机械瓣膜替换术后抗凝血浆蛋白C含量改变的意义

目的探讨机械瓣膜替换术后口服华法令者 ,血浆蛋白 C,PC)的改变以及与其他凝血因子改变的关系。方法采用酶联免疫吸附法测定 PC含量 ,采用经典一期法测定凝血因子 X∶ C、凝血酶原时间并计算国际正常化比值 (INR)。结果正常对照组 (n=45 ) ,口服华法令组 (n=78) PC含量分别为 (5 .0 0± 0 .6 4) m g/ L、(2 .5 4± 2 .18)mg/ L ,两者差异有极显著性 (P<0 .0 0 1)。服药时间 1～ 6个月、7～ 2 4个月、2 5～ 132个月者 PC含量分别为 (4.0 2±3.6 0 ) mg/ L、(2 .5 2± 1.5 6 ) m g/ L、(2 .40± 1.6 6 ) m g/ L。 PC含量改变与因子 X、凝血酶原时间 (PT)、INR间无明显相关性。结论机械瓣膜替换术后口服华法令者血浆蛋白 C含量减低 ,并与服药时间长短有关 ,蛋白 C的改变存在较大的个体差异。在抗凝治疗初期 ,对蛋白 C含量的监测有着特别重要的意义。     

人造机械瓣膜替换术后护理

心瓣膜病是指心脏瓣膜受到各种致病因素损伤后或先天性发育异常所形成的器质性病变。表现为瓣膜口狭窄和/或关闭不全。病变累及一个瓣膜,或几个瓣膜同时或先后受累,最常见于二尖瓣,其次是二尖     

心脏瓣膜替换术后抗凝治疗的健康宣教

目的：研究向人工瓣膜替换术后患进行健康宣教的目的、内容及方法。方法：对施行心脏瓣膜替换术的３７１例进行健康宣都,着重进行抗凝指导,结果：３７１例术后均用华法林终身抗凝,因服用华法林并发出血９例,其中脑出血５例,消化道出血４例,治愈５例。结论：心脏瓣膜替换术后要加强健康宣教,着重抗凝治疗的必要性、方法出院后复查凝血酶原时间。     

心脏机械瓣膜替换术后妊娠20例次报告

我院自1990年6月至1996年6月,经治心脏机械瓣膜替换术后妊娠18人20次妊娠,其中6人6次分娩,1人1次剖宫产,因计划生育行人流13人次。现总结报告如下。 1 临床资料 本组18例,年龄21～32岁,平均26.6岁。机械瓣膜国产倾碟瓣15例,st.Jude Medical双叶碟瓣4例。二尖瓣替换术后16例,主动脉瓣替换术1     

心脏瓣膜替换术后监测

心脏瓣膜替换手术创伤大、管道多,均有不同程度功能损害。肺通气弥散功能减退,凝血机制差,病情变化迅速,易发生各种并发症。通过60例心脏瓣膜替换术后监护分析,从循环系统、呼吸系统、中枢神经系统、抗凝治疗及健康教育等方面提出了切实可行的护理措施,提高了治愈率,缩短住院日,减轻患者经济负担。     

二尖瓣狭窄闭式扩张术后的瓣膜替换术

介绍二尖瓣闭式扩张术后瓣膜替换术经验,回顾１９８８年１月－１９９８年１月５２例二尖瓣闭式扩张术后瓣膜替换术的资料,瓣膜替换时平均年龄４５．１７岁±７．９７岁。均为择期手术,两次手术间隔为１２．０５岁±５．７５年。均在低温体外循环下手术,其中二尖瓣替换术４２例二尖瓣及主动脉瓣替换术７例,二尖瓣及三尖瓣替换术２例,三瓣膜替换术１例,术后早期死亡５例,其１９９２年前为１９．０５％（４／２１）,１９９２年     

30例儿童心脏瓣膜替换术后的护理

笔者总结30例14岁以下儿童心脏瓣膜替换术后的护理经验。主要是儿童瓣膜替换术后预防低心排血量综合征,加强呼吸道、皮肤护理,防止并发症,严密观察心律变化及有无出血倾向,认为机械瓣膜替换术后低强度抗凝治疗是安全可靠的。     

儿童心脏瓣膜替换术30例术后护理

目的:探讨儿童心脏瓣膜替换术后的护理干预.方法:将30例行心脏瓣膜替换术患儿随机分为护理组和对照组各15例,护理组采用精心的术后护理干预,对照组采用常规护理措施.结果:两组患儿在平均住院天数、平均代谢当量、皮肤压伤及肺部并发症等方面比较差异有统计学意义(P<0.05).结论:对儿童心脏瓣膜替换术后进行护理干预,可显著改善患儿的心功能全身状况、并发症、精神心理等方面,获得满意效果.     

蛋白C抗凝系统在尿毒症维持性血液透析中的变化及意义

目的 :探讨血浆抗凝因子蛋白 C(PC)、蛋白 S(PS)及血栓调节蛋白 (TM)在尿毒症、凝血异常导致出血并发症中的作用。方法 :采用双抗夹心酶联免疫吸附法 (EL ISA)及发色底物法测定 4 5例尿毒症血液透析 (血透 )患者及正常对照组血浆 PC抗原 (PC:Ag)、PC活性 (APC)、血浆总 PS(TPS)、血浆游离 PS(FPS)及 TM含量。结果 :尿毒症患者 PC:Ag、TPS、FPS、TM和 D二聚体 (DD)含量及 APC明显高于正常对照组 (P<0 .0 5或P<0 .0 0 1) ;维持性血透患者血浆 APC、TPS、FPS及 DD血透后明显升高 (P<0 .0 5或 P<0 .0 0 1) ;TM血透后明显降低 (P<0 .0 0 1) ;有出血并发症者血浆 PC:Ag、FPS、DD含量及 APC明显升高 (P<0 .0 5或 P<0 .0 1)。结论 :尿毒症患者蛋白 C抗凝活性降低 ,与尿毒症时高凝倾向和血栓形成有关。血透可激活原本已处于高凝状态的凝血系统 ,使体内蛋白 C抗凝途径的抗凝活性增强。     

Plasma levels of protein C and vitamin K-dependent coagulation factors in patients on long-term oral anticoagulant therapy

Plasma levels of protein C (PC) and vitamin K-dependent coagulation factors (factors II, VII, IX and X) were measured in 100 specimens from patients on long-term warfarin therapy. Both activities and antigens of these coagulation factors were decreased, depending on the thrombotest values. Factor II activity/antigen ratio and factor X activity/antigen ratio were correlated well with thrombotest values, indicating that the concentration of inactive molecules (PIVKAs) relative to normal proteins increases with increasing intensity of anticoagulation. Although PC antigen (PC:Ag) was also decreased, the ratios between PC:Ag and vitamin K-dependent coagulation factor antigens remained constant, being independent of the intensity of warfarin therapy. These findings indicate that long-term oral anticoagulant therapy results in the suppression of the synthesis of both vitamin K-dependent coagulation factors and PC, but the production of the coagulant and anticoagulant proteins is well-balanced.     

维持性血透患者血浆抗凝血因子的变化及意义

目的 探讨血浆抗凝血因子PC，PC，TM在尿毒症止血、凝血异常导致出血并发症中的作用。方法 采用双抗夹心ELJSA法，发色底物法测定45例尿毒症血透患者血浆PC(PCAg，APC)，PC(TPS，FPS)，TM含量。结果尿毒症患者PCAg,TPS，FPS，TM含量明显高于正常对照组(P＜0．05，P＜0．001)，而PC活性(APC)明显低于对照组(P＜0．001)。维持性血透患者血浆APC，TPS，FPS血透后明显升高(P＜0．05，P＜0．001)；TM血透后明显降低(P＜0．001)。有出血倾向的尿毒症患者血浆APC均明显升高(P＜0．05)。结论 尿毒症患者蛋白C抗凝活性降低(APC)，与尿毒症时高凝倾向和血栓形成有关。血液透析治疗的尿毒症患者在原有高凝状态基础上，透析后仍可激活凝血系统，使体内蛋白C抗凝途径的抗凝活性增强。     

High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C

Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels are associated, respectively, with either increased risk or apparent protective effects for atherothrombosis. The ability of purified LDL and HDL to downregulate thrombin formation, a contributor to atherothrombotic processes, was assessed. Purified HDL, but not LDL, significantly enhanced inactivation of coagulation factor Va by activated protein C (APC) and protein S, and HDL stimulated protein S–dependent proteolytic inactivation of Va by APC, apparently due to cleavage at Arg306 in Va. In normal plasma, added HDL enhanced APC/protein S anticoagulant activity in modified prothrombin-time clotting assays. When the anticoagulant potency of HDL was compared with phospholipid (PL) vesicles of well-defined composition using this assay, HDL appeared qualitatively different from PL vesicles because HDL showed only good anticoagulant activity, whereas PL vesicles were rather procoagulant. When 20 normal plasmas were tested using this clotting assay, apoA-I levels correlated with anticoagulant response to APC/protein S (r = 0.47, P = 0.035), but not with activated partial thromboplastin time–based APC resistance ratios. Because HDL enhances the anticoagulant protein C pathway in vitro, we speculate that HDL may help downregulate thrombin generation in vivo and that this anticoagulant action is one of HDL's beneficial activities.     

Relationship between protein C antigen and anticoagulant activity during oral anticoagulation and in selected disease states

Protein C is a natural vitamin K-dependent plasma anticoagulant, deficiencies of which have been found in patients with recurrent thrombosis and warfarin-induced skin necrosis. To appreciate more fully the role of protein C in disease states and during oral anticoagulation, a new functional assay for protein C involving adsorption of plasma protein C on a Ca+2-dependent monoclonal antibody, elution, quantitative activation, and assessment of plasma anticoagulant activity, has been developed. When oral anticoagulation is initiated, the anticoagulant activity of protein C decreases to a greater extent than either the amidolytic or immunologic levels. During stabilized warfarin treatment, there is no correlation between either amidolytic or antigenic levels and the functional protein C activity, suggesting that measurement of protein C anticoagulant activity may be necessary to reflect adequately the anticoagulant protection afforded by this protein. In contrast, there was a strong correlation between anticoagulant and amidolytic and immunologic levels in liver failure and disseminated intravascular coagulation. Two patients with thromboembolic disease have been identified who exhibit a marked decrease in anticoagulant activity, but who have normal immunologic and amidolytic levels. Thus, this assay permits assessment of protein C in individuals who have received anticoagulant treatment and identification of a new class of protein C-deficient individuals.     

综合护理干预在心脏瓣膜术后患者华法林抗凝治疗的应用效果

目的 探讨综合护理干预在心脏瓣膜术后患者华法林抗凝治疗中的应用效果。 方法 选取2015年2月-2017年2月接受心脏瓣膜置换术且术后采用华法林抗凝的患者100例,随机分为观察组与对照组各50例。对照组予以心脏瓣膜术后常规护理,观察组行综合护理干预。比较2组患者华法林抗凝治疗的依从性、不良反应发生情况以及患者满意度情况。 结果 观察组患者华法林抗凝治疗完全依从性显著高于对照组(Z=-2.568,P=0.010)。出血以及血栓的发生率均低于对照组(χ²=5.473,P=0.019; χ²=4.332,P=0.037)。患者满意度高于对照组(χ²=6.061,P=0.014)。 结论 综合护理应用于心脏瓣膜术后华法林抗凝中,可显著提高患者依从性,降低不良反应发生率,提高患者满意度。     

Molecular recognition in the protein C anticoagulant pathway

Summary.  The protein C (PC) anticoagulant system provides specific and efficient control of blood coagulation. The system comprises circulating or membrane-bound protein components that take part in complicated multimolecular protein complexes being assembled on specific cellular phospholipid membranes. Each of the participating proteins is composed of multiple domains, many of which are known at the level of their three-dimensional structures. The key component of the PC system, the vitamin K-dependent PC, circulates in blood as zymogen to an anticoagulant serine protease. Activation is achieved on the surface of endothelial cells by thrombin bound to the membrane protein thrombomodulin. The endothelial PC receptor binds the Gla domain of PC and stimulates the activation. Activated PC (APC) modulates the activity of blood coagulation by specific proteolytic cleavages of a limited number of peptide bonds in factor (F)VIIIa and FVa, cofactors in the activation of FX and prothrombin, respectively. These reactions occur on the surface of negatively charged phospholipid membranes and are stimulated by the vitamin K-dependent protein S. Regulation of FVIIIa activity by APC is stimulated not only by protein S but also by FV, which, like thrombin, is a Janus-faced protein with both pro- and anticoagulant potential. However, whereas the properties of thrombin are modulated by protein–protein interactions, the specificity of FV function is governed by proteolysis by pro- or anti-coagulant enzymes. The molecular recognition of the PC system is beginning to be unravelled and provides insights into a fascinating and intricate molecular scenario.