前列腺素E1在治疗急性肾功能衰竭中的作用

目的:为了探讨前列腺素E1在治疗急性肾功能衰竭中的作用.方法:分别设立治疗组与对照组,对治疗组给予前列腺素E1,两组患者均观察2W,按疗效判定标准判定疗效.结果:治疗组治愈率为30%,好转率为50%,均高于对照组;而无变化情况占20%低于对照组.结论:应用前列腺素E1治疗急性肾功能衰竭,对于缩短其疗程起到了令人满意的效果.     

一氧化氮在内皮素-1诱导神经元凋亡中的作用

目的:证实内皮素-1(endothelin-1,ET-1)(2×10-7M)诱导培养大鼠大脑皮层神经元凋亡及刺激神经元释放内源性一氧化氮(NO)的作用;了解NO在该浓度ET-1诱导神经元凋亡中的作用。方法:神经元培养取自乳鼠大脑皮质细胞,培养5d后分3组实验:对照组(空白)、ET-1组(2×10-7M)、ET-1 L-NAME(左旋精氨酸甲酯,NO合成抑制剂,100mM)组,继续培养24h。收集细胞,用流式细胞仪定量检测凋亡率;收集培养上清液,用硝酸还原酶法检测NO浓度。结果:ET-1(20nM)处理后24h,培养大鼠大脑皮层神经元的凋亡率显著高于对照组(P<0.001)。L-NAME明显阻断了ET-1诱导神经元凋亡的作用,与ET-1组比较,凋亡率降幅为40%(P<0.05)。经ET-1处理后24h,神经元培养液中NO浓度均较对照组显著高(P<0.001)。而L-NAME完全抑制了ET-1引起的培养液中NO的升高。结论:ET-1(20nM)有诱导培养大鼠大脑神经元凋亡的作用;该作用与ET-1刺激培养大鼠大脑神经元合成和释放内源性谷氨酸和NO增加有关;NO合酶抑制剂能显著减轻ET-1诱导的神经元凋亡率。提示ET-1诱导培养大鼠大脑神经元凋亡通过NO途径。     

肾通注射液对急性肾衰家兔内皮素和一氧化氮的影响

目的：探讨活血化瘀药肾通注射液对急性肾衰家兔肾血管活性物质的影响。方法：健康雄性大耳白兔40只，随机平分为正常组、模型组、肾通治疗组和丹参治疗组，分别观测各组血肌酐（Scr）、尿素氮（BUN）、24h尿蛋白排泄率、滤过钠排汇分数（FENa）、内生肌酐清除率（Ccr）、血Na^ 、K^ 以及内皮素（ET）和一氧化氮（NO）水平，同时检测肾组织ET（NET）和NO（NNO）含量变化。结果：急性肾衰家兔经肾通、丹参注射液治疗后，肾功能各项指标均有显著改善（肾通效果似优于丹参，但两者无显著性差异），肾血管活性物质产生明显变化，血ET显著下降，NO水平升高，肾局部ET和NO与模型组比较差异更为显著。结论：肾通注射液对急性肾衰有防治作用，广泛调节肾血管活性物质，特别是对肾局部ET和NO的调节从而显著改善肾血流动力学是其重要的作用机理之一。     

血液透析对慢性肾功能衰竭患者血浆内皮素影响的研究

为了研究内皮素（ＥＴ）在慢性肾功能衰竭（ＣＲＦ）患者中的变化，及血液透析（ＨＤ）对ＥＴ的影响，对４５例ＣＲＦ患者和３０例正常人采用放射免疫分析法（ＲＩＡ）测定血浆ＥＴ水平。结果显示，ＣＲＦ患者血浆ＥＴ明显升高，ＨＤ组明显高于非透析组；ＨＤ后血浆ＥＴ明业降低，ＣＲＦ组ＥＴ与血清肌酐（Ｓｃｒ）呈正相关，提示ＣＲＦ患者血浆ＥＴ的升高与肾功能损害有关；ＨＤ后ＥＴ下降与ＨＤ后钠潴留减少有关。     

血液透析对慢性肾功能衰竭患者血浆内皮素水平的影响及临床意义

目的　观察血液透析对慢性肾衰患者血浆内皮素 (ET)水平的影响以及ET水平与血压和超滤量之间的关系。方法　正常对照 2 0例、慢性肾功能衰竭维持性血透患者 30例 ,放射免疫法测定血浆ET ,同时检测血清Scr、BUN。结果　对照组血浆ET为 (5 2 .30± 7.2 6 )pg ml;患者组透析前后ET分别为(2 5 6 .0 6± 139.6 8)pg ml ,(2 2 5 .83± 10 7.5 2 )pg ml;慢性肾衰患者血透前后血浆ET水平浓度明显高于对照组(P <0 .0 1,P <0 .0 1) ;血透后ET水平较血透前降低 ,但无统计学意义 (P >0 .0 5 ) ,伴高血压的血透患者血浆ET水平明显高于血压正常者 ,超滤量 >2 .0kg者血ET水平较超滤量 <2 .0kg者显著增高 (P <0 .0 1)。结论　血浆ET水平增高与高血压互为促进因素 ,可形成恶性循环 ,加速肾功能损害 ;故应保持血透间期体重增加 <2 .0kg ,以降低ET增高幅度。     

内皮素-1在暴发性肝功能衰竭发生中的作用

目的　观察内皮素 (ET) - 1在暴发性肝功能衰竭发生中的作用。方法　以硫代乙酰胺 (TAA)灌胃染毒的方法建立大鼠暴发性肝功能衰竭模型 ,利用生化方法测定血浆内毒素及内皮素水平 ,采用 ET抗血清拮抗 ET- 1的作用。结果　 TAA组血浆内皮素、内毒素和血清丙氨酸转氨酶水平显著高于正常对照组 (P<0 .0 5 ) ;TAA +ET- Ab组血浆内皮素、内毒素和丙氨酸转氨酶水平显著低于 TA A组 (P<0 .0 5 ) ,内皮素与内毒素水平呈显著正相关 (P<0 .0 1) ,内皮素抗血清可以拮抗 ET- 1的作用并可减轻肝坏死的程度。结论　内皮素可上调血浆内毒素水平 ,与暴发性肝功能衰竭的发生密切相关     

内皮素-1和一氧化氮／一氧化氮酶测定在2型糖尿病中的意义

目的探讨内皮素-1（ET-1）和一氧化氮（NO）／一氧化氮酶（NOS）在2型糖尿病的发生、发展及预后的临床价值。方法将受试者分为2型糖尿病组和健康对照组检测其血浆ET-1和血清NO／NOS水平。结果2型糖尿病组血浆ET-1和血清NOS水平均高于健康对照组（P〈0．01）;而NO水平低于健康对照组（P〈0．01）。有并发症组血浆ET-1和血清NOS水平均高于无并发症组（P〈0．01,P〈0．05）;NO水平低于无并发症组（P〈0．01）。结论2型糖尿病的发生、发展及预后可能与血中ET-1、NO／NOS失衡有一定的联系。     

内皮素在慢性肾衰中的水平及意义

内皮素 (ＥＴ)三个成员中ＥＴ 1活性最强。肾脏是ＥＴｓ合成的主要场所 ,也是清除的场所。 1996年1月～ 1998年 12月我们检测慢性肾功能衰竭(ＣＲＦ)及肾衰合并高血压 2 4例患者血浆中的ＥＴ 1水平 ,并与原发性高血压患者及正常健康者进行对比 ,以探讨ＥＴ 1在ＣＲＦ中的意义。对象与方法对象 :ＣＲＦ组 2 4例 ,男 18例 ,女 6例 ,平均年龄52 2岁 ;其中合并高血压 19例为ＣＲＦ高血压组。原发性高血压组 16例 ,男 11例 ,女 5例 ,平均年龄50 4岁。健康对照组 2 0例 ,男 12例 ,女 8例 ,平均年龄 39 9岁。方法 :空腹采静脉血 2ｍｌ,注入…     

阿昔洛韦致急性肾功能衰竭1例

患者，女，59岁，平素体健，无高血压、糖尿病、肾病和药物过敏史，乙肝病毒携带者。2005年7月12日在皮肤病专科医院诊断为：右侧头颈带状疱疹。给予0．9％氯化钠注射液250ml＋阿昔洛韦0．5g（丽珠科益，批号：050509）ivd，qd；同时口服阿昔洛韦胶囊0．2g，tid；泼尼松10mg，po，bid；凉血解毒口服液10ml，bid；重组基因干扰素100万iu。im，qod，（长春长征基因药业，批号：041005—4）。     

免疫球蛋白和补体在慢性肾功能衰竭和急性肾功能衰竭鉴别诊断中的临床意义

目的 探讨免疫球蛋白及补体在慢性肾功能衰竭和急性肾功能衰竭鉴别诊断中的临床意义.方法 对80例慢性肾功能衰竭患者、64例急性肾功能衰竭患者和50例健康对照者采用速率散射比浊法检测免疫球蛋白及补体.结果 (1)慢性肾功能衰竭患者与健康对照相比较,IgG、IgM和补体C3、C4有显著性差异(分别是P＜0.001、P＜0.001、P＜0.001和P＜0.05);(2)急性肾功能衰竭与健康对照相比较,IgC、IgA有显著性差异分别是(P＜0.05和P＜0.001);(3)急性肾功能衰竭与慢性肾功能衰竭患者相比较,IgG、IgM和补体C3、C4有显著性差异(分别是P＜0.01、P＜0.001、P＜0.001和P＜0.05).结论 血清免疫球蛋白及补体的检测对慢性肾功能衰竭和急性肾功能衰竭的鉴别诊断有重要临床意义.     

Protective effect of nitric oxide on ischemia/reperfusion-induced renal injury and endothelin-1 overproduction

To elucidate the role of nitric oxide (NO) in the pathogenesis of ischemic acute renal failure, we examined the effects of (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409) and N(G)-nitro-L-arginine methyl ester (L-NAME) as a NO donor and a non-selective NO synthase inhibitor on ischemia/reperfusion-induced renal injury and renal endothelin-1 content. Ischemic acute renal failure was induced by occlusion of the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. At 24 h after reperfusion, renal function in untreated acute renal failure rats markedly decreased and histological examination revealed severe renal damage. In addition, increases in renal endothelin-1 contents were evident in the acute renal failure rats at 2, 6, and 24 h after reperfusion, respectively. Pretreatment with FK409 (1 or 3 mg/kg, i.v.) attenuated ischemia/reperfusion-induced renal dysfunction, histological damage, and endothelin-1 overproduction after reperfusion. In contrast, pretreatment with L-NAME (1 or 10 mg/kg, i.v.) aggravated renal injuries of acute renal failure rats at 24 h after reperfusion, and the effect is accompanied by further increases in the renal endothelin-1 content at 2 and 6 h, but not at 24 h, after reperfusion. These results suggest that suppressive effects of NO on the renal endothelin-1 overproduction induced by ischemia/reperfusion in an early phase are probably responsible for the protective effect of NO against ischemic acute renal failure.     

单纯性肾病综合征患儿血中NO与ET的测定

目的:了解小儿肾病综合征发病过程中血浆中NO,ET浓度的变化特点。方法:采用分光光度法及放射免疫分析法检测了27例单纯性肾病综合征患儿及20例健康对照儿童血浆中NO,ET浓度。结果:血浆NO,NOS,ET在肾病患儿,正常对照组分别为(44.90±9.74μmol/L,13.84±3.44 U/mL,194.41±46.42 pg/ml);(80.46±13.43μmol/L,32.20±3.80U/mL,79.02±13.37pg/ml)。肾病患儿NO,NOS值显著降低(P<0.01),ET值显著增高。NO与NOS呈正相关(r=0.8798),NO与ET呈负相关(r=-0.6965)。结论:血浆NO,ET的浓度变化在肾病综合征患儿的病理生理过程中起着一定作用。     

参附注射液对重症急性胰腺炎大鼠NO和ET-1的影响

目的本研究通过对参附注射液在SD大鼠重症急性胰腺炎模型上的使用,观察其对血清及胰腺组织NO和ET-1的影响,探讨其作用机理,为临床使用提供实验依据。方法48只SD大鼠随机分为3组：假手术组（n=16）、SAP组（n=16）、SF组（n=16）。假手术组开腹后仅翻动肠管,SAP组、SF组以3％牛磺胆酸钠2mL／kg逆行注入胆胰管,复制重症胰腺炎模型。制模成功后,SF组大鼠,尾静脉注射参附注射液,假手术组、SAP组给予等量生理盐水,每12h1次。各组分别于制模后12h、24h两个时间点取材。观测腹水,检测血清淀粉酶及血清和胰腺组织NO、ET-1浓度,并计算ET1／NO比值,胰腺组织行HE染色光镜检查形态学变化。结果各时点血清淀粉酶活性、胰腺病理评分：SAP组、SF组显著高于假手术组（P〈0．01）,SF组低于SAP组（P〈0．01）;血清、胰腺组织内ET-1、NO浓度：SAP组、SF组显著高于假手术组（P〈0．01）,SF组显著低于SAP组（P〈0．01）;血清、胰腺组织内ET-1／NO比值,SAP组显著高于假手术组（P〈0．01）,SF组与SAP组相比降低（P〈0．05,P〈0．01）。结论SF组与模型组相比较,血清、胰腺组织NO、ET-1浓度下降差异有统计学意义,与此同时血清淀粉酶活性,胰腺湿干重比值降低,表明参附注射液可减轻胰腺组织损害,对胰腺组织有保护作用。     

肝硬化门静脉高压症患者血浆NO和ET-1的临床意义

目的探讨肝硬化门脉高压患者血浆一氧化氮(NO)和内皮素1(ET-1)水平与食管静脉曲张和腹水的关系。方法76例肝硬化患者血浆NO、ET-1与其食管静脉曲张内镜评分、门静脉内径、腹水分级评分、血清白蛋白等四项指标进行非参数统计等级相关分析。结果血浆NO、ET-1与食管静脉曲张程度和门静脉内径呈正相关，与血清白蛋白呈负相关；血浆ET-1与腹水程度呈正相关。结论血浆NO和ET-1参与肝硬化门静脉高压症的病理机制。     

偏头痛患者外周血一氧化氮和内皮素含量变化的探讨

目的探讨偏头痛患者发作期、间歇期外周血NO、ET-1含量的变化。方法采用分光光度计及放射免疫法分别测定45例偏头痛患者发作期、41例偏头痛患者间歇期血清NO、ET-1含量,同时与健康查体者进行对照。结果偏头痛患者发作期血清NO、ET—1含量均明显高于健康对照组;间歇期患者血清NO含量明显下降,接近于健康对照组,而ET－1含量仍维持较高水平,与发作期患者比较无明显差异,而与健康对照组比较则差异明显。结论偏头痛患者发作期外周血NO、ET－1含量明显增高;间歇期患者NO含量接近正常水平,而ET－1含量仍维持在较高水平;NO及ET－1含量增高及平衡紊乱是偏头痛发生的重要影响因素。     

The effects of extended nitric oxide release on responses of the human non-pregnant myometrium to endothelin-1 or vasopressin

BackgroundUterotonic mediators: endothelin-1 (ET-1), arginine vasopressin (AVP), and nitric oxide (NO) play important roles in the regulation of uterine contractility. We hypothesize that NO affects both ET-1 or AVP. Therefore, this study investigated the involvement of extended exogenous NO release in the regulation of responses of the human non-pregnant myometrium to ET-1 and AVP.MethodsSpecimens were obtained from 10 premenopausal women, undergoing hysterectomy for benign gynecological disorders. Responses of the myometrial strips to ET-1 or AVP in the absence and presence of an exogenous NO donor (diethylenetriamine; DETA/NO; 10⁻⁴ mol/L) were recorded under isometric conditions. To inhibit endogenous NO, a competitive inhibitor of NO synthase, L-N^G-nitroarginine (L-NNA) was added to the organ bath.ResultsET-1 enhanced the spontaneous contractile activity of the myometrium more powerfully (p < 0.01) than AVP. Preincubation with exogenous NO weakened ET-1- or AVP-induced increases in this contractile activity (p < 0.05). However, unexpected results were obtained after preincubation with L-NNA and with DETA/NO then added. Both ET-1 and AVP induced augmented contractile effects in almost all concentrations compared with the responses to these peptides alone or after NOS synthase inhibition (both p < 0.01).ConclusionsThis study demonstrated for the first time that extended incubation with a NO donor influences the uterine muscle response evoked by ET-1 and AVP. Both endogenous and exogenous NO is involved in the control of the uterine responses to ET-1 or AVP of non-pregnant myometrium. Furthermore, both peptides stimulate increased uterine contractility when the local imbalance between the constrictive and relaxing mediators takes place.     

慢性肺心病患者血浆内皮素-1、一氧化氮和降钙素基因相关肽含量分析

目的　分析慢性肺心病 (CCP)患者血浆内皮素 1(ET 1)、一氧化氮 (NO)和降钙素基因相关肽(CGRP)检测的临床意义。方法　应用实验研究策略 ,分别测定CCP急性加重期 (A组 ,4 4例 )、缓解期 (B组 ,4 4例 )和健康对照组 (C组 ,30例 )ET 1、NO和CGRP的血浆含量。结果　ET 1血浆含量在A组、B组和C组分别是 ( 5 8 5 92± 2 2 4 70 ) pg/ml、( 4 7 6 70± 17 85 4 )pg/ml和 ( 39 0 5 0± 2 0 36 7) pg/ml,差异有显著意义 (F=8 5 5 8,P =0 0 0 0 )。NO血浆含量在A组、B组和C组分别是 ( 70 92 2± 31 5 81) μmol/L、( 5 8 110± 2 5 2 11)μmol/L和 ( 5 0 2 6 0± 18 2 4 8) μmol/L ,差异有显著意义 (F =5 873,P =0 0 0 4 )。CGRP血浆含量在A组、B组和C组分别是 ( 6 7 344± 32 0 92 ) pg/ml、( 5 2 2 0 5± 2 3 912 ) pg/ml和 ( 39 5 6 7± 15 75 3)pg/ml,差异有非常显著意义 (F =10 74 1,P =0 0 0 0 )。结论　CCP急性加重期ET 1、NO和CGRP血浆含量增高 ;缓解期ET 1和NO不增高 ,而CGRP仍高     

丹参多酚酸盐治疗早期慢性肾衰竭及对血浆ET-1和CGRP水平的影响

目的探讨丹参多酚酸盐在治疗早期慢性肾衰竭中的作用及机制。方法 54例患者随机分为2组,常规治疗组27例（简称常规组）;常规＋丹参多酚酸盐治疗组27例（简称研究组）。观察丹参多酚酸盐治疗前后肾功能、尿蛋白及血浆ET-1和CGRP水平的变化。结果 CRF患者血浆ET-1水平高于对照组,而血浆CGRP水平偏低;两者在治疗后均显著改善,但以研究组改善更为显著,与常规组治疗后比较,血浆ET-1水平降低（P〈0.05）,而血浆CGRP水平增高（P〈0.01）。CRF患者血浆ET-1水平与血清Scr、尿蛋白呈正相关;而血浆CGRP水平与后两者均呈负相关;血浆ET-1水平与CGRP呈负相关。丹参多酚酸盐治疗后,血浆ET-1水平与Scr、尿蛋白及血浆CGRP之间的相关关系和治疗前一致。结论丹参多酚酸盐能降低CRF患者血浆ET-1水平,增加血浆CGRP水平,减少尿蛋白,改善肾功能,故值得临床应用。     

Intrarenal haemodynamics and renal dysfunction in endotoxaemia: effects of nitric oxide synthase inhibition

1. This study investigated the effects of low dose endotoxin (lipopolysaccharide, LPS) on (i) systemic haemodynamics, (ii) renal blood flow (RBF), (iii) renal cortical and medullary perfusion and (iv) renal function in the anaesthetized rat. We have also investigated the effects of nitric oxide (NO) synthase (NOS) inhibition with N^G-methyl-L-arginine (L-NMMA) on the alterations in systemic and renal haemodynamics and renal function caused by endotoxin.
2. Infusion of low dose LPS (1 mg kg⁻¹ over 30 min, n=6) caused a late fall in mean arterial blood pressure (MAP, at 5 and 6 h after LPS), but did not cause an early (at 1–4 h after LPS) hypotension. The pressor effect of noradrenaline (NA, 1 μg kg⁻¹, i.v.) was significantly reduced at 1 to 6 h after LPS (vascular hyporeactivity). Infusion of L-NMMA (50 μg kg⁻¹ min⁻¹ commencing 60 min before LPS and continued throughout the experiment, n=7) abolished the delayed hypotension and significantly attenuated the vascular hyporeactivity to NA (at 2–6 h).
3. Infusion of LPS (1 mg kg⁻¹ over 30 min, n=6) caused a rapid (within 2 h) decline in renal function (measured by inulin clearance) in the absence of a significant fall in MAP or renal blood flow (RBF). L-NMMA (n=7) attenuated the impairment in renal function caused by LPS so that the inulin clearance in LPS-rats treated with L-NMMA was significantly greater than in LPS-rats treated with vehicle (control) at 3–6 h after infusion of LPS.
4. Endotoxaemia also caused a significant reduction in renal cortical, but not medullary perfusion (measured as Laser Doppler flux). Infusion of L-NMMA caused a significant further fall in cortical perfusion and a significant fall in medullary perfusion in the absence of changes in RBF.
5. Infusion of LPS resulted in a progressive increase in the plasma levels of nitrite/nitrate (an indicator of the formation of NO), so that the plasma concentration of nitrite/nitrate was significantly higher than baseline at 150 to 330 min after LPS. Infusion of L-NMMA attenuated the rise in the plasma concentration of nitrite/nitrate (at 270 and 330 min, P<0.05) caused by LPS.
6. Thus, the renal dysfunction caused by injection of low dose of endotoxin in the rat occurs in the absence of significant falls in blood pressure or total renal blood flow. Inhibition of NOS activity with L-NMMA attenuates the renal dysfunction caused by endotoxin (without improving intrarenal haemodynamics), suggesting that an overproduction of NO may contribute to the development of renal injury and dysfunction by causing direct cytotoxic effects.