低分子肝素治疗肾病综合征临床疗效观察

目的 观察低分子肝素（LMWH）对原发性肾病综合征的疗效和安全性。方法 30例原发性肾病综合征病人随机分为两组，对照组给予强的松。LMWH组在强的松治疗的基础上每日加用LMWH皮下注射。结果 LMWH组血纤维蛋白原（FIB），D－二聚体浓度明显下降，24h尿蛋白明显下降，血浆白蛋白明显上升。结论 LMWH可以明显改善原发性肾病综合征的高凝状态，延缓肾功能。     

实验性肾病综合征中的胰岛素样生长因子-1

目的 :了解实验性阿霉素肾病综合征 (NS)的大鼠血清、尿及肝脏组织中胰岛素样生长因子 -1(IGF -1)浓度的变化 ,探讨肾病综合征生长障碍的发病机制。方法 :检测Wistar系雄性大鼠阿霉素致肾病综合征组和正常对照组的24h尿蛋白排泄量和血、尿、肝组织的IGF -1水平。IGF -1的测定采用放射免疫法。结果 :与正常对照组相比 ,肾病组大鼠血清IGF -1明显降低 (P<0.01) ;尿IGF -1明显升高 (P<0.01) ;两组肝组织内的IGF -1浓度差别无统计学意义 (P>0.05)。尿IGF -1浓度与血清IGF -1浓度呈负相关 (r= -0.78,P<0.01),而与24h尿蛋白排泄量呈正相关 (r=0.78,P<0.01)。结论 :NS大鼠伴随着尿蛋白排泄的增多 ,其尿IGF -1的排泄也增多 ,导致其血清IGF -1水平降低     

低分子肝素钙治疗肾病综合征临床观察

目的：观察低分子肝素钙（LMWH）治疗肾病综合征（NS）的临床效果。方法：随机选择36例NS患者分为两组,对照组18例常规治疗,治疗组18例在常规治疗基础上加用LMWH治疗2周;观察24小时尿蛋白定量,血白蛋白、血脂、血胆固醇、尿量,水肿情况。结果：治疗2周后,与对照组比较,治疗组24小时尿蛋白定量,血白蛋白,血脂、血胆固醇、尿量、水肿、并发症（出血及血栓形成）方面,较对照组显著下降（P〈0.05）。结论：LMWH能减少NS患者尿蛋白,缓解高凝状态,是治疗抗凝和NS安全有效的药物。     

低分子肝素钙治疗小儿原发性肾病综合征的疗效观察

目的 观察低分子肝素钙（LMWH）对小儿原发性肾病综合征（NS）的临床疗效。方法 将63例小儿原发性NS分为常规组和LMWH治疗组对比观察。结果 LMWH组4周后尿蛋白和总胆固醇下降,血清白蛋白增高,D－二聚体（D－D）浓度下降,且均较常规组明显（P＜0．05）,利尿、消肿及尿蛋白转阴时间相应缩短（P＜0．05）。结论 LMWH治疗后可改善小儿原发性NS高凝状态,有利于其早期缓解,且出血危险性小,使用方便安全。     

激素治疗对肾病综合征肾小管功能的影响

目的：探讨激素治疗肾病综合征(NS)时对肾小管功能的影响。方法：测定28例NS患者激素治疗前、治疗后和27例正常人血清白蛋白(ALB)、24h尿蛋白定量和圆盘电泳、尿NAG、GAL、尿酸化功能和渗透压。结果：用药前NS患者尿NAG、GAL明显高于正常组，用药后明显下降，且与血清白蛋白呈负相关，与尿蛋白定量、尿大和中相对分子质量蛋白比例呈正相关；尿渗透压明显低于正常组，但用药前后差别无统计学意义；酸化功能3组相比差别无统计学意义。结论：激素治疗NS能降低尿蛋白、升高血清白蛋白，促进受损的近端小管上皮细胞修复，改善近端小管功能，对远端小管和集合管无明显影响。     

低分子肝素治疗原发性肾小球肾炎的临床探讨

目的探讨低分子肝素(LMWH)对原发性肾小球肾炎治疗的作用及机理.方法21例病理诊断原发性肾小球肾炎患者,随机分为两组,对照组中表现慢性肾炎综合征者单用洛汀新,表现肾病综合征(NS)者加强的松;观察组再加用LMWH、法安明.[HTH〗结果治疗8周后两组尿蛋白、内生肌酐清除率(Ccr)、血清白蛋白、血脂及肾脏病理均改善,其中Ccr及病理改善观察组明显优于对照组(P＜0.01及＜0.05);抗Xa因子活性(AXa)观察组明显高于对照组,而两组肝功能及凝血指标无显著差异.结论LMWH可减轻原发性肾小球肾炎病理损害及延缓肾功能进展,且出血等副作用小.     

卡托普利联合低分子肝素在肾病综合征治疗中的效果

目的:探讨卡托普利联合低分子肝素在肾病综合征治疗中的效果。方法:纳入研究的40例患者,均为我院于2016年1月~2018年1月收治的肾病综合征患者,采用电脑随机分组的方式,分为20例对照组以及20例研究组。对照组接受卡托普利治疗,研究组接受卡托普利联合低分子肝素治疗,对比观察24h尿蛋白、血浆白蛋白、总胆固醇。结果:研究组24h尿蛋白、总胆固醇低于对照组,血浆白蛋白高于对照组,差异具有统计学意义(P<0.05)。结论:肾病综合征接受卡托普利联合低分子肝素治疗,能有效缓解临床症状,促进疾病的好转,疗效显著,值得在临床上推广。     

1,25(OH)2D3对阿霉素肾病大鼠HGF表达的影响

目的:观察肝细胞生长因子(hepatocyte growth factor,HGF)在阿霉素肾病大鼠血液及肾组织中的表达,探讨1,25(OH)2D3对微小病变肾病综合征(MCNS)HGF表达的影响及其对微小病变肾病综合征的保护机制.方法:雄性Wistar大鼠110只随机分为正常组(32只)、肾病组(78只).肾病组单次尾静脉注射阿霉素5mg/kg,建立MCNS模型,正常组给予注射等量生理盐水.造模后第7天检测全部大鼠24h尿液中尿蛋白含量,尿蛋白＞30mg/24h者为MCNS造模成功.剔除5只,将造模成功的大鼠(共73只)再随机分为两组:肾病对照组(n=37),治疗组(n=36).于造模后第7d、14d、28d、42d测定各组大鼠24h尿蛋白、血清白蛋白、胆固醇含量,同时采用夹心ELISA方法检测各组大鼠血液、肾组织中HGF的水平.结果:与正常组比较对照组大鼠血液及肾组织中HGF表达有所增加(P＜0.01).治疗组HGF的表达水平较对照组显著升高(P＜0.01).而尿蛋白排泄量与对照组比较,则有明显降低(P＜0.01).结论:1,25(OH)2D3对于微小病变肾病综合征至少有部分保护作用,其机制可能为通过上调HGF的表达,从而对阿霉素肾病大鼠肾脏起保护作用.     

低分子肝素在肾病综合征中应用观察

目的探讨肾病综合征患者应用低分子肝素治疗前后的变化。方法36例肾病综合征患者在常规治疗基础上加用低分子肝素,对照组20例常规治疗,使用低分子肝素2周,观察24小时尿蛋白定量,血白蛋白、血脂、血胆固醇、尿量,浮肿,并发症(急性肾功能不全)情况。结果肾病综合征患者在治疗2周后,24小时尿蛋白定量,血白蛋白,血脂、血胆固醇、尿量、浮肿,并发症(急性肾功能不全)方面,较对照组显著下降(P<0.05)。结论肾病综合征患者抗凝治疗应作为常规手段,对目前患者症状、预防并发症有重要作用。     

低分子肝素钙联合贝那普利辅助治疗原发性肾病综合征的疗效观察

目的 观察低分子肝素钙联合贝那普利辅助治疗原发性肾病综合征(PNS)患者的疗效.方法 将80例PNS患者随机分为2组,对照组40例采用泼尼松和环磷酰胺治疗,观察组40例则在对照组治疗的基础上加用低分子肝素钙联合贝那普利治疗.观察、比较2组治疗前后血浆白蛋白、尿白蛋白定量、肌酐清除率、尿素氮、血脂变化,血浆凝血酶原时间、活化部分凝血活酶时间,纤维蛋白原及不良反应等.结果 2组患者治疗后血浆白蛋白升高,24 h尿蛋白定量减少,肌酐清除率、尿素氮及血脂下降,与治疗前比较差异有统计学意义(P<0.05);观察组治疗后疗效优于对照组(P<0.05).观察组治疗后几项凝血指标较治疗前及对照组治疗后均降低,差异均有统计学意义(P<0.05或P<0.01).观察组总有效率95%及完全缓解率80.0%显著高于对照组的80.0%,60%,差异有统计学意义(P<0.05).低分子肝素钙和贝那普利可改善高凝状态,降低尿蛋白,升高血清白蛋白,改善肾功能.结论 低分子肝素钙联合贝那普利辅助治疗原发性肾病综合征可明显提高疗效,可作为抗凝的常规措施,对改善患者症状,预防并发症有重要作用.     

Excretion of metabolites of prostacyclin and thromboxane by rats with nephrotoxic nephritis: effects of interleukin-1.

1. To obtain direct evidence of abnormal eicosanoid biosynthesis in rats injected with anti-glomerular-basement-membrane antibodies (a-GBM), products derived from thromboxane A2 (TXA2) and prostacyclin (PGI2) were measured in 24 h urine collections before and after a-GBM. 2. Administration of a-GBM (9.5 mg) caused albuminuria, decreased creatinine clearance, increased numbers of intra-glomerular neutrophils and increased excretion of TXB2, 2,3-dinor-TXB2 (products of TXA2) and 6-oxo-PGF 1 alpha and 2,3-dinor-6-oxo-PGF 1 alpha (products of PGI2) at 24 h. 3. Interleukin-1 (IL-1 beta; 5 micrograms) alone caused an increase in PGI2 metabolite excretion but had no effect on TXA2 metabolites. It had no effect on creatinine clearance but increased numbers of glomerular neutrophils by approximately 4-5 fold compared to a-GBM. 4. Pretreatment of rats with IL-1 beta before a-GBM synergistically increased albumin excretion but only additively increased eicosanoid excretion. Numbers of intra-glomerular neutrophils and creatinine clearance were unchanged compared to IL-1 beta alone. 5. The cyclo-oxygenase inhibitor, ibuprofen (10 mgkg-1 i.p., twice daily for 4 days) inhibited both serum TXB2 production and urinary prostaglandin excretion. It also caused an almost complete attenuation of albumin excretion. Creatinine clearance and glomerular neutrophils remained unchanged after a-GBM/IL-1 beta. 6. We conclude that the 50% inhibition of thromboxane production induced by ibuprofen does not modify the fall in creatinine clearance of accumulation of neutrophils in the glomerulus caused by the a-GBM. This degree of inhibition of eicosanoid production was associated with a striking decrease in proteinuria, but this may reflect a haemodynamic rather than a disease modifying action.     

Delay of the initiation of hypertension in spontaneously hypertensive rats by CV-4151, a specific thromboxane A2 synthetase inhibitor

When CV-4151, a specific thromboxane (TX) A2 synthetase inhibitor, was given orally to 4 week old (4w) spontaneously hypertensive rats (SHR) daily for 3 weeks, the initiation of hypertension was delayed by about one week. The agent increased urinary excretion of water, sodium and creatinine, reduced that of TXA2 (as TXB2), increased that of PGI2 (as 6-keto-PGF1 alpha) and enhanced urinary PGI2/TXA2. In 4w Wistar-Kyoto rats (WKY) and 18w SHR was established hypertension, the agent had little effect on blood pressure and renal function. In isolated, perfused kidneys of 6w SHR, CV-4151 markedly inhibited both arachidonic acid-induced pressor action and production of TXA2. TXA2 synthetase activity in renal cortical microsomes of 5w SHR was approximately 1.5 times higher than that in age-matched WKY. CV-4151 inhibited TXA2 synthetase activity of medullary and cortical microsomes more effectively in 5w SHR than in age-matched WKY. Thus, in young SHR, the TXA2 synthetase inhibitor seemed to improve renal function by altering the balance of renal TXA2 and PGI2 biosynthesis and subsequently caused a delay in the initiation of hypertension. The present findings lend support to the idea that an imbalance in the renal TXA2-PGI2 biosynthesis may be involved in the initiation of hypertension in SHR.     

富硒平菇和亚硒酸钠对老年大鼠有关指标的影响

目的　探讨有关硒对老年大鼠 (18月龄 )凝血和纤溶功能有关指标的影响以及富硒平菇和亚硒酸钠对老年鼠合适的补充剂量 ,并比较富硒平菇和亚硒酸钠的优劣。方法　对 18月龄老年鼠进行实验 ,实验期12 3d ,分别观察添加亚硒酸钠或富硒平菇干粉的饲料 (含硒量为 0 2、0 2 5、0 4、0 6mg/kg)对血浆血栓素、前列环素、D 二聚体 (DD)、谷胱甘肽过氧化酶 (GSH PX)、超氧化物歧化酶 (SOD)、脂质过氧化物 (LPO)以及丙氨酸转氨酶(ALT)和实验前后体重变化的差异。结果　适量硒 0 2mg/kg饲料 ,补硒 0 4mg/kg饲料 ,对于老年大鼠前列环素 (PGI2 )含量的增高有促进作用 ,对血栓素A2 (TXA2 )有降低作用 ,对于PGI2 /TXA2 的比值和GSH PX活性的提高及LPO的降低均有促进作用。 0 6mg/kg饲料不能降低PGI2 /TXA2 的比值 ,并能造成D D含量增高和ALT活性有所提高 ,0 6mg/kg饲料组亚硒酸钠还能引起老年鼠体重下降 ,结果还提示富硒平菇优于亚硒酸钠。 结论　补硒应当慎重。     

六味地黄方对高脂血症大鼠血浆 ET、TXA2、PGI2水平及动脉内皮保护的影响

目的：研究六味地黄方对高脂血症大鼠血浆ET、TXA2、PGI2水平及动脉血管内皮保护的影响。方法：通过高脂饮食建立高脂血症大鼠模型,观察大鼠外周循环内皮细胞（CEC）、主动脉病理学、内皮素（ET）、前列腺素I2（PGI2）、血栓素A2（TXA2）的变化。结果：六味地黄方能减少高脂血症大鼠外周CEC及主动脉内皮细胞损伤;降低高脂大鼠血清ET、血浆TXA2,升高血浆PGI2水平。结论：六味地黄方对高脂血症大鼠内皮细胞具有保护作用,其作用机制可能与改善内皮细胞分泌功能有关。     

Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia

Prostacyclin (PGI2), thromboxane A2 (TXA2) and F2-isoprostanes, prostaglandin F2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI2, TXA2 and F2-isoprostanes in patients with hypertension and hyperlipidemia (HH group), we measured the major urinary metabolites of PGI2: 6-keto PGF1alpha (Keto) and 2,3-dinor-6-keto PGF1alpha, (Dinor), those of TXA2:TXB2 and 11-dehydro TXB2 (Dehydro), and urinary 8-isoprostane (Iso) in 34 patients. Urinary excretion of Dinor was significantly lower in patients than in controls and that of Dehydro was significantly higher in patients than in controls. Keto, TXB2 and Iso were not significantly different between them. Antiplatelet agents decreased not only TXA2 metabolites but also PGI2 metabolites. Urinary C-peptide immunoreactivity was correlated with Dinor and Dehydro. After administration of eicosapentaenoic acid (EPA), total cholesterol (T-cho) and triglycerides (TG) significantly decreased. Although prostanoids did not show significant change, changes in T-cho were correlated with changes in Dinor and changes in Iso. These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI2, TXA2 and F2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism.     

卡托普利对肾血管性高血压大鼠血小板胞浆[Ca^2＋]i及血浆TXA2／PGI2…

AIM: To study the effect of captopril (Cap) on platelet cytosolic free calcium concentration ([Ca2+]i), platelet aggregation (PAg), and plasma TXA2/PGI2 ratio in the renovascular hypertensive rats. METHODS: Blood pressure was measured once a week by tail-cuff microphonic manometer. Platelet [Ca2+]i was measured by Fura 2-AM. Plasma angiotensin II (Ang), thromboxane A2 (TXA2), and prostacycline (PGI2) were measured by radioimmunoassay. RESULTS: Platelet [Ca2+]i and PAg increased (P < 0.01), while plasma Ang and TXA2/PGI2 ratio elevated (P < 0.05) in the renovascular hypertensive rats; platelet [Ca2+]i and plasma TXA2/PGI2 ratio reduced markedly after i.g. Cap 100 mg.kg-1.d-1 compared with saline for 2 wk. CONCLUSION: The altered TXA2/PGI2 after Cap treatment contributed to the improvement of the platelet [Ca2+]i and PAg.     

甲基莲心碱及与牛磺酸合用对大鼠血小板聚集和血栓形成的影响

甲基莲心碱（Ｎｅｆ）ｉｇ抑制大鼠血栓形成，单用Ｎｅｆ及与牛磺酸（Ｔａｕ）合用抑制率分别为５３．３１％和７４．３０％；对ＡＤＰ、胶原、凝血酶诱导的血小板聚集抑制率，Ｎｅｆ及Ｎｅｆ＋Ｔａｕ分别为５５．８％和７３．４％，４３．４５％和５９．３％，６５．３３％和７８．５％。两药对血浆纤维蛋白原、优球蛋白溶解时间均无明显影响。Ｎｅｆ能有效抑制ＡＤＰ诱导的血小板ＴＸＡ２释放，与Ｔａｕ合用抑制作用增强，而对血浆ＰＧＩ２含量无作用，Ｎｅｆ在ｉｖ后３０ｍｉｎ内对大鼠血清总胆固醇含量亦无影响，但与Ｔａｕ合用后能降低血清总胆固醇水平。     

Arachidonic acid metabolism in glucocorticoid-induced hypertension

1. Products of metabolism of arachidonic acid, such as 20-hydroxyeicosatetraenoic acid (20-HETE), thromboxane A(2) (TXA(2)) and prostaglandin I(2) (PGI(2)), regulate vascular tone. Among them, 20-HETE is a potent constrictor in small arteries that also has natriuretic properties. The present study investigated changes in urinary concentrations of 20-HETE and metabolites of TXA(2) and PGI(2) in glucocorticoid-hypertension in rats, a sodium-independent model. 2. Male Sprague-Dawley rats were treated with saline, adrenocorticotrophic hormone (ACTH; 0.2 mg/kg) or dexamethasone (20 microg/kg) by daily s.c. injection for 12 days. Systolic blood pressure (SBP) was measured using the tail-cuff method. Metabolic cages were used for 24 h urine collection. Thymus weight and urinary concentrations of 20-HETE, TXA(2) and PGI(2) were determined. 3. In the present study, SBP was increased by both ACTH (from 102 +/- 2 to 134 +/- 7 mmHg; n = 10; P < 0.01) and dexamethasone (from 106 +/- 5 to 122 +/- 4 mmHg; n = 10; P < 0.01). Thymus weight, a marker for glucocorticoid activity, was significantly decreased by both ACTH and dexamethasone (56 +/- 9 and 76 +/- 5 mg/100 g bodyweight, respectively; n = 10; P' < 0.01) compared with the saline control (151 +/- 5 mg/100 g bodyweight; n = 20). Urinary 20-HETE excretion was increased by ACTH (501 +/- 115 pmol/g creatinine; n = 10; P' < 0.05) but not by dexamethasone (126 +/- 13 pmol/g creatinine; n = 10) compared with the saline control (219 +/- 54 pmol/g creatinine; n = 20). Neither ACTH nor dexamethasone affected urinary excretion of TXB(2) or PGI(2) compared with the saline control. 4. In conclusion, ACTH but not dexamethasone increased urinary 20-HETE excretion in male Sprague-Dawley rats. Urinary concentrations of the metabolites TXB(2) and PGI(2) were unchanged in both models of glucocorticoid-hypertension. The vasoconstrictor 20-HETE may play a role in the genesis of ACTH-induced hypertension.     

川芎嗪对急性胰腺炎大鼠胰腺血流量影响与治疗作用

应用牛磺胆酸钠诱发大鼠急性胰腺炎(AP)模型.观察了川芎嗪(TMP)对AP大鼠胰腺血流量和存活率的影响.发现TMP显著增加胰腺相对血流量及灌注量.减轻胰腺病理形态损伤.提高大鼠存活率。通过测定血浆TXB_2、6-酮PGF_la及血小板聚集率.显示TMP能纠正AP时TXA_2-PGI_2失衡.降低血小板聚集率。提示TMP的治疗作用可能系通过调节TXA_2-PGI_2平衡而改善AP时胰腺血液循环紊乱而实现。     

小麦胚芽油抗动脉粥样硬化的药效学研究

目的：观察小麦胚芽油（wheat germ oil,WGO）对动脉粥样硬化（atherosclerosis,AS）大鼠的治疗效果,并探讨其抗 AS 的可能作用机制。方法连续高脂乳剂灌胃4周,制作 AS 大鼠模型,分别给予各组大鼠连续灌胃不同剂量 WGO 8周;HE 染色光镜下观察大鼠主动脉弓病理形态的改变;酶联免疫吸附试验（ELISA）法检测各组大鼠血清中前列环素（Prostacyclin 2, PGI2）、血栓素 A2（Thromboxane 2,TXA2）及内皮素-1（Endothelin-1,ET-1）的含量。结果2．0 g·kg －1的 WGO 能明显改善 AS大鼠主动脉弓的病理状态,基本恢复正常状态;与模型组比较,1．0、2．0 g·kg －1 WGO 均可显著提高 AS 大鼠血清中 PGI2含量,明显降低 TXA2、ET-1水平（P ＜0．05）。结论WGO 能明显改善 AS 大鼠的动脉粥样硬化状态。其作用机制可能为小麦胚芽油具有良好的调节 PGI2、TXA2平衡,抑制血栓形成,修复内皮损伤以及较强的抗氧化作用。