CHANGES IN PLATELET SIZE AND SPLEEN VOLUME IN RESPONSE TO SELECTIVE AND NON-SELECTIVE β-ADRENOCEPTOR BLOCKADE IN HYPERTENSIVE PATIENTS

• 1 The spleen contains approximately one‐third of all the body's platelets. These platelets are relatively larger and haemostatically more active than platelets in the systemic circulation and can be released into the systemic circulation by stimulation of α‐adrenoceptors or inhibition of β‐adrenoceptors. In the present study, we evaluated the effects of selective (bisoprol) and non‐selective (carvedilol) beta‐blockers agents on mean platelet volume (MPV) and spleen size in hypertensive patients at rest and after exercise.
• 2 Blood pressure, heart rate, platelet count, MPV and spleen volume were measured in 18 newly diagnosed hypertensive patients, as well as in nine healthy control subjects, subjected to treadmill exercise test at their first visit and, for the hypertensive group, after 15 and 30 days of treatment with the selective β₁‐adrenoceptor antagonist bisoprolol 5 mg/day (n = 9) or the non‐selective α₁‐, β₁‐ and β₂‐adrenoceptor antagonist carvedilol 25 mg/day (n = 9).
• 3 Increases in resting MPV values with concomitant decreases in spleen volume were found after 15 and 30 days treatment with either bisoprolol or carvedilol. The pronounced decrease in splenic volume after exercise and the increased MPV and platelet counts seen at first visit were halved after 15 and 30 days of treatment with either drug.
• 4 We conclude that in hypertensive patients treated with either selective or non‐selective beta‐blockers, the spleen contracts and MPV increases, which may increase the risk of atherothrombosis.

     

急性冠脉综合征患者血小板计数和平均血小板体积变化的临床观察

目的 :研究急性冠脉综合征 (ACS)患者血小板计数 (BPC)和平均血小板体积 (MPV )的变化。方法 :选择274例经冠脉造影证实的ACS患者 (急性心肌梗死和不稳定心绞痛 )和76例冠脉造影结果未见异常的正常人群做对照组 ,用COULTERJT_IR型半自动血液分析仪测定BPC和MPV。结果 :ACS组BPC较对照组显著减少(P<0.01) ,MPV较对照组显著增大 (P<0.05)。结论 :ACS患者MPV增大而血小板数量减少 ,可能与本征的发病有关。     

机采和手工血小板在血液病治疗中的效果分析

目的观察机采血小板和手工血小板在临床血液病输血治疗中提升血小板的疗效,为临床合理应用不同种类的血小板制剂提供参考。方法选择本院2009年9月～2012年9月输注机采血小板患者139例,输注手工血小板患者96例,观察输注后24h两组患者的止血效果、输血反应,比较计算血小板增加数校正值（CCI）、血小板回升率（PPR）。结果机采血小板组与手工血小板组比较CCI明显升高,PPR升高,输血反应发生率较低（5．0％vs 15．6％）,止血效果较好。结论输注机采血小板能有效提高患者的血小板值,止血效果优于手工血小板．且能减少输血反应的发生。     

PLATELET KINETICS AFTER TRANSFUSION

A kinetics model is proposed for platelet disposition after transfusion of platelets. In this model, transfusion of platelets and production of endogenous platelets contribute to an increase in the number of platelets in patients, and the life span and age of each platelet contribute to a decrease. The time course of the number of platelets after transfusion of platelets is theoretically described by this model to be a straight line followed by a concave curve. When the platelets have a life span without any variation, a linear pattern is observed in spite of their different ages at the transfusion. This model with a constant life span was applied to three patients receiving platelet transfusion, and the model parameters were calculated by curve fitting the observed platelet levels to the model using the nonlinear least-squares method. As a result, the life span, distribution volume per body weight, and endogenous platelet level (averages for three patients) were calculated as 6·29 d, 0·137 L kg⁻¹, and 1·40×10⁴ counts μL⁻¹, respectively. The calculated platelet levels in individual patients were compared with the observed ones during the next transfusions, and the relative and absolute differences between calculated and observed values were 2·0±15.3% and −0·075±0·443×10⁴ counts μL⁻¹ (mean±SD, 15 observed points for three patients), respectively. These case studies suggest that the model could be clinically useful for individual platelet transfusion.     

磷酯酶C对家兔血小板聚集和超微结构的影响

目的　应用电镜研究磷酯酶C(phospholipaseC ,PLC)对家兔血小板聚集和超微结构的影响 ,以探讨用药后PLC抗血小板聚集作用的机制。方法　家兔颈动脉插管取血 ,制备PRP ,将其分为 4组 :①空白对照组 ;②生理盐水组 ;③ 0 5UPLC组 ;④ 2 5UPLC组。 2～ 4组分别用ADP诱导聚集 ,测出其聚集抑制率 ,各组分别制成超薄切片样品进行电镜观察、摄片。结果　 0 5、2 5UPLC明显抑制血小板聚集反应 ,聚集抑制率分别为 86 0 3 %± 12 6%和 82 47%±5 49% ;0 5UPLC抑制血小板形成伪足 ,α颗粒和致密颗粒较多 ,OCS管腔较小 ,其超微结构较生理盐水组变化小 ;2 5UPLC处理血小板的形态结构和超微结构与空白对照组无差异 ,血小板呈圆形或椭圆形 ,边缘光滑 ,无伪足样突起 ,α颗粒、致密颗粒、OCS等正常分布于胞质中。结论　PLC明显抑制ADP诱导的血小板聚集反应及其超微结构的改变 ,这可能是PLC抗血小板聚集作用的重要原因之一     

老年病血液流变学100例分析

目的 了解老年病各类疾病血液流变学特点。方法 对我院100例老年病人进行血液流变学检测，并分组归类分析：A组：缺血性心脑血管病40例（冠心病28例，脑梗塞12例）；B组：与动脉硬化、血栓形成密切相关病类42例（高血压病26例，糖尿病16例）；C组：一般病类18例，包括消化性溃疡、支气管炎等，并设健康对照组30例。结果 A、B、C三组血栓长度、重量、红细胞刚性指数（IR）、红细胞电泳时间（EFT）均明显高于对照组；红细胞比积（HCT）各组无差异；A、B组胆固醇（TC）、甘油三酯（TG）、纤维蛋白原（Fib）升高；低切变时（40S^-1，10S^-1）全血表现粘度（BAV）升高，尤以A组为重；血小板粘附率（PadT）A组升高。结论 老年病血栓容易形成，红细胞聚集性（EA）增高，变形能力（ED）下降。缺血性心脑血管病危险因素多而严重，糖尿病、高血压病次之。血栓形成、血管内膜病变过程中，细胞因素占重要地位。     

妊娠期高血压疾病孕妇凝血功能的对照研究

目的对妊娠期高血压疾病孕妇凝血功能进行对照研究。方法选取2011年7月～2013年6月在我院妇产科住院分娩的妊娠期高血压疾病孕妇272例作为研究对象,分为3个亚组;随机选取来本院产检的正常孕妇55例作为对照组,对凝血功能进行测定。结果研究组Ⅰ与对照组比较,PT缩短显著,APTT和TT延长（P〈0．05）,而两组INR比较,差异不显著。两组Fbg、血小板和红细胞比积比较,差异有统计学意义（P〈0．05）。分组比较,PT差异无统计学意义（P〉0．05）,APTT和TT有显著性延长（P〈0．05）,Fbg有显著性减少（P〈0．05）。D-二聚体升高的百分率,研究组明显高于对照组,差异有统计学意义（P〈0．05）。而研究组Ⅰ、Ⅱ、Ⅲ组间D-二聚体升高的百分率比较差异无统计学意义（P〉0．05）。结论妊娠期高血压疾病患者具有较高的凝血状态,且存在血管内凝血消耗的情况。     

灯盏花素对高血压大鼠血小板游离钙浓度和聚集率及心脏重塑的影响

目的:研究灯盏花素、福辛普利、依那普利对自发性高血压大鼠(SHR)血小板游离钙浓度、血小板聚集率和心脏重塑的影响.方法:24只10月龄伴有左心室肥厚(LVH)的SHR 随机分为灯盏花素组、福辛普利组、依那普利组和生理氯化钠溶液组(NS组)4组进行为期8周的干预治疗,观察其对SHR收缩压、心率、左心室肥厚指数、心肌细胞超微结构、血小板胞浆游离钙和血小板聚集率的影响.结果:6只SHR的收缩压、左心室肥厚指数、血小板胞浆游离钙浓度和血小板聚集率均显著高于同龄Wistar Kyoto (WKY)大鼠(P均＜0.01).可见心肌细胞肥大、心肌肌浆网扩张和心肌线粒体增生等超微结构改变.血小板胞浆游离钙浓度和血小板聚集率与左心室肥厚指数呈显著正相关(P均＜0.01).与NS组比较,3药均能显著降低左心室肥厚指数、血小板胞浆游离钙浓度和血小板聚集率(P均＜0.01),并改善SHR的心肌细胞超微结构;福辛普利和依那普利还能显著降低SHR的收缩压(P均＜0.01).结论:血小板内钙代谢异常和血小板功能改变可能在SHR心脏重塑中起重要作用.灯盏花素、福辛普利和依那普利均能显著降低SHR的血小板胞浆游离钙浓度和血小板聚集率,从而改善SHR心脏重塑.     

The actions of lovastatin on platelet function and platelet eicosanoid receptors in type II hypercholesterolaemia

Summary We have studied the effects of 12 weeks of lovastatin (20 mg per day) on platelet function and thromboxane formation in 18 patients with type II hypercholesterolaemia in a double-blind, placebo-controlled, prospective study.Lovastatin significantly reduced total serum and LDL-cholesterol by 20% and 25% respectively. Washed platelets of lovastatin-treated patients had significantly reduced collagen-induced aggregation and thromboxane formation ex vivo. There was no change in ADP-induced platelet aggregation, but a significant increase in prostacyclin (iloprost)-stimulated platelet cyclic AMP concentrations in lovastatin-treated patients. This was associated with a significant increase in the number of prostacyclin receptors in platelet membranes prepared from lovastatin-treated patients. There was also an increase in platelet thromboxane receptors. There were no such changes in the placebo group.These data confirm our original observation of normalization of platelet function in hypercholesterolaemia by HMGCoA reductase inhibitors and suggest changes in platelet membrane composition at the megakaryocyte level as a possible site of action.     

Inhibitory effects of endogenous L-arginine analogues on nitric oxide synthesis in platelets: role in platelet hyperaggregability in hypertension

1. An increase in plasma concentrations of endogenous L-arginine analogues, which are inhibitors of nitric oxide (NO) synthesis, may be involved in platelet activation and the increased risk of thrombosis in essential hypertension. Nitric oxide is synthesised in platelets from the amino acid L-arginine by inducible and constitutive isoforms of NO synthase (NOS), which leads to increased levels of cGMP. 2. In the present study, we investigated basal intraplatelet cGMP levels, platelet aggregation and pro-inflammatory biomarkers in hypertensive patients. The effects of endogenous (N(G)-monomethyl-L-arginine (L-NMMA) and asymmetric dimethylarginine (ADMA); both at 1 mmol/L) and exogenous (aminoguanidine and N(G)-nitro-L-arginine; both at 1 mmol/L) L-arginine analogues and the neutral amino acid L-leucine (1 mmol/L) in inhibiting NOS activity in platelets were also investigated. 3. Twelve healthy controls and 18 hypertensive patients participated in the study. Platelet aggregation induced by collagen was increased in hypertensive patients (95 +/- 5%) compared with controls (72 +/- 5%). Basal NOS activity and intraplatelet cGMP levels were reduced in hypertensive platelets. Moreover, ADMA, L-NMMA and L-leucine were effective inhibitors of NO synthesis in both hypertensive and control platelets. Essential hypertension led to an inflammatory response, with increased plasma concentrations of fibrinogen, C-reactive protein and cytokines. 4. These findings provide evidence that, in essential arterial hypertension, the enhanced plasma levels of endogenous L-arginine analogues ADMA and L-NMMA, potent inhibitors of L-arginine transport and NO synthesis in platelets, may play a role in increased platelet aggregation via a cGMP-dependent mechanism.