues of Vit D₃ alone, or combinations of both agents. Differentdoses and routes of administration were compared. The followingmarkers of disease activity were evaluated: mortality, peakproteinuria, serum IgE concentrations, and renal immunoglobulindeposition. RESULTS.: Disease activity was markedly attenuated in all rats treatedwith CsA alone. Vit D₃ and certain of its synthetic analoguesadministered alone also tempered the autoimmune process, butto a lesser extent than did CsA. The effect of CsA alone wasso potent, that no additive or synergistic effects could bedemonstrated when CsA was administered in combination with VitD₃. CONCLUSIONS.: Despite similar described immunomodulatory effects in vitro,CsA is clearly more effective than Vit D₃ in preventing HgCl₂autoimmune disease in BN rats. This suggests that there is adifference in the cellular targets of these two agents in vivo,and/or a difference in the potency with which HgCl2-triggeredimmune activation is suppressed.     

大鼠颌下腺切除对CCl4所致肝损伤修复的影响

实验大鼠分为颌下切除＋ＣＣｌ４组，假手术＋ＣＣｌ４对照组及正常对照组，结果假手术＋ＣＣｌ４第２ｄ时Ⅲ带细胞轻度受损，第４ｄ、８ｄ时受损面积略大，第１２ｄ时大部分细胞恢复，而颌下腺切除＋ＣＣｌ４组则损伤明显，第８ｄ时胞质极度稀疏，１２ｄ时大部分细胞尚未恢复，与假手术组比较，该组Ｆｅｕｌｇｅｎ反应略弱，ＰＡＳ反应减弱，第４～８ｄ时较明显，Ｇ－６－Ｐ，ＳＤＨ活性均减弱。结果表明颌下腺切除导致内源性表皮生     

Role of vasopressin on excitatory amino acids mediated pressor responses in the periaqueductal gray area

In order to evaluate the role played by vasopressin on pressor responses elicited by stimulation of the periaqueductal gray (PAG) area by excitatory amino acids we carried out in vivo studies in genetically vasopressin deficient rats (Brattleboro). Microinjections of l-glutamic acid (glutamate, 0.6 to 60 nmol/rat) or N-methyl-d-aspartic acid (NMDA, 0.07 to 7 nmol/rat) into the PAG area of freely moving Brattleboro rats induced increases of arterial blood pressure values significantly lower than those obtained in Long Evans rats (control) (glutamate in Brattleboro rats: from +2±1 mmHg to 16±3 mmHg; glutamate in Long Evans rats: from +16±2 mmHg to +36±4 mmHg; NMDA in Brattleboro rats: from +5±2 mmHg to +34 ±8 mmHg; NMDA in Long Evans rats: from +18±7 mmHg to 80±9 mmHg; n=5). Similarly, in anaesthetized Brattleboro rats (urethane 1.2 g/kg i.p.) pressor responses to NMDA microinjections (0.7 nmol/rat) into the PAG area were significantly lower than in Long Evans rats (controls) (+15±3 mmHg vs +24±4 mmHg). In Long Evans rats NMDA injection also reversed blood pressure decrease induced by ganglionic blocker, hexamethonium and/or losartan (3 mg/kg i.v.), an AT1 receptor antagonist. In Brattleboro rats, NMDA injection did not reverse blood pressure decreases induced by hexamethonium (5 mg/kg i.v.). Moreover, hexamethonium induced blood pressure decrease was not reversed by acetylcholine injection (137 nmol/rat) into the PAG area of anaesthetized Long Evans rats, but if injected before hexamethonium, acetylcholine was able to increase blood pressure (+25±3 mmHg). Our results document: i) the importance of the PAG area in the control of cardiovascular system; ii) the involvement of excitatory amino acids in the neural control of vasopressin release; iii) the close relationship between glutamate and vasopressin in the central blood pressure regulation. Received: 1 April 1997 / Accepted: 2 February 1998