Coagulation-physiological studies on the prevention of thromboembolism with dextran 60. II. Changes in coagulation and fibrinolysis

The postoperative behavior of different parameters of coagulation and fibrinolysis have been studied in three groups of 20 patients each. Group A got only 4-hydroxycumarin, group B 500 ml Dextran 60 intraoperatively in addition to that, group C 500 ml Dextran 60 during surgery and on the 1., 2., 4., 7. and 10. postoperative day. The results show that the hypercoagulability which occurs immediately after surgery can be prevented by infusion of Dextran 60. On the other hand there is no evidence that Dextran 60 may cause a consumptive coagulability. There is only little influence on fibrinolysis, so that no defect of haemostasis can be expected. So it is possible to use Dextran 60 both for bridging over the phase of early embolism after surgery until the change to other anticoagulants and as a substance which can be applicated for a longer period of time in prophylaxis of thromboembolism. It is referred to the additional properties of Dextran 60 in prevention of thrombosis due to reduction of blood viscosity and improvement of microcirculation.     

The effect of dexamethasone on platelet function

To assess the effects of dexamethasone on platelet function, aggregation studies were performed on nine healthy adults before and after ingestion of a single dose of dexamethasone 10 mg, and on six patients receiving daily dexamethasone. Bleeding times were done on 14 volunteers before and after a similar drug dose. Platelet aggregation by ADP, epinephrine and collagen was unchanged after dexamethasone in the healthy subjects and aggregation curves in the patient group were comparable to the normals. Bleeding times were moderatley prolonged in women (from 284 +/− 58 seconds to 389 +/− 114 seconds) but not in men. This prolongation was much less pronounced than that which occurs with low doses of aspirin and no subject experienced delayed bleeding. Dexamethasone in single high doses probably does not cuase a clinically important effect on platelet function.     

国外静脉血栓栓塞症预防研究的文献计量学分析

目的分析国外静脉血栓栓塞症(venous thromboembolism,VTE)预防研究的现状及热点趋势,为国内护理人员开展临床工作及相关研究提供参考依据。方法检索科学网核心数据库(Web of Science Core Collection,WOSCC)中与VTE预防有关的核心期刊文献,检索时限为2005年1月1日—2020年4月27日,借助CiteSpace 5.0软件进行文献计量和聚类分析。结果国外VTE预防研究发文量整体呈上升趋势,主要聚焦物理预防、药物预防、并发症观察、危险人群识别、不同疾病人群VTE预防等5个方面,其中"预防持续时长""间歇性充气加压装置""脑卒中""抗凝""临床实践指南"和"新型口服抗凝药物"是目前的研究热点。结论 VTE预防已受到国外学者的重视,建议通过将VTE预防研究的焦点具体化、拓宽VTE重点预防人群范围、制订VTE预防护理指南等方法,推动国内VTE预防护理研究的发展,并不断提高临床护理质量,减少VTE的发生。     

住院患者静脉血栓栓塞症防治管理效果评价

目的 推进院内住院患者静脉血栓栓塞症(VTE)防治管理科学化、规范化,提升医疗质量,保障患者安全.方法 通过构建院内VTE防治体系,组织院内VTE培训活动,优化VTE管理系统及VTE不良事件追踪管理等干预手段,对2016—2019年干预前后(2016—2017年共237840例出院患者作为对照组,2018—2019年共...     

The effect of low molecular weight dextran on haemodynamics and respiratory function during endotoxin-induced shock.

The effects of low molecular weight dextran (LMWD) infusion, on gas exchange and haemodynamics were evaluated in sheep during endotoxin shock. The infusion of LMWD was started after signs of shock and lung injury were evident. After a stabilization period 10 micrograms kg-1 E. Coli endotoxin was infused i.v.. Endotoxin infusion resulted in an marked increase in pulmonary artery pressure (PAP) and decrease in mean arterial pressure (MAP), respiratory compliance, arterial oxygen tension (PaO2) and oxygen delivery index (DO2l). After 3 h MAP, PaO2, DO2l and compliance improved significantly in LMWD treated animals. The PAP had also decreased significantly in the LMWD-treated animals, but remained high in the controls (P less than 0.01). It was concluded that LMWD infusion improves haemodynamics and gas-exchange in sheep during endotoxin shock.     

阿司匹林在冠心病患者中C反应蛋白及血小板的影响

目的研究阿司匹林(ASP)对冠心病(CHD)患者血浆C-反应蛋白(CRP)及血小板(Platelet)功能的影响,了解它们与CHD的关系。方法将90例CHD病人,随机分为两组:I组口服ASP 50 mg/d,II组ASP 150 mg/d,早餐后顿服;8周后检验两组患者的血浆CRP浓度、血小板膜表面α颗粒膜蛋白(GMP-140)和血小板聚集率的变化。结果与治疗前比较,除I组CRP浓度变化差异无显著性外,其余各项指标均有显著性差异(P>0.05),组间比较差异有显著性(P>0.05)。结论使用ASP 150 mg/d能直接降低血浆CRP浓度、GMP-140水平和抑制血小板活化和聚集,能有效地防止冠状血管的进一步损害。     

In vitro and in vivo studies of the effect of aztreonam on platelet function and coagulation in normal volunteers.

The in vitro effects of aztreonam on platelet aggregation were compared with those of cefotaxime, moxalactam, piperacillin, and carbenicillin. In addition, the in vivo effects of intravenously administered aztreonam on blood coagulation and platelet function were examined in 10 normal male volunteers in a randomized crossover study. In vitro, at concentrations of greater than 6.25 mM (2.7 mg/ml), aztreonam inhibited ADP-induced platelet aggregation in a dose-dependent manner. The effect was less than that produced by equimolar concentrations of cefotaxime, moxalactam, piperacillin, or carbenicillin. At all concentrations tested, aztreonam and cefotaxime inhibited epinephrine-induced aggregation least. All antibiotics inhibited collagen-induced aggregation, but only at inordinately high concentrations (25 mM). In vivo studies in 10 male subjects, randomly infused intravenously with 2 g of aztreonam or saline placebo every 6 h for 21 consecutive doses in a single-blind crossover study, revealed no evidence of bleeding or visible adverse side effects. Although plasma coagulation and platelet adhesion remained within normal limits in all subjects throughout the study, inhibition of ADP-induced platelet aggregation significantly (P less than 0.0001) increased on days 3 and 6, but still was below 40%. With the exception of one subject who had a mean template bleeding time of 7.3 min (normal, 2 to 7 min at 95% confidence limits) on day 6 of aztreonam administration, all volunteers exhibited bleeding times within the normal range. No abnormalities in platelet morphology were observed. Mean peak serum aztreonam concentrations on days 1 and 6 were 90.1 +/- 16.7 and 95.9 +/- 13.7 micrograms/ml, respectively; accumulation did not occur. Thus, in normal volunteers, aztreonam produced no significant recognizable abnormalities of hemostasis after 6 days of maximal recommended doses.     

脑梗死患者血中一氧化氮与血小板功能

目的 研究脑梗死患者血中一氧化氮(NO)含量与血小板功能之间的关系及临床意义。方法 将20例脑梗死患者分为发病初期组、缓解期组,正常对照组15例,采用硝酸还原酶法测NO含量;用血小板聚集凝血因子分析仪和流式细胞仪分别测定血小板聚集率(PAgT)和血小板α-颗粒膜蛋白(GMP-140)的含量。结果:血清中NO水平在发病初期较正常对照组明显增高(P<0.01)。同时,血小板PAgT明显减低,与正常对照有显著性差异(PADP<0.05,P<0.01);GMP-140在发病初期和稳定期减低,较正常对照都有显著性差异(P<0.01)。结论 实验结果表明,脑梗死患者发病初期随着血中NO水平的增高,PAgT受抑,GMP-140水平减低。认识上述病理变化对脑梗死发病机制的探讨有着重要意义。同时提示N0含量、PAgT、GMP-140测定可作脑梗死患者诊断、治疗及预后观察的一项客观指标。     

The effect of exercise on platelet beta-adrenoceptor function and platelet aggregation in healthy human volunteers

Summary. Plasma levels of adrenaline and noradrenaline, platelet cyclic-AMP (cAMP) content, platelet aggregation, platelet release of beta-thromboglobulin, and platelet factor 4 and serum content of thromboxane B₂(TXB₂) and 6-keto-PGF_1α were measured in 12 healthy male volunteers (age 38–72, mean 54·2 years) who were tested at rest and immediately after five min light cycle exercise. The plasma levels of adrenaline and noradrenaline increased significantly after exercise (P<0·01). The platelet cAMP level was not changed by exercise. The functional capacity of platelet beta-adrenoceptors, determined as cAMP production after beta-adrenoceptor stimulation in vitro, decreased highly significantly after exercise in all 12 volunteers (P<0·01). No alteration was observed in platelet aggregation induced by adrenaline or in platelet release of beta-thromboglobulin or platelet factor 4. No change was observed in the serum levels of TXB₂ and 6-keto-PGF_1α. In conclusion: light cycle exercise results in a decreased functional capacity of platelet beta-adrenoceptors, but has no effect on platelet aggregation or platelet release. This might indicate a concomitant and equal decreased functional capacity of platelet alpha-adrenoceptors.     

The effect of hydroxyethyl starch on in vitro platelet and granulocyte function

The effect of hydroxyethyl starch (HES) on granulocyte and platelet functions was assessed. No alteration of granulocyte viability, morphology, phagocytic ability, or bactericidal capacity was detected after incubation with 6 per cent HES at 25 C for two hours. Platelet morphology, size distribution, aggregation, nucleotide and serotonin release, and platelet factor-3 availability were also unchanged after exposure to HES. It is concluded that HES has no adverse effect on cell function and appears to be a suitable adjuvant agent for blood cell component collection.     

Time-dependent effect of statins on platelet function in hypercholesterolaemia

BACKGROUND: Reduction of platelet activity induced by statins has been described as a positive effect exerted by such molecules on vascular thrombotic events. However, the relations among cholesterol (LDL-C) reduction, the timing of the antiplatelet effect, the involved mechanisms and the doses of each statin able to reduce platelet function are not actually well known. The aim of our study was to evaluate the impact of simvastatin (20 mg day-1), atorvastatin (10 mg day-1), fluvastatin (40 mg day-1) and pravastatin (40 mg day-1) on platelet function in hypercholesterolaemic subjects with relation to (LDL-C), oxidized-LDL (ox-LDL) and antiport mechanism modifications. MATERIALS AND METHODS: Sixteen subjects were assigned to each treatment (40 males, 24 females, mean age 48.7 +/- 13.4, LDL-C 5.13 +/- 0,23 mmol L-1) and evaluated for platelet surface P-selectin (P-sel), lipid profile, ox-LDL, platelet-associated ox-LDL (Pox-LDL), platelet cholesterol content, antiport mechanisms, and intracellular and systemic NO synthase every 7 days for one month. RESULTS: Our data show a strong relation between enhanced P-sel and Pox-LDL (r = 0.68, P < 0.01). Simvastatin, atorvastatin, fluvastatin and pravastatin reduce platelet activity after 1, 2, 3 and 4 weeks of treatment, respectively (P < 0.001, P < 0.001, P < 0.01, P < 0.05). Pox-LDL are modulated early by simvastatin, atorvastatin and fluvastatin Pox-LDL (r = 0.66, 0.65 and 0.52; P < 0.001, 0.001 and 0.01, respectively) whereas LDL-C and ox-LDL reductions associated to modifications of antiport activity act later. Moreover, they are the most relevant finding in pravastatin-related subjects. CONCLUSIONS: Our data suggest a different impact of several statins on platelet function, which is initially related to interference with Pox-LDL rather than LDL-C reduction.     

Disorders of platelet function.

Platelets provide for primary hemostasis by forming a hemostatic plug at sites of vascular damage. They also provide a surface for the assembly of the coagulation protein complexes that generate thrombin, serve as a nidus for fibrin clots, and secrete factors involved in wound repair. Normal platelet function can be divided into four phases: adhesion, aggregation, secretion, and expression of procoagulant activity. Platelet adhesion initiates plug formation as platelets adhere to the connective tissue at the edges of a wound within seconds after vascular damage. When damage occurs in regions of slow blood flow, platelets adhere to subendothelial collagen, fibronectin, and laminin. However, when damage occurs in regions of rapid flow, platelet adhesion requires the presence of subendothelial von Willebrand factor (vWf) and a specific platelet receptor, the glycoprotein Ib/IX (GPIb/IX) complex. Following initial adhesion, platelets aggregate to complete the formation of a hemostatic plug. Platelet aggregation requires active platelet metabolism, platelet stimulation by agonists such as ADP, thrombin, collagen, or epinephrine; the presence of calcium or magnesium ions and specific plasma proteins such as fibrinogen or vWf; and a platelet receptor, the glycoprotein IIb/IIIa (GPIIb/IIIa) complex. Thus, platelet stimulation results in the generation of intracellular second messengers that transmit the stimulus back to the platelet surface, exposing protein binding sites on GPIIb/IIIa. Fibrinogen (or vWf) then binds to GPIIb/IIIa and crosslinks adjacent platelets to produce platelet aggregates. Platelet stimulation also results in platelet secretion and the elaboration of platelet procoagulant activity. During secretion, substances are released to propagate the aggregation response and to promote wound healing; the expression of procoagulant activity localizes thrombin generation to the site of vascular damage. Disorders of platelet function can be divided into those of congenital and those of acquired origin. Although congenital disorders are uncommon, acquired disorders are encountered frequently in clinical practice. Congenital absence of GPIb/IX and GPIIb/IIIa results in the Bernard-Soulier syndrome (BSS) and Glanzmann thrombasthenia (GT), respectively. Each is an autosomal recessive bleeding disorder in which absence of a protein complex renders the affected platelets incapable of undergoing either vWf-mediated adhesion (BSS) or fibrinogen-mediated aggregation (GT).(ABSTRACT TRUNCATED AT 400 WORDS)     

The effects of irradiation on platelet function

Current medical practice involves the irradiation of blood components, including platelet concentrates, before their administration to patients with severe immunosuppression. The authors studied the effect of irradiation on in vitro platelet function and the leaching of plasticizers from the bag, both immediately and after 5 days of storage. The platelet count, white cell count, pH, glucose, lactate, platelet aggregation and release reaction, and serotonin uptake were not altered by the irradiation of random-donor or apheresis units with 2000 rads carried out at 0 and 24 hours and 5 days after collection. The leaching of di(2-ethylhexyl)phthalate from the plastic bags followed by the conversion to mono(2-ethylhexyl)phthalate was not increased by irradiation. Therefore, it is possible to irradiate platelet concentrates on the day of collection and subsequently store them for at least 5 days while maintaining in vitro function. This procedure could have considerable benefit for blood banks involved in the provision of many platelet products.