杜仲绿原酸对高脂小鼠血液流变学作用研究

旨以研究杜仲绿原酸对高脂高胆固醇诱导的高血脂模型小鼠血液流变学的影响,以昆明小鼠为实验动物,随机分成5组:阴性对照组,模型对照组和低剂量(25 mg/kg BW)、中剂量(50 mg/kg BW)、高剂量(100 mg/kg BW)杜仲绿原酸组,每组10只.后4组饲以高脂饲粮,同时小鼠灌胃杜仲绿原酸4周,实验结束,分别测定各组小鼠血液流变学参数、血清和肝脏的抗氧化酶活性和脂质过氧化产物MDA含量及其总抗氧化能力和羟自由基清除率.高脂血症小鼠的全血粘度、血浆粘度、红细胞压积、血沉、纤维蛋白原、红细胞刚性指数和聚集指数显著降低(P＜0.05),红细胞变形指数显著提高(P＜0.05),小鼠血清和肝脏SOD、GSH-Px水平、总抗氧化能力和羟自由基清除能力均显著升高(P＜0.05),MDA水平显著降低(P＜0.05).在高脂膳食条件下,杜仲绿原酸能有效提高血液的抗氧化防御功能(包括抗氧化力、抗氧化酶活性)、改变血液流变学参数等,降低血液粘度、红细胞刚性和聚集,增强变形能力,使细胞膜的流动性增高,其中以中剂量效果相对较好.     

急性低氧性缺氧小鼠血液粘度与红细胞流变性变化

目的:观察小鼠急性低氧性缺氧(AHH)后红细胞流变性与血液粘度的变化。方法:32只健康昆明小鼠均分为:对照组、AHH组(复制模型,分为5 min、8 min、11 min三个亚组),在相应时间点,快速颈部脱臼后,从心尖取血,检测各组小鼠血液粘度与红细胞流变性指标。结果:与对照组相比,低氧5 min组各切变率下的全血粘度、全血相对粘度、全血还原粘度均显著降低,红细胞变形指数显著升高;低氧8 min组和低氧11 min组的群体细胞电泳时间显著延长、细胞电泳长度与细胞迁移率显著降低;低氧8 min组的全血相对粘度、全血还原粘度、红细胞聚集指数均显著高于、红细胞变形指数显著低于低氧5 min组。结论:AHH可引起小鼠血液粘度降低、红细胞电泳能力下降。     

小鼠网织红细胞微观流变学特性的研究

按Bishop方法,在小鼠血液里诱导生成大量网织红细胞,然后提取网织红细胞,对其电泳率、渗透脆性、膜的流动性、细胞的变形能力和取向性进行了系统研究。研究结果表明网织红细胞在转变为成熟红细胞的短短时间内,其微观流变学特性发生了明显的变化：电泳率变小、渗透脆性变好、膜的流动性变大、细胞的变形能力变强、取向性变好,最终发育成具有全面功能的成熟红细胞。     

不同品种实验兔血液流变学特性

目的分析比较市售中国白兔与我院自繁培育的封闭群新西兰白兔血液流变学特性的差异。方法采集新西兰白兔和中国白兔的血液样品,分别检测比较其WBV（高、中、低切变率）、PV、HCT、ESR等14项血液流变学指标。结果 （1）新西兰白兔与中国白兔不同性别间血液流变学特性没有显著性差异（P〉0.05）;（2）新西兰白兔和中国白兔血液流变学指标中,血浆粘度ηP,还原粘度低切Rls,还原粘度中切Rms,还原粘度高切Rhs及红细胞电泳指数RIE5个指标间有显著差异（P〈0.05）。其余9项指标差异不显著（P〉0.05）。结论实验兔的血液流变学特性与品种有一定的相关性。     

葛根素对肺心病大鼠血液流变学和肺动脉压的影响

目的:观察葛根素对肺心病大鼠血液流变学和肺动脉压的影响。方法:40只SD大鼠随机分为4组(n=10):对照组,模型组,葛根素低剂量(300 mg/kg ip)和高剂量组(600 mg/kg ip),参考薛氏常压低氧方法建立肺心病大鼠模型,常压低氧4周后测定大鼠血浆粘度,全血粘度,红细胞容积,纤维蛋白原和红细胞聚集指数等血液流变学指标和平均肺动脉压。结果:葛根素能显著降低肺心病大鼠血浆粘度,全血粘度,红细胞容积,纤维蛋白原(P<0.05),对红细胞聚集指数无显著性作用(P>0.05),显著降低模型组降低肺动脉压(P<0.05)。结论:葛根素对肺心病大鼠有治疗效果,为临床治疗肺心病提供实验依据。     

临产孕妇血液流变性研究

研究临产孕妇血液流变性的11项指标的改变,并与健康育龄妇女进行对照.结果表明临产孕妇体外血栓形成的长度、血栓湿重、血栓干重、血浆比粘度、红细胞电泳时间及血沉方程K 值等均明显高于对照组(P<0.01).全血比粘度与红细胞压积低于对照组(P<0.05),全血还原粘度、红细胞内粘度和 TK 值在两组间无显著差异.认为在妊娠后期孕妇血液呈高凝状态.其主要原因是红细胞聚集性增高及血浆粘度增高,与红细胞变形能力及红细胞压积关系不明显.文中还探讨了各因素的相互影响。     

低强度激光对人红细胞生物物理特性的影响

研究不同功率的低强度He-Ne激光对正常人体红细胞流变学特性影响。以正常人体红细胞为研究对象,测量了低强度He-Ne激光在不同照射时间、不同功率条件下红细胞的变形、取向、膜流动性、膜的微粘度和渗透脆性的变化情况。结果表明:照射后红细胞的变形性和膜流动性增强、渗透脆性下降。照射对红细胞流变学特性影响显著,其中激光能量为0.24 J、照射血样为2 mL时取得的照射效果最佳。     

肝郁脾虚证模型大鼠血流变及TXB2、PGF1a的变化

目的:探查中医肝郁脾虚证模型的血流变及相关调节因子的状态。方法:采用慢性束缚应激 过度疲劳 饮食失节法建立大鼠肝郁脾虚证模型,测定大鼠造模三周、自然恢复一周时的血流变和血浆TXB2、PGF1a。结果:与正常组相比,模型组大鼠造模三周150/s、38/s、10/s、5/s切变率下的全血粘度和还原粘度均显著升高(P＜0．001),红细胞聚集指数显著降低(P＜0．001),红细胞压积显著升高(P＜0．01),红细胞变形指数无显著性差异(P＞0．05);血浆TXB2显著升高(P＜0．001),6-keto-PGF1a显著降低(P＜0．05), TXB2/PGF1a显著升高(P＜0．01);模型组大鼠第四周150/s、38/s、10/s、5/s切变率下的全血粘度和还原粘度仍显著升高(P＜0．001或P＜0．01);红细胞聚集指数显著降低(P＜0．001);红细胞压积与变形指数无显著性差异(P＞0．05);血浆TXB2和TXB2/PGF1a显著降低(P＜0．05),6-keto-PGF1a显著升高(P＜0．05)。结论:肝郁脾虚证大鼠存在血液高粘和血栓易形成状态,恢复期血液高粘同时伴有扩血管因素的加强。提示肝郁脾虚证有血流变的异常和血浆TXA2-PGI2的平衡失调,主要涉及到血小板和血浆因素的参与。     

糖基化磷脂酰肌醇锚定高密度脂蛋白结合蛋白1——影响血浆甘油三酯代谢的新基因

近年研究发现,脂蛋白脂酶(lipoprotein lipase,LPL)水解血浆富含甘油三酯的脂蛋白这一脂解过程中,糖基化磷脂酰肌醇锚定高密度脂蛋白结合蛋白1(glycosylphosphatidylinositol-anchoredhigh density lipoprotein-binding protein 1,GPIHBP1)起到了非常重要的作用。它能够结合LPL和乳糜微粒,发挥脂解平台的作用;同时它也参与LPL向毛细血管内皮细胞的转运。GPIHBP1基因敲除小鼠和GPIHBP1基因突变的病人发生严重高乳糜微粒血症。GPIHBP1的发现丰富了人们对于血浆脂蛋白代谢的认识,并为治疗高乳糜微粒血症提供了新的途径。     

全身稳恒磁场暴露对糖尿病性动脉粥样硬化大鼠血脂和血液流变学的影响

目的:探索全身暴露强度为4.0 m T中强度稳恒磁场对于糖尿病性动脉粥样硬化的血脂和血液流变学影响,以明确稳恒磁场对糖尿病性动脉粥样硬化的潜在作用效果。方法:选择3月龄雄性SD大鼠30只,随机等分至空白对照组、糖尿病组及糖尿病磁场暴露组。糖尿病和糖尿病磁场暴露组的大鼠采用链脲佐菌素+维生素D3+高脂饮食组合作用法建立糖尿病性动脉粥样硬化大鼠模型,对糖尿病磁场暴露组施加2小时/天、强度为4.0 m T的全身稳恒磁场暴露,连续刺激8周后,检测空腹血糖、血清胰岛素、血脂四项(血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇以及低密度脂蛋白胆固醇)以及血液流变参数(低切全血粘度、中切全血粘度、高切全血粘度以及血浆粘度)。结果:稳恒磁场暴露显著抑制了糖尿病动脉粥样硬化大鼠血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇的升高(P0.05),同时也显著降低了低切、中切和高切全血粘度以及血浆粘度(P0.05),但对血糖和血清胰岛素的影响不显著(P0.05)。结论:中强度稳恒磁场可显著降低糖尿病性动脉粥样硬化大鼠的血脂水平并改善其血液流变学。     

Hemorheological abnormalities in lipoprotein lipase deficient mice with severe hypertriglyceridemia

Severe hypertriglyceridemia (HTG) is a metabolic disturbance often seen in clinical practice. It is known to induce life-threatening acute pancreatitis, but its role in atherogenesis remains elusive. Hemorheological abnormality was thought to play an important role in pathogenesis of both pancreatitis and atherosclerosis. However, hemorheology in severe HTG was not well investigated. Recently, we established a severe HTG mouse model deficient in lipoprotein lipase (LPL) in which severe HTG was observed to cause a significant increase in plasma viscosity. Disturbances of erythrocytes were also documented, including decreased deformability, electrophoresis rate, and membrane fluidity, and increased osmotic fragility. Scanning electron microscopy demonstrated that most erythrocytes of LPL deficient mice deformed with protrusions, irregular appearances or indistinct concaves. Analysis of erythrocyte membrane lipids showed decreased cholesterol (Ch) and phospholipid (PL) contents but unaltered Ch/PL ratio. The changes of membrane lipids may be partially responsible for the hemorheological and morphologic abnormalities of erythrocytes. This study indicated that severe HTG could lead to significant impairment of hemorheology and this model may be useful in delineating the role of severe HTG in the pathogenesis of hyperlipidemic pancreatitis and atherosclerosis.     

A Case Of Severe Neuropat Hy Associated With Hypertriglyceridemia

ObjectiveTo describe a case of severe neuropathy associated with hypertriglyceridemia.MethodsWe describe the clinical and laboratory findings of the study patient and review the relevant literature.ResultsA 45-year-old woman presented to the emergency department with recurrent abdominal pain and severe peripheral neuropathy. Her laboratory data revealed elevated lipase and a very high triglyceride concentration (> 10 000 mg/dL), consistent with a diagnosis of recurrent hypertriglyceridemia-induced pancreatitis. Workup for peripheral neuropathy showed normal concentrations of thyrotropin, fasting blood glucose, vitamin B₁₂, and creatinine, as well as a normal hemoglobin A_1c level, serum protein electrophoresis, and urine protein electrophoresis. Rapid plasma reagin antibodies, antinuclear antibodies, and lyme antibodies were not detected. In the absence of other identifiable causes, hypertriglyceridemia was deemed the likely etiology of severe neuropathy in this patient.ConclusionsPeripheral nerve conduction abnormalities can be identified in patients with mild hypertriglyceridemia in the absence of symptoms. Early recognition and aggressive management of hypertriglyceridemia may prevent the complications of severe peripheral neuropathy.(Endocr Pract. 2008;14:1020-1022)     

血流变学指标及血清学指标在骨折延迟愈合患者中的临床意义

目的:探讨血流变学和血清学指标在骨折延迟愈合患者中的变化及其临床意义。方法:随机选取2010年1月~2016年6月在我院进行手术治疗的骨折延迟愈合及骨折正常愈合患者各90例,分别为观察组与对照组,对比分析两组患者术后第1、8、12周时血清可溶性血管细胞黏附分子1(sVCAM-1)、胰岛素样生长因子1(IGF-1)、血小板衍生生长因子(PDGF)及人可溶性细胞间黏附分子1(sICAM-1)和红细胞刚性指数、红细胞聚集指数、血浆黏度的差异。结果:术后第1、8、12周两组血清学及血流变学各指标整体相比差异均具有统计学意义(均P0.05),且组内两两比较均具有统计学差异(均P0.05)。术后8、12周观察组血清s ICAM-1、sVCAM-1、红细胞刚性指数、红细胞聚集指数、血浆黏度均高于对照组,而血清PDGF、IGF-1均低于对照组,比较差异均具有统计学意义(均P0.05)。结论:骨折患者血清sICAM-1、PDGF、IGF-1、sVCAM-1及红细胞刚性指数、红细胞聚集指数、血浆黏度水平会随着病程进展发生变化,并且血清sICAM-1、sVCAM-1及红细胞刚性指数、红细胞聚集指数、血浆黏度水平的升高,血清PDGF、IGF-1水平的降低可能是引起骨折延迟愈合的重要因素,对于骨折患者的临床治疗具有重要临床意义。     

Cells, proteins, and certain physical-chemical properties of brook trout (Salvelinus fontinalis) blood

Laboratory brook trout were used to evaluate, refine, or develop biochemical procedures for the analysis of fish blood. Analytical values were obtained for the following blood properties: total and differential leucocytes and erythrocytes; erythrocyte and plasma proteins (by electrophoresis); plasma refractive index; erythrocyte sedimentation rate; erythrocyte osmotic fragility; blood surface tension and density; haemoglobin; and packed cell volume. These blood factors are discussed with reference to fish health and disease and to changes caused by deleterious quantities of water pollutants.     

"从督论治"针刺治疗颈性眩晕的随机对照临床研究

摘要 目的：观察"从督论治"针刺治疗颈性眩晕的临床应用价值。方法：选取上海市中医医院2020年5月~2022年3月期间收治的296例颈性眩晕患者，采用双色球法将其分为研究组、对照组，各为148例。研究组接受"从督论治"针刺治疗，对照组接受常规针刺治疗。对比两组中医疗效、临床症状评分[颈性眩晕症状与功能评估量表（ESCV）、视觉疼痛模拟评分（VAS）]、动脉血流速度、血液流变学指标。结果：研究组的临床总有效率高于对照组（P<0.05）。治疗后，研究组ESCV评分高于对照组，VAS评分低于对照组（P<0.05）。治疗后，研究组基底动脉（BA）和大脑双侧（L、R）椎动脉（VA）的血管搏动指数（PI）低于对照组，平均血流速度（Vm）高于对照组（P<0.05）。治疗后，研究组全血粘度-高切（HBV）、全血粘度-低切（LBV）、红细胞压积（HCT）、血浆粘度（PV）、红细胞聚集指数（AI）、全血还原粘度（RV）、红细胞刚性指数（IR）、血沉（ESR）、纤维蛋白原（FIB）、红细胞电泳时间（EET）低于对照组（P<0.05）。结论："从督论治"针刺治疗颈性眩晕，可有效改善疼痛、眩晕症状，调节脑血流速度、血液流变学指标。     

葛根素对U14宫颈癌小鼠血液流变学、脾淋巴细胞增殖及细胞毒性影响

摘要 目的：研究葛根素治疗对U14宫颈癌小鼠血液流变学、脾淋巴细胞增殖活性及对宫颈癌细胞毒性的影响。方法：45只雌性昆明小鼠随机分为对照组、模型组和葛根素组。模型组和葛根素组小鼠通过腋下注射U14小鼠宫颈癌细胞建立U14宫颈癌移植瘤小鼠,并且葛根素小鼠通过葛根素灌胃进行治疗,对照组和模型组小鼠给予等量生理盐水。比较各组小鼠血流变学、脾淋巴细胞增殖活性及对宫颈癌细胞毒性。结果：经葛根素治疗的葛根素组宫颈癌小鼠肿瘤重量显著低于模型组小鼠（P<0.05）,葛根素治疗宫颈癌小鼠的抑瘤率是（42.91±12.91）%。宫颈癌小鼠低切/高切全血粘度、血浆粘度值以及血细胞比容均显著升高（P<0.05）,而葛根素治疗可显著降低宫颈癌小鼠低切/高切全血粘度、血浆粘度值以及血细胞比容（P<0.05）。宫颈癌小鼠脾脏重量、脾脏指数和脾淋巴细胞体外增殖能力均显著下降（P<0.05）,而葛根素治疗可显著提高宫颈癌小鼠脾脏重量、脾脏指数和脾淋巴细胞体外增殖能力（P<0.05）。此外,经葛根素治疗的宫颈癌小鼠脾淋巴细胞对U14宫颈癌细胞细胞毒性显著高于模型组宫颈癌小鼠（P<0.05）。结论：葛根素治疗可降低U14宫颈癌小鼠血液粘度、改善血流变性质,并且可以提高脾淋巴细胞的增殖活性和对宫颈癌细胞的杀伤力。     

Multimerization of Glycosylphosphatidylinositol-anchored High Density Lipoprotein-binding Protein 1 (GPIHBP1) and Familial Chylomicronemia from a Serine-to-Cysteine Substitution in GPIHBP1 Ly6 Domain

GPIHBP1, a glycosylphosphatidylinositol-anchored glycoprotein of microvascular endothelial cells, binds lipoprotein lipase (LPL) within the interstitial spaces and transports it across endothelial cells to the capillary lumen. The ability of GPIHBP1 to bind LPL depends on the Ly6 domain, a three-fingered structure containing 10 cysteines and a conserved pattern of disulfide bond formation. Here, we report a patient with severe hypertriglyceridemia who was homozygous for a GPIHBP1 point mutation that converted a serine in the GPIHBP1 Ly6 domain (Ser-107) to a cysteine. Two hypertriglyceridemic siblings were homozygous for the same mutation. All three homozygotes had very low levels of LPL in the preheparin plasma. We suspected that the extra cysteine in GPIHBP1-S107C might prevent the trafficking of the protein to the cell surface, but this was not the case. However, nearly all of the GPIHBP1-S107C on the cell surface was in the form of disulfide-linked dimers and multimers, whereas wild-type GPIHBP1 was predominantly monomeric. An insect cell GPIHBP1 expression system confirmed the propensity of GPIHBP1-S107C to form disulfide-linked dimers and to form multimers. Functional studies showed that only GPIHBP1 monomers bind LPL. In keeping with that finding, there was no binding of LPL to GPIHBP1-S107C in either cell-based or cell-free binding assays. We conclude that an extra cysteine in the GPIHBP1 Ly6 motif results in multimerization of GPIHBP1, defective LPL binding, and severe hypertriglyceridemia.     

Lithium-Induced Hypothyroidism: Oxidative Stress and Osmotic Fragility Status in Rats

The present study was conducted to explore the possible effects of different doses of lithium carbonate on thyroid functions, erythrocyte oxidant–antioxidant status, and osmotic fragility. Twenty-four Wistar-type male rats were equally divided into three groups: groups I and II received 0.1 and0.2 % lithium carbonate in their drinking water, respectively, for 30 days. The rats in group III served as controls, drinking tap water without added lithium. At the end of the experimental period, the erythrocyte osmotic fragility and the levels of triiodothyronine (T₃), thyroxine (T₄), thyroid-stimulating hormone (TSH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were measured in blood samples. Compared to controls, there was a statistically significant increase of TSH but decreases of the T₃ and T₄ levels in group II. Both experimental groups showed a statistically significant increase of the maximum osmotic fragility limit. The minimum osmotic fragility values of the animals in group II were statistically higher than those of controls. The standard hemolytic increment curve of both experimental groups was shifted to the right when compared to the curve obtained from the controls. Also, relative to controls, the activities of MDA and SOD were significantly higher and the GSH level lower in group II, but not so in group I. The results of the present study show that treatment with lithium carbonate may result in thyroid function abnormalities, increased oxidative damage, and possible compromise of the erythrocyte membrane integrity resulting from increased osmotic fragility.     

解毒通络生津颗粒联合羟基氯喹对原发性干燥综合征患者血液流变学及血清IgG、IgA、CRP水平的影响

目的:探讨解毒通络生津颗粒联合羟基氯喹对原发性干燥综合征(pSS)患者血液流变学及血清免疫球蛋白G(Ig G)、免疫球蛋白A(Ig A)、C-反应蛋白(CRP)水平的影响。方法:选取2017年1月-2017年9月期间我院收治的60例pSS患者为研究对象,采用随机数字表法将患者分为对照组(n=30)和观察组(n=30)。对照组给予硫酸羟基氯喹治疗,观察组在此基础上联合解毒通络生津颗粒治疗,比较两组患者的血液流变学指标、Ig G、Ig A和CRP水平,同时评价两种治疗方案的疗效和不良反应。结果:治疗前两组患者血液流变学指标相比差异均无统计学意义(P0.05)。治疗后观察组全血高切粘度、全血低切粘度、血浆粘度和红细胞沉降率(ESR)均较治疗前降低,且观察组全血低切粘度和血浆粘度低于对照组(P0.05)。治疗前两组患者Ig G、Ig A和CRP水平相比差异均无统计学意义(P0.05)。治疗后观察组Ig G、Ig A和CRP水平均较治疗前降低,且低于对照组(P0.05)。观察组的不良反应发生率为13.33%,低于对照组的46.67%,差异有统计学意义(P0.05)。对照组总有效率为43.33%,低于观察组的为70.00%,差异有统计学意义(P0.05)。结论:解毒通络生津颗粒和硫酸羟基氯喹联合应用能够有效改善pSS患者血液流变学及免疫学指标,增强患者免疫力,且安全性较好,值得进一步推广使用。     

Increased plasma apoM levels impair triglyceride turnover in mice

ObjectiveApolipoprotein M (apoM) is an essential transporter of plasma Sphingosine-1-Phosphate (S1P), typically attached to all lipoprotein classes, but with a majority bound to high density lipoproteins (HDL). ApoM-deficient mice display an increased activity in brown adipose tissue and a concomitant fast turnover of triglycerides. In what manner apoM/S1P affect the triglyceride metabolism is however still unknown and explored in the present study.MethodsTriglyceride turnover and potentially associated metabolic pathways were studied in the female human apoM transgenic mouse model (apoM-Tg) with increased plasma apoM and S1P levels. The model was compared with wild type (WT) mice.ResultsApoM-Tg mice had a reduced plasma triglyceride turnover rate and a lower free fatty acid uptake in subcutaneous adipocytes compared to WT mice. Screening for potential molecular mechanisms furthermore revealed a reduction in plasma lipase activity in apoM-Tg animals. Overexpression of apoM also reduced the plasma levels of fibroblast growth factor 21 (FGF21).ConclusionsThe study features the significant role of the apoM/S1P axis in maintaining a balanced triglyceride metabolism. Further, it also highlights the risk of inducing dyslipidaemia in patients receiving S1P-analouges and additionlly emphasizes the apoM/S1P axis as a potential therapeutic target in treatment of hypertriglyceridemia.