原发性高血压患者纤溶系统功能的变化

目的 观察未经治疗的原发性高血压患者的纤溶指标的变化及临床意义。方法 选取36例初次就诊的原发性高血压患者[男17例。女19例，平均年龄(52&;#177;7)岁]及3l例血压正常者[男16例，女15例，平均年龄(5l&;#177;7)岁]。两组受试者的临床特点无明显差别。用发色底物法测定他们的血浆组织型纤溶酶原激活物(t-PA)及其抑制剂(PAI—1)的活性和a2-PI活性。结果 原发性高血压患者血浆t-PA和a2-PI活性明显低于对照者，P&;lt;0．05。PAI-1，活性明显高于对照组，P&;lt;0．05。结论 原发性高血压患者存在内源性纤溶功能低下。     

组织型纤溶酶原激活物及纤溶酶原激活物抑制剂对系统性红斑狼疮的检测价值

<正>自身免疫介导并累及多个系统、临床表现起伏是系统性红斑狼疮(systemic lupus erythematosus,SLE)的显著特征,血液、造血系统受损较常见,其发病机制仍不十分清楚[1]。SLE可以引起全身多器官损害并常存在高凝状态,甚至发生血栓或     

复发性缺血性脑卒中患者血纤溶系统的变化及其临床意义

目的：探讨复发性缺血性脑卒中患者血纤溶系统变化的临床意义。方法：观察41例复发缺血性脑卒中、58例初发缺血性脑卒中患者及42例健康对照组血液组织型纤溶酶原激活物（tPA)，纤溶酶原激活物抑制剂（PAI－1），纤溶酶的（Plg)，纤溶酶（Plm)及纤维蛋白原（Fig) 含量。结果：复发性缺血性脑卒中与初发缺血性脑卒中患者血tPA-1水平均明显高于对照组，初发缺血性脑卒中患者Plg明显升高，与对照组比较有显著差异；血纤维蛋白原水平在复发中风组明显高于初发中风组和对照组。TPA－1与房颤和中风家族史呈正相产；Plm与冠心病心绞痛呈正相关。结论：缺血性脑卒中的复发与多种危险因素有关，其中血纤维蛋白原水平的增加和纤溶功能的降低在复发中起着重要作用；降低血纤维蛋白原的水平和纠正降低的血纤溶功能在预防缺血性脑卒中的复发方面有重要意义。     

高血压患者血浆期纤溶活性变化的意义

研究发现 :高血压存在着凝血纤溶失衡及内皮细胞的损伤[1] ,是心血管疾病和脑血管意外的危险因素之一。本文探讨了高血压的严重程度与纤溶活性的关系 ,以及同时合并冠心病时其纤溶系统的变化和临床意义。1　对象与方法1 1　高血压组　 40 8例患者中 ,高血压Ⅱ期 12 0例 ,平均年龄 (6 2 0 9± 9 88)岁。男 86例 ,女 34例 ;急性脑梗死 10 0例 ,平均年龄 (6 6 2 8± 7 94)岁。男 82例 ,女 18例 ;陈旧性脑梗死 40例 ,平均年龄 (6 6 4 5± 8 32 )岁。男 35例 ,女 5例 ;腔隙性脑梗死 2 0例 ,平均年龄 (6 4 95± 5 17)岁。男 18例 ,女 2例 ;急…     

冠心病患者行为类型与纤溶激活系统的关系

目的：研究不同行为类型冠心病患者之间纤溶激活系统的变化，为冠心病患者心理干预提供理论依据。方法：用A型行为问卷评定56例冠心病患者和52例健康人群，用发色底物法测定他们血浆中的纤溶激活系统中纤溶酶原激活物抑制剂1(plasminogen activator inhibitor1，PAI-1)、组织型纤溶酶原激活物(tissue plasminogen activator，t-PA)活性。结果：冠心病患者PAI-1活性(AU／mL)高于正常人群(1．04&;#177;0．18比0．52&;#177;0．07，t=20．42，P&;lt;0．001)，t-PA活性(IV／mL)低于正常人群(0．35&;#177;0．09比0．38&;#177;0．04，t=2．81，P&;lt;0．01)；这种改变在不同，伺为类型之间比较，与非A型行为类型的冠心病患者比，A型行为类型PAI-1的活性高(1．19&;#177;0．19比0．90&;#177;0.12，t=5．25，P&;lt;0.01)，而t-PA活性低(0．30&;#177;0．08比0．37&;#177;0．09，t=3、53，P&;lt;0.01)，差异有显著性。结论：冠心病患者随着A型行为的增加，血浆中PAI-1活性上升，t-PA活性下降，导致凝血功能亢进，纤溶功能下降，血液处于高凝状态，促浏血栓形成和发展，从而导致各种血管性事件的发生。     

冠心病患者行为类型与纤溶激活系统的关系

目的:研究不同行为类型冠心病患者之间纤溶激活系统的变化,为冠心病患者心理干预提供理论依据。方法:用A型行为问卷评定56例冠心病患者和52例健康人群,用发色底物法测定他们血浆中的纤溶激活系统中纤溶酶原激活物抑制剂1(plasminogenactivatorinhibitor1,PAI-1)、组织型纤溶酶原激活物(tissueplasminogenactivator,t-PA)活性。结果:冠心病患者PAI-1活性(AU/mL)高于正常人群(1.04±0.18比0.52±0.07,t=20.42,P<0.001),t-PA活性(IU/mL)低于正常人群(0.35±0.09比0.38±0.04,t=2.81,P<0.01);这种改变在不同行为类型之间比较,与非A型行为类型的冠心病患者比,A型行为类型PAI-1的活性高(1.19±0.19比0.90±0.12,t=5.25,P<0.01),而t-PA活性低(0.30±0.08比0.37±0.09,t=3.53,P<0.01),差异有显著性。结论:冠心病患者随着A型行为的增加,血浆中PAI-1活性上升,t-PA活性下降,导致凝血功能亢进,纤溶功能下降,血液处于高凝状态,促进血栓形成和发展,从而导致各种血管性事件的发生。     

慢性心力衰竭患者血浆组织型纤溶酶原激活物和纤溶酶原激活物抑制物-1含量变化及其临床意义

目的　研究慢性心力衰竭 (CHF)患者血浆组织型纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制物 1(PAI 1)含量的变化及其临床意义。方法　用酶联免疫吸附法 (ELISA)检测 6 0例CHF患者 (CHF组 )和 2 0例健康体检者 (正常对照组 )血浆t PA及PAI 1抗原含量。结果　CHF组血浆t PA和PAI 1平均含量都明显高于对照组 (P<0 .0 1)。CHF患者血浆PAI 1含量增高随心功能恶化而愈加明显。结论　CHF患者纤溶功能明显下降 ,可用血浆t PA、PAI 1含量作为判断病情的参考指标之一。     

厄贝沙坦对高血压患者纤溶活性内皮素一氧化氮降钙素基因相关肽的影响

目的　观察厄贝沙坦治疗原发性高血压(EH)时对纤溶活性、内皮素(ET)、一氧化氮(NO)、降钙素基因相关肽(CGRP)的影响。方法　6 2例健康体检者作为正常对照组,6 8例EH患者用厄贝沙坦治疗8周,观察用药前后血压、血浆组织型纤溶酶原激活物(t -PA)及其抑制物(PAI)活性及内皮素、一氧化氮、降钙素基因相关肽浓度的变化。结果　EH患者t PA活性、CGRP和NO浓度明显低于正常对照组(P <0 .0 1) ;而PAI活性、ET浓度明显高于正常对照组(P <0 .0 1) ,厄贝沙坦治疗后,血压显著低于治疗前(P <0 .0 1) ,血t -PA活性、NO、CGRP浓度均较治疗前显著升高(P <0 .0 1) ;血ET浓度显著下降(P <0 .0 1)。结论　EH患者存在纤溶活性和内皮功能异常;厄贝沙坦可改善EH患者纤溶活性和内皮功能。     

肝硬化患者纤溶活性指标的检测及其临床意义

目的 探讨肝硬化患者纤溶活性指标的变化及意义。方法 将80例肝硬化患者根据Child-Pugh分级分为三组：A级组30例,B级组32例,C级组18例。均同时检测组织纤溶酶原激活物（tPA）,组织纤溶酶原激活物抑制物（PAD、纤维蛋白（原）降解产物（FDP）和D-聚体。结果 随病情的加重,肝硬化患者纤维蛋白原活性明显下降,D-聚体和t—PA显著升高,差异有统计学意义（P〈0．05）。PAI活性变化不大,差异无统计学意义（P〉0．05）。结论 t-PA随病情加重而显著性升高．PAI无显著性变化,t-PA与肝硬化程度密切相关,其检测有利于了解肝硬化的进程。     

Alteration of serum enzymes in primary hypothyroidism.

In order to study the relationships between serum enzymes and the degree of hypothyroidism, 114 patients with primary hypothyroidism aged from 7 to 65 years were investigated. Forty one percent of patients exhibited normal levels of serum enzymes, while 59% had high levels either alone or in combination. The frequency of enzyme elevation was as follows: creatine kinase: 37%, aspartate aminotransferase: 35%, alanine aminotransferase: 29%, amylase: 15%, alkaline phosphatase: 3%. No significant correlation between thyroid stimulating hormone and serum enzyme levels was observed. This was due to highly variable release of enzymes from cells resulting presumably from individual metabolic set-point. Replacement therapy with thyroxine resulted in remarkable lowering of creatine kinase not only from high level to normal as early as 3 weeks even before normalization of thyroid stimulating hormone, but also from high normal to low normal level. The elevation of amylase and its response to thyroxine is being reported for the first time.     

Alteration of platelet glucose transport system in atherosclerosis

Functional and biochemical alterations of platelets in patients suffering from atherosclerosis were studied in our laboratory. One of the most striking alterations observed is in the platelet active glucose transport system. The Na+/K+ gradient dependent active transport system of glucose is found to be absent in the platelets of atherosclerotics. The platelet glucose transport kinetics in these subjects give unsaturable and linear kinetics. Furthermore, the specific glucose binding protein activity detected in the incubation fluid after cold osmotic shock to the platelets of normal subjects is found to be absent in the platelets of atherosclerotics. The platelet active glucose transport system is normal in juvenile onset diabetics, whereas it is impaired in maturity onset diabetics with clinical manifest atherosclerosis. The release inducers like ADP, adrenalin and collagen exert no effect on the platelet active glucose transport system. The specific glucose-binding protein is an unreleasable protein in the platelets of normal subjects. Hence, the absence of active glucose transport system in atherosclerotics is not due to the activated platelets in circulation.     

Understanding primary pulmonary hypertension

Primary pulmonary hypertension (PPH) is a severe and progressive disease. It is characterized by persistent elevation of pulmonary artery pressure without any known cause. The hemodynamics demonstrates high pulmonary artery pressure and resistance to blood flow through the lung circulation. PPH is a diagnosis of exclusion. The diagnosis is often delayed because the initial symptoms may be mild and the exam findings subtle. The mean age of survival is 2.8 years without treatment. With treatment patients can survive for more than 10 years. Current lifetime treatment includes anticoagulation, oxygen, digoxin, calcium channel blockers, vasodilators, and diuretics. Promising results have been obtained with prostacyclin and endothelin receptor antagonists. Lung transplantation can be considered for patients with advances PPH and those not responding to medical therapy.     

Prothrombotic mechanisms in primary pulmonary hypertension

Pulmonary hypertensive states are associated with an increased propensity for thrombosis. This prothrombotic state appears to be a result of pulmonary hypertension promoting endothelial dysfunction and altered hemodynamic status. In some patients with primary pulmonary hypertension, however, a primary prothrombotic state directly induces the pulmonary hypertensive state. This review focuses on the evidence for the association between prothrombotic states, especially increased platelet activation, and the development of pulmonary hypertension.     

Hypomagnesemia and hypertension in primary hyperparathyroidism

A retrospective study of 89 patients with surgically proven primary hyperparathyroidism was done to gain insight into the pathogenesis of hypertension associated with this condition. The 43 patients (48%) who were hypertensive did not differ significantly from the normotensive patients with regard to age, sex, serum calcium and phosphate levels, and creatinine clearance. However, the mean serum magnesium level was significantly lower in hypertensive hyperparathyroid patients (1.52 +/- 0.24 mEq/L) than in normotensive hyperparathyroid patients (1.76 +/- 0.18 mEq/L; P less than .001), irrespective of use of diuretics in the former group. Although some studies implicate hypomagnesemia in the pathogenesis of essential hypertension, we are unaware of any previous human study reporting a link between hypomagnesemia and hypertension associated with primary hyperparathyroidism. This study suggests that a low level of serum magnesium may play a role in the pathogenesis of hypertension associated with primary hyperparathyroidism, a finding that needs further evaluation.     

Once-daily metoprolol in primary hypertension.

The antihypertensive effect of the selective beta-1-adrenoceptor blocker, metoprolol, administered once daily was evaluated in 32 patients with primary hypertension. After a 4-wk placebo period, the patients were treated with either 150 mg or 300 mg of metoprolol, once daily, for 8 wk. Initially and during the treatment periods blood was drawn for analysis of metoprolol in plasma, plasma renin activity (PRA), and electrolytes, and urine was collected for determination of the urinary aldosterone excretion. Metoprolol reduced the blood pressure measured up to 26 hr after the last dose. The percentage of responders to metoprolol (decrease of mean arterial pressure greater than or equal to 10% over placebo) was 40% for patients on 150 mg and 71% for patients on 300 mg. Except in the standing position, heart rates were reduced for 26 hr after a 150-mg dose. There was a correlation between pretreatment PRA levels and antihypertensive effect of metoprolol in patients on 300 mg metoprolol but not in patients on 150 mg. Urinary aldosterone decreased equally during treatment in responders and nonresponders. Antihypertensive effects and side effects did not correlate with plasma metoprolol concentrations.