海水肺内灌注对血小板聚集和凝血功能的影响

目的:了解海水淹溺对血小板聚集和凝血功能的影响。方法:用Modell方法向犬肺内灌注海水,模拟海水淹溺;将气管导管钳闭造成窒息作对照。定时抽血作血小板聚集和凝血功能有关指标检测。结果:淹溺组血小板计数于10～60分钟明显降低,血小板最大聚集率由基础值42.0％降至4.45％,凝血时间明显延长。窒息组血小板聚集仅于10分钟时短暂降低,凝血时间虽有延长,但于60分钟后已接近基础值。结论:海水肺内灌注较单纯窒息对血小板聚集和凝血功能的影响更明显。     

4%琥珀酰明胶、6%羟乙基淀粉和12%缩合葡萄糖对血小板聚集功能的体外研究

目的研究4％琥珀酰明胶(佳乐施，GF)、6％羟乙基淀粉(贺斯，HES)和12％缩合葡萄糖(益极疏，PG)三种胶体液对血小板聚集功能的影响。方法采健康人静脉血(n=10)，分为对照组(NS组)、GF组、HES组和PG组。以全血值为基础值，每组分为8：2和6：4两个稀释度。以二磷酸腺苷(ADP)为诱导剂．观察各组血小板最大聚集率(PAg Tmax)和聚集坡度(Slope)的变化(涡流密度测量法)。结果排除稀释因素影响，各胶体组均不同程度地抑制血小板聚集，PG的抑制作用最强，其次是HES，GF作用最小。结论胶体液抑制血小板聚集的作用是其抑制凝血功能的重要组成部分，临床应根据病人凝血功能状态合理选择不同的胶体液，以策安全。     

乌司他丁对剖宫产患者凝血及血小板聚集功能的影响

目的 观察乌司他丁对剖宫产患者术中凝血及血小板聚集功能的影响.方法 选择60例无血液疾病及凝血功能障碍、肝肾功能异常或服用相应药物的择期剖宫产患者,ASA Ⅰ或Ⅱ级,随机均分为乌司他丁组和生理盐水组.分别于胎儿娩出后给药前(T0)、给药后1 h(T1)、2 h(T2)、4 h(T3)采血测定凝血酶原时间(PT)、部分凝血活酶时间(APFT)、凝血酶时间(TT)、纤维蛋白原(FIB)、国际标准化比率(INR)及血小板1 min,5 min聚集率及最大聚集率(PAG1、PAG5、PAGM).结果 与T0时比较,乌司他丁组T1时PT、APTT延长(P＜0.05);T2时TT延长(P＜0.05).与生理盐水组比较,乌司他丁组T1时APTF、T2时TT延长(P＜0.05).两组PAG1、PAG5、PAGM组内及组间比较差异均无统计学意义.结论 围术期静脉滴注乌司他丁5 000 U/kg可改善剖宫产患者术中的高凝血状态,有助于预防术后深静脉血栓形成.     

异丙酚对上腹部手术病人血小板聚集及凝血功能的影响

目的评价异丙酚麻醉对病人血小板聚集及凝血功能的影响。方法41例择期行上 腹部手术病人,ASA I或Ⅱ级,年龄24-56岁,体重46—75 kg。静脉注射异丙酚、芬太尼、维库溴铵行 麻醉诱导,气管插管后行异丙酚靶控输注(TCI)麻醉,设定效应室靶浓度4μg／ml。分别于麻醉诱导前 (T0)、术前异丙酚TCI 30 min(T1)、术前异丙酚TCI 60 min(T2)、术前异丙酚TCI 120 min(T3)采集静脉 血,比浊法测量血小板最大聚集率,双波长荧光比值法测定血小板内游离Ca2 浓度([Ca2 ]i),以及测 定血栓弹性描记图参数和凝血四项指标:血浆部分凝血活酶时间、血浆凝血活酶时间、凝血酶原时间、 血浆纤维蛋白原浓度。结果与T0相比,T1-3时血小板最大聚集率及激活后[Ca2 ]i峰值均下降(P <0．01),静息状态[Ca2 ]i差异无统计学意义,凝血功能参数差异无统计学意义(P>0．05)。结论 异丙酚通过抑制Ca2 内流对血小板聚集产生抑制作用,而对凝血功能无明显影响。     

氟比洛芬酯对骨癌大鼠肾功能、凝血功能及其血小板聚集的影响

目的 连续7d腹腔注射氟比洛芬酯注射液,研究其对骨癌痛大鼠肾脏、凝血功能、血小板聚集影响. 方法 36只成熟雌性SD大鼠完全随机分为6组:肿瘤+生理盐水组(C组)、肿瘤+氟比洛芬酯10 mg· kg1·d-1组(CK10组)、肿瘤+氟比洛芬酯25 mg·kg-1·d-1组(CK25组)、肿瘤+氟比洛芬酯50 mg· kg-1·d-1组(CK50组)、氟比洛芬酯50 mg· kg-1·d-1单纯组(K50组)和假手术组+生理盐水组(sham组),每组6只.制作骨癌痛模型14 d后,每天分别腹腔注射相应剂量氟比洛芬酯或生理盐水2次,连续7d后处死大鼠.腹主动脉采血,检测血尿素氮(blood urea nitrogen,BUN)、肌酐(creatinine,Cr)、Na+、K+、凝血酶原时间(protrombin time,PT)、活化部分凝血活酶时间(activated partial thromboplastin time,APTT)、纤维蛋白原(fibrinogen,Fib)、血小板聚集功能(platelet aggregation,PA)及其观察肾病理学变化.结果 腹腔给予氟比洛芬酯7d后,分别与sham组和C组比较,CK50组(9.9±1.5) mmol/L、K50组(9.7±1.4)mmol/L血BUN水平明显增高(P＜0.05),CK50组(137±8) mmol/L、K50组(138±8)mmol/L Na+和CK50组(3.9±0.3)mmol/L、K50组(3.9±0.4) mmol/L K+显著降低(P＜0.05),Cr、PT、APTT、Fib和PA值变化无统计学意义(P＞0.05);CK10、CK25组血BUN、Cr、PT、APTT、Fib、Na+、K+和PA值分别与sham组、C组比较,差异无统计学意义(P＞0.05).CK50、K50组病理学变化为肾小球缩小,肾小球毛细血管充盈不足;C组、sham组、CK10、CK25组肾组织结构清晰,未见异常变化. 结论 腹腔重复注射不同剂量氟比洛芬酯对骨肿瘤大鼠凝血功能及其血小板聚集功能无明显影响,然而大剂量氟比洛芬酯(50 mg·kg-1·d-1)影响尿素氮、钠钾离子的代谢及肾小球毛细血管充盈.     

小剂量阿司匹林治疗血小板聚集功能异常复发性流产的临床效果分析

目的：观察对血小板聚集功能异常所导致的复发性流产患者使用小剂量阿司匹林治疗的临床效果。方法选取2011年6月～2013年9月收治血小板聚集功能异常复发性流产患者42例,随机分为观察组与对照组,对照组肌肉注射黄体酮进行治疗,观察组在此基础上加用小剂量阿司匹林进行联合治疗,对比两组患者临床疗效。结果观察组患者足月分娩率与治疗有效率均明显高于对照组,治疗后血小板聚集功能水平明显降低,且低于对照组,差异有统计学意义（P＜0.05）。结论使用小剂量阿司匹林治疗血小板聚集功能异常导致复发性流产,能够有效调节其血小板聚集功能,改善临床妊娠结局,具有理想的临床疗效。     

吸入麻醉药对人血浆和血小板血栓素B2生成与血小板聚集的影响

目的：探讨吸入麻醉剂氟烷、安氟醚和异氟醚对人血浆血栓素Ｂ２（ＴＸＢ２），血小板ＴＸＢ２生成与血小板聚集的影响。方法：血浆ＴＸＢ２和血小板ＴＸＢ２的生成量用放免分析法测量，血小板聚集率用比浊法测量。结果：吸入１ＭＡＣ氟烷３０分钟后，血浆ＴＸＢ２浓度、二磷酸腺苷（ＡＤＰ）和肾上腺素（Ｅ）诱导的血小板ＴＸＢ２生成量与血小板聚集率显著下降，吸入１ＭＡＣ安氟醚３０分钟后，血浆ＴＸＢ２浓度和血小板ＴＸＢ２生成量与血小板聚集率亦显著下降，其降低的程度比氟烷轻。吸入１ＭＡＣ异氟醚对上述指标无明显影响。血小板ＴＸＢ２生成的减少与血小板聚集率的下降呈显著正相关。结论：氟烷显著抑制血小板聚集，安氟醚次之，异氟醚对血小板聚集无明显影响。其机制可能与氟烷和安氟醚通过抑制血小板上血栓素Ａ２受体的亲和力，降低ＡＤＰ和Ｅ诱导的血小板ＴＸＢ２的生成有关。     

The effects of citrate and urine on calcium oxalate crystal aggregation

Summary The rate of crystal sedimentation in a suspension of calcium oxalate monohydrate (COM) crystals was determined spectrophotometrically in the presence and absence of dialysed urine and citrate. A reduced rate of crystal sedimentation after stirring was recorded in suspensions containing citrate in concentrations between 0.33 and 1.67 mmol/l. The sedimentation rate was reduced in the presence of a 0.3–3.3% concentration of dialysed urine, with increased inhibition of crystal sedimentation when the concentration of urine was increased. A comparison of the inhibition of COM crystal sedimentation in whole urine and in dialysed urine from normal subjects and stone-formers disclosed significantly higher values (P<0.05) in the dialysed urine. The results support previous observations that physiological concentrations of citrate might efficiently inhibit the aggregation of COM crystals. Furthermore even low concentrations of both whole urine and dialysed urine are apparently very efficient inhibitors of COM crystal aggregation.     

硝普钠复合异丙酚控制性降压对血小板聚集功能的影响

目的 研究硝普钠与异丙酚联合应用于控制性降压对血小板聚集功能的影响。方法56例患者随机分为四组,A组为对照组,B组为异丙酚组,C组为硝普钠组,D组为异丙酚加硝普钠组,C、D组均进行控制性降压。分别于术前、应用控制性降压后30min、1h、术后2h,监测血小板聚集功能、血浆凝血酶原时间（PT）和血浆中一氧化氮（NO）水平。结果 C组、D组在应用降压后30min、1h血小板聚集功能与麻醉前相比,显著受抑制（P<0.05）,D组抑制最明显（P<0.01）,术后2h各组间无显著差异。应用降压后30min、1h NO水平,C组、D组明显高于术前（P<0.05）,D组明显高于其他组（P<0.01）,组间各时点PT无明显差异（P>0.05）。结论 硝普钠复合异丙酚可升高内源性NO水平,对血小板的聚集功能抑制更加明显,但并不抑制机体的凝血机制。     

The effect of s-nitroso-glutathione on platelet and leukocyte function during experimental extracorporeal circulation

Treatment with extracorporeal membrane oxygenation ECMO) is associated with side effects, e.g., blood cell consumption and activation. Our group has earlier shown that nitric oxide administered as a gas reduces platelet consumption and activation. In the present work we have studied the effect of the NO-donor S-nitroso-glutathione GSNO) on platelets and leukocytes in an in vitro extracorporeal circuit. Two complete ECMO circuits were perfused with fresh heparinized human blood for 24 hours. GSNO was administered as a continuous infusion to one circuit at a rate of 0.7 mg/hour in four paired experiments and at a rate of 3.5 mg/hour in another four paired experiments. The other circuit was used as a control. Blood samples were withdrawn from both circuits before the start of the experiments and at 0.5, 1, 3, 12, and 24 hours of perfusion. The samples were analyzed for red blood cell count, leukocyte count, platelet count, platelet membrane expression of glycoproteins GP) Ib and GPIIb/IIIa, leukocyte membrane expression of cluster of differentiation CD) 11b/CD18, as well as plasma concentration of tumor necrosis factor TNF)-alpha, interleukin IL)-1beta, and IL-8. No difference in these parameters between the GSNO and the control circuit at any time point was assayed. In this study, no significant effect of GSNO on circulating platelets or leukocytes during experimental extracorporeal circulation could be shown.     

Effect of urinary macromolecules on aggregation of calcium oxalate in recurrent calcium stone formers and healthy

Summary The inhibitory activity of urinary macromolecules on the aggregation of calcium oxalate crystals was studied using an aggregometer originally devised to measure thrombocyte aggregation capacity by means of the optical turbidity at 660 nm. The macromolecular fraction of the urine (molecular weight above 5000) of recurrent calcium stone formers showed much less inhibitory activity than that of healthy controls (P0.05). It was speculated on the basis of the results of gel filtration that there were some proteins (molecular weight about 10000–30000) which had inhibitory activities for the aggregation of calcium oxalate. This gives support to the assumption that macromolecules are important during the phase of aggregation of calcium oxalate crystals.     

Quantitative electron microscopic study of calcium accumulation in cerebral ischemia mitochondria

Formation of calcium deposits in mitochondria is a consistent feature of irreversible injury in ischemic myocardium. We studied calcium accumulation in nerve cell mitochondria in a cat model 30 and 60 minutes after cerebral ischemia localized in the anterior part of the caudate nucleus and adjacent internal capsule. In control animals, calcium deposits were visible in synaptic vesicles, Golgi apparatus, mitochondria, lysosomes, and in glial and neuronal nuclei. After cerebral ischemia, findings included astrocytic swelling and degeneration of neurons, with an increase in calcium pyroantimoniate mitochondrial deposits. Content of intramitochondrial calcium deposits is related to duration of ischemia as well as the amount of cellular lesions.     

The effect of epoprostenol on platelet activation and consumption during experimental extracorporeal perfusion

Hemorrhages are major complications experienced in 10-35% of neonates treated with extracorporeal life support (ECLS). The increased bleeding tendency is partly due to an ECLS induced thrombocytopenia and impaired platelet function. In the present study, we evaluated the effect of epoprostenol on the ECLS induced platelet consumption and activation. In terms of the methods, identical in vitro ECLS circuits were primed with fresh heparinized human blood and circulated for 24 h. Epoprostenol (2.4 microg/L blood/h) was added to one of the circuits in each pair. In total, 6 paired experiments were performed. The platelet count, neutrophil count, plasma concentration of hemoglobin, and platelet membrane expression of glycoproteins (GP) Ib and IIb/IIIa were assayed before the start and at 0.5, 1, 3, 12 and 24 h of perfusion. Higher platelet counts were observed in the experimental circuits. However, no difference in the platelet membrane expression of GPIb and GPIIb/IIIa could be observed between the circuits. In conclusion, epoprostenol reduces platelet consumption during ECLS without affecting the membrane expression of GPIb and GPIIb/IIIa.     

Influence of UW solution on in vitro platelet aggregability

Abstract  Bleeding problems in or-thotopic liver transplantation (OLT), starting immediately after reperfusion of the graft, are complicating the outcome of transplantation. Platelets may be involved in this situation, but there is still a lack of information about the influence of UW solution on platelet function. We evaluated the effect of UW solution on in vitro platelet aggreg ability in healthy volunteers using whole blood electrical aggregometry and concluded, that UW solution causes impaired platelet aggregabil ity and may contribute to bleeding problems during OLT. The mechanism of impairment remains un clear, since central pathways as well as membrane receptors seem to be involved. Furthermore. our data support the necessity of extended flushing of the liver graft after re perfusion.     

Simultaneous measurements of calcium oxalate crystal nucleation and aggregation: impact of various modifiers

Rates of nucleation and aggregation of calcium oxalate crystals were derived from 20-min time course measurements of OD₆₂₀ after mixing solutions containing CaCl₂ and K₂C₂O₄ at 37°C, pH 5.7, ionic strength (IS) 0.21, with constant stirring (500 rpm); final assay concentrations were 4.25 mM calcium and 0.5 mM oxalate, respectively. The maximum increase of OD₆₂₀ with time, termed S _N, mainly reflects maximum rate of formation of new particles and thus crystal nucleation. After equilibrium has been reached, OD₆₂₀ progressively decreases despite ionized calcium staying constant and no new particles being formed, due to crystal aggregation. Rate of aggregation, S _A, is derived from the maximum decrease in OD₆₂₀ with time. S _N and S _A are not independent, as indicated by a positive correlation (r=0.844, P=0.0001). Among the modifiers studied, citrate at 0.5–2.5 mM lowered both S _N and S _A in a concentration-dependent manner (P<0.01 for all comparisons vs control). Chondroitin-6-sulfate at 6.25–25 mg/l moderately lowered S _N, whereas it strongly inhibited aggregation (P<0.01 vs control). At 6.8–20.4 mg/l, albumin did not affect nucleation, whereas it inhibited aggregation in a concentration-dependent manner (P<0.005 vs control for all comparisons).     

The effects of bicarbonate and acetate haemodialysis on platelet cyclic AMP concentration,thromboxane B2 release and aggregation

The effects of chronic uraemia and serial acetate (HDA) or bicarbonate (HDB) hacmodialysis on the aggregation, thromboxane B₂ (TXB₂) release and cyclic AMP (cAMP) concentration of platelets from arterial blood were studied in 14 uraemic patients (6 dialysed and 8 conservatively treated) and 10 controls. Platelets from uraemic patients, either dialysed or treated conservatively, exhibited a significantly higher cAMP level (P<0.005), a lower TXB₂ level (P<0.01), and a lower aggregability (P<0.001) than the controls. The platelet cAMP level was more markedly decreased after HDB than after HDA (P<0.05). Greater increases in platelet aggregation (P<0.05) and TXB₂ formation were observed after HDB than after HDA. The concentration of platelet cAMP and aggregability, and also the platelet cAMP and the TXB₂ level showed a significantly negative correlation (r=–0.7,P<0.05 andr=–0.60,P<0.05, respectively). There was a positive correlation between the platelet-derived TXB₂ and the aggregability (r=0.67,P<0.05). Although most patients had secondary hyperparathyroidism, the serum parathyroid hormone level did not correlate closely with the cAMP, TXB₂ or aggregation results. The dysfunction of uraemic platelets accompanied by a reduced TXB₂ release may be explained by an increased cAMP and a decreased arachidonic acid availability. HDB improves the platelet function to a greater degree than does HDA.     

Toborinone and olprinone,phosphodiesterase III inhibitors,inhibit human platelet aggregation due to the inhibition of both calcium release from intracellular stores and calcium entry

Purpose We investigated the inhibitory effects of toborinone and olprinone on human platelet aggregation and calcium mobilization.Methods Washed human platelets were preincubated with toborinone or olprinone, then exposed to 0.015U·ml^–1 of thrombin. Aggregation curves were measured using an aggregometer. Effects of toborinone or olprinone on changes in intracellular calcium concentration ([Ca²⁺]_i) were measured fluorometrically using fura-2 acetoxymethyl ester (fura-2). Levels of intracellular cyclic 3,5-adenosine monophosphate concentration ([cAMP]_i) were also measured, using enzyme-linked immunosorbent assay (ELISA) techniques.Results The concentrations required to cause 50% inhibition of aggregation (IC₅₀) induced by thrombin were 9.7 ± 0.9µM for toborinone and 3.6 ± 0.2µM for olprinone. Both drugs at IC₅₀ significantly elevated [cAMP]_i levels and significantly inhibited Ca²⁺ release from intracellular stores. Release of [Ca²⁺]_i induced by thrombin was 272.9 ± 87.1nM, 153.3 ± 28.7nM, and 138.9 ± 58.2nM in the control, toborinone, and olprinone groups, respectively (P 0.02). Calcium influx through calcium channels in the plasma membrane was also suppressed by toborinone and olprinone.Conclusion Toborinone (9.7µM) and olprinone (3.6µM) inhibit human platelet aggregation, though these concentrations are higher than their therapeutic plasma concentrations. The inhibitory effects of both drugs are related to the inhibition of both Ca²⁺ release and Ca²⁺ entry through [cAMP]_i elevation.     

Transmission electron microscopic study of calcium phosphate formation in supersaturated solutions seeded with apatite

Summary The present study examined crystal growth on enamel and synthetic apatite seed surfaces in dilute supersaturated solutions by means of transmission electron microscopy. At all supersaturations, new growth initially appeared on the ends of the seed crystal. In solutions undersaturated with respect to octacalcium phosphate (OCP), this growth was needlelike in appearance. Above the solubility point for OCP, the growth frequently took the form of thin, platelike crystals. The relevance of these findings to precursor phase formation is discussed.     

人参多糖对家兔肝缺血/再灌注损伤时血小板聚集功能的影响

目的探讨人参多糖对家免肝缺血/再灌注损伤时血小板聚集功能的影响。方法30只家免,随机均分为对照组（C组）、缺血/再灌注组（IR组）和人参多糖组（GP组）。观察血小板最大聚集率（Ptmax）、最大聚集时间（PtT）、聚集坡斜率（PtS）及谷丙转氨酶（ALT）的变化,电镜观察肝组织形态学改变。结果IR组与C组比较,各时间点Ptmax、PtS、ALT明显升高,PtT显著缩短,肝组织超微结构发生异常改变;人参多糖可逆转上述指标的异常变化。结论人参多糖可通过抑制血小板聚集功能,改善肝脏微循环,从而防治肝脏缺血/再灌注损伤。