氯吡格雷对早期糖尿病肾病患者血液流变学及尿MA的影响

早期糖尿病肾病患者（尿微量白蛋白：20—200mg／L）60例随机分为常规治疗组（n=30）和氯吡格雷治疗组（n=30），氯吡格雷组在常规治疗组基础上加用氯吡格雷75mg每晚口服，持续1月，测定各组治疗前、后血液流变学指标及血糖、血脂、U—mAlb。结果氯吡格雷组的全血粘度、血浆比粘度、血浆纤维蛋白原浓度、血小板聚集率及尿微量自蛋白均显著低于常规治疗组（P〈0．05），结论氯吡格雷对早期糖尿病肾病患者血液流变学有不同程度的改善并能有效降低尿微量白蛋白。     

脑心通胶囊对短暂性脑缺血发作的疗效及对血液流变学的影响

目的研究脑心通胶囊对短暂性脑缺血发作（TIA）的疗效及对血流变学的影响。方法对32例TIA患者使用脑心通胶囊治疗，并进行开放性自身对照研究，在治疗前后检测红细胞比容、血浆黏度、全血黏度（中切）、全血还原黏度（中切）、纤维蛋白原及血小板聚集率并观察疗效。结果治疗开始后TIA发作相继减少，停止发作时间分别为1d内4例，3d内16例，6d内8例，9d内4例，随访半年无复发，未见脑梗死病例发生，无药物不良反应发生。治疗前后血浆黏度、全血黏度（中切）、红细胞比容、纤维蛋白原、血小板聚集率间差异均有统计学意义（P〈0．01）。结论脑心通胶囊能明显改善TIA患者血流变并获得疗效，可作为缺血性脑卒中的治疗和预防用药。     

老年突发性耳聋患者血液流变学和甲襞微循环的改变

目的探讨突发性耳聋（突聋）与血液流变学和甲襞微循环的改变的关系。方法检测35例突聋患者的全血黏度、血浆黏度、纤维蛋白原、血小板聚集率和甲襞微循环指标，并与健康体检者进行对照分析。结果突聋组全血黏度、血浆黏度、纤维蛋白原、血小板聚集率、甲襞微循环的改变均明显高于正常对照组（P〈0.05～0.01）。结论血液流变学及甲襞微循环的改变可能与突聋的发生相关。     

缺血性股骨头坏死患者与正常受试者血浆糖盏蛋白水平的比较其临床意义

目的探讨缺血性股骨头坏死患者血浆糖盏蛋白水平的改变及其临床意义。方法检测在华中科技大学同济医学院附属协和医院骨伤科病房与门诊就诊的52例缺血性股骨头坏死患者和48名健康志愿者的血浆糖盏蛋白水平、血小板聚集率和纤维蛋白原含量,对每位受试者均做Harris评分。结果缺血性股骨头坏死患者血浆糖盏蛋白水平较正常人升高,血小板聚集率较正常人降低。血浆糖盏蛋白水平与股骨头坏死危险因素不相关,与Harris评分及纤维蛋白原呈正相关。血小板聚集率4 min和10 min时与纤维蛋白原正相关,2 min时与纤维蛋白原不相关。结论高含量纤维蛋白原促进糖盏蛋白的产生,其通过竞争性抑制血小板聚集缓解临床症状。血浆糖盏蛋白升高可能是缺血性股骨头坏死的一种自我保护机制。     

灯盏细辛注射液对高血压病病人血液流变学的影响

目的探讨灯盏细辛注射液对高血压病病人血液流变学的影响.方法选取30例1级～2级高血压病病人,给予灯盏细辛注射液20 mL(90 mg)溶于生理盐水250 mL中静脉输注,每日1次,连用10 d,观察用药治疗前后全血高切黏度、低切黏度、红细胞聚集指数、血浆黏度、血小板黏附率及纤维蛋白原的改变情况.结果 30例1级～2级高血压病病人经灯盏细辛注射液20 mL(90 mg)治疗10 d后,全血高切黏度、低切黏度、红细胞聚集指数、血浆黏度、血小板黏附率、纤维蛋白原均有明显改善,治疗前后自身比较有统计学意义.结论灯盏细辛注射液能降低高血压病病人的血液黏滞度,减少心脑血管阻塞事件的发生.     

复方七芍降压片治疗高血压病的临床研究

目的探讨复方七芍降压片治疗高血压病的临床疗效及作用机制.方法采用随机单盲对照法设置治疗组30例,对照组30例,治疗组服用复方七芍降压片,对照组服用卡托普利.观察两组治疗前后的血浆神经肽Y(NPY)变化及血小板聚集率的变化.结果两组均能降低血压及血浆NPY的含量;治疗组中医证候总有效率优于对照组;治疗组可降低血浆纤维蛋白原的含量及改善血小板聚集率,对照组则降低作用不明显.结论复方七芍降压片治疗高血压病有较好的临床疗效且无明显毒副反应.     

血液透析患者血小板聚集功能的变化

对１５例维持性血液透析（ＨＤ）患者进行了血小板聚集试验和部分凝血参数测定。结果显示，ＨＤ组血小板聚集率和血小板ＡＴＰ释放均显著低于正常对照组（Ｐ＜０．０１），表明ＨＤ患者存在血小板功能缺陷。血液透析后血小板聚集率和血浆血栓烷Ｂ２水平显著增高（Ｐ＜０．０１），提示血透过程中血小板被激活。凝血多数测定结果显示ＨＤ组血浆纤维蛋白原和ＶＷＦ水平显著高于对照组（Ｐ＜０．０５），而抗凝血酶Ⅲ活性和纤溶酶原活性则低于对照组（Ｐ＜０．０５）。作者初步讨论了这些变化的机理及其对止血凝血功能的影响，认为它们是引起ＨＤ患者出血倾向和血栓栓塞现象的重要原因。     

肺心病患者血小板膜蛋白P－selectin与血小板功能的变化

采用同位素标记的单克隆抗体（￣（１２５）Ｉ－ＳＺ＿（５１））观察了３０例慢性肺心病患者血小板膜蛋白Ｐ－ｓｅｌｅｃｔｉｎ的变化及血小板粘附、聚集功能变化的关系。结果显示，慢性肺心病患者的血小板膜蛋白Ｐ－ｓｅｌｅｃｔｉｎ较慢性肺病组及与正常人群比较显著升高（Ｐ＜０．０１），同时与血小板的粘附功能、聚集功能具有良好的相关性（Ｐ＜０．０１），血浆中的ｖｏｎＷｉｌｌｅｂｒａｎｄ因子（ｖＷＦ）、纤维蛋白原水平升高并促进血小板粘附及聚集。     

血液生物平衡疗法治疗血液流变学异常者的观察

目的：探讨血液生物平衡法治疗血液流变学异常的疗效。方法：对21例血液流变学异常进行血液生物平衡治疗，20例采用传统方法治疗作为对照。结果：采用血液生物平衡治疗在降低血浆粘度、红细胞压积、全血粘度、血纤维蛋白原及血小板聚集率等方面疗效显（P＜0．01），而对照组治疗前后均无明显改变（P＞0．05）。结论：血液生物平衡疗法治疗血液流变学异常疗效好，且方便易行，便于临床推广。     

脑梗死患者凝血功能的分析

目的分析脑梗死患者凝血图及血小板数目、体积变化情况，探讨脑梗死发生发展的理论依据。方法对80例发病时间在6～24h内的脑梗死患者测定其血小板数目（PLT）、平均血小板体积（MPV）及凝血图，并与正常人比较。结果脑梗死患者的血浆纤维蛋白原含量（FIB）及平均血小板体积（MPV）均显著高于正常人。结论平均血小板体积（MPV）和血浆纤维蛋白原含量（FIB）的异常与脑梗死的发生发展密切相关。     

Effects of antihypertensive treatment on platelet function in essential hypertension.

To evaluate the effect of antihypertensive therapy on platelet activation in essential hypertension, the plasma levels of beta-thromboglobulin (beta-TG) were examined in 45 patients with essential hypertension and 20 age-matched normotensive control subjects. Hypertensive patients were assigned to monotherapy with one of five different antihypertensive drugs for 6 months, and the change of plasma levels of beta-TG was reexamined after the completion of the monotherapy. The plasma beta-TG increased in hypertensive patients compared with levels in normotensive control subjects. Monotherapy with each drug resulted in sufficient blood pressure control in all hypertensive patients. The plasma beta-TG decreased significantly after monotherapy with an alpha-blocker or an angiotensin-converting enzyme inhibitor (ACEI). The plasma beta-TG increased with the use of a diuretic but did not change with the use of a beta-blocker or calcium antagonist. The platelet activation observed in patients with essential hypertension is reversed by monotherapy with an alpha-blocker or an ACEI. It is possible that these drugs reduce the development of hypertensive vascular complications due to suppression of platelet activation in patients with essential hypertension.     

Beta-thromboglobulin and platelet aggregation in essential hypertension and the influence of prazosin therapy

Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or ADP) were determined in twenty-eight normotensive subjects and thirty patients with untreated essential hypertension. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measurements were repeated in eighteen essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline- and ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on platelet aggregation. The results show that increased in vivo activation as well as increased platelet aggregation need not be restored to normal after effective decrease of blood pressure. The results suggest that a combination of drugs with an antihypertensive and antiplatelet (antiaggregating) effect (or use of a drug with both an antihypertensive and antiaggregating effect) can further decrease the development of severe complications of essential hypertension.     

Circulating atrial natriuretic polypeptide in essential hypertension

To investigate the significance of atrial natriuretic polypeptide (ANP) in essential hypertension, we measured plasma ANP concentrations in 43 subjects with essential hypertension uncomplicated by cardiac or renal failure, in 16 subjects with borderline hypertension, and in 17 normotensive control subjects. Plasma ANP levels were significantly higher in hypertensive subjects compared to borderline hypertensive subjects (p less than 0.05) and normotensive control subjects (p less than 0.05). Hypertensive subjects with left ventricular hypertrophy (LVH) had higher plasma ANP levels than the hypertensive group as a whole (p less than 0.05). A significant positive correlation was observed between mean blood pressure and plasma ANP level in the hypertensive group (n = 43, gamma = 0.77, p less than 0.01). Furthermore, plasma ANP level was decreased significantly after 4 weeks of effective antihypertensive therapy compared with the initial value (p less than 0.05). These results suggest that plasma ANP is frequently elevated in hypertensive subjects with markedly high blood pressure or LVH, and it can be reduced by effective therapy with antihypertensive drugs.     

氟伐他丁对老年高血压伴高脂血症者内皮素及血小板聚集功能的影响

探讨老年原发性高血压伴高胆固醇血症者抗高血压同时行调脂治疗对内皮素 (ET)及血小板聚集率(PAG)的影响。方法　 86例老年原发性高血压伴高胆固醇血症者随机分为治疗组 43例和对照组 43例 ,在行调脂饮食及降压治疗的同时观察用氟伐他丁 (2 0～ 40mg/d)前及 12周后的血脂、ET和PAG的变化。结果　治疗组经 12周调脂治疗后血胆固醇下降了 19% (P <0 .0 0 1) ,甘油三酯下降了 9% (P <0 .0 1) ,低密度脂蛋白胆固醇降低了18% (P <0 .0 0 1) ,高密度脂蛋白胆固醇上升了 5 % ;ET显著下降 (P <0 .0 1) ,PAG亦显著下降 (P <0 .0 5 ) ;而对照组血脂水平、ET、PAG虽有降低 ,但无显著性差异。结论　老年原发性高血压伴高脂血症者降压治疗同时使用氟伐他丁不仅可降低血脂 ,同时可改善ET及血小板聚集功能。     

Age and 5HT 2-receptor blockade with ketanserin in essential hypertension

Platelet derived serotonin (5HT) contributes to blood pressure elevation and the development of thromboembolic complications. Among the pathophysiological mechanisms involved in these vascular events, derangements in 5HT kinetics and exaggerated platelet response to 5HT may be part of the major triggering factors. An age-dependent attenuation platelet 5HT kinetics was revealed in normotensive control subjects but not in patients with essential hypertension. In older hypertensive patients, particularly in men, platelet 5HT uptake was decreased. In parallel, platelet reactivity was increased with advancing age as shown by a greater 5HT induced platelet aggregation and higher plasma concentration of beta-thromboglobulin. Antihypertensive treatment with the 5HT2-receptor antagonist ketanserin attenuated platelet 5HT turnover and inhibited 5HT induced platelet aggregation; the latter was more pronounced in older patients. The clinical efficacy and tolerability of ketanserin 20-40 mg twice daily given as mono- or combination therapy was evaluated in 188 patients with mild to moderate essential hypertension for a period of 12 weeks. A greater fraction of patients greater than or equal to 60 years achieved diastolic target pressure of less than or equal to 95 mgHg. Complaints related to the central nervous system or the peripheral circulation were greatly reduced in patients older than 60 years. In older patients, over and above the antihypertensive effect, 5HT2-receptor blockade may play an important role in the prevention of thromboembolic complications by inhibition of 5HT induced platelet activation.     

Alpha 2-adrenergic receptors and arterial pressure

The aim of this work was to investigate the influence of blood pressure levels on human platelet alpha 2-adrenergic receptivity. The study was carried out on 12 mild essential hypertensive patients and 7 normotensive parkinsonians with orthostatic hypotension. Alpha 2-adrenoceptors number and affinity were determined by 3H-yohimbine binding, plasma catecholamines were measured by HPLC and adrenaline-induced platelet aggregation by turbidimetry. Results obtained were compared with those of two groups of 12 normotensive control subjects. In hypertensive patients, both platelet alpha 2-adrenoceptors (139 +/- 6 vs 176 +/- 18 fmol/mg protein) and velocity of adrenaline-induced platelet aggregation were decreased whereas plasma adrenaline and noradrenaline remained unchanged. In patients with orthostatic hypotension, there was an increased number of platelet alpha 2-adrenoceptors (313 +/- 52 vs 168 +/- 8 fmol/mg protein) associated with a significant decrease in plasma noradrenaline (62 +/- 11 vs 190 +/- 25 pg/ml). In none of the two groups of patients there was any change in receptor affinity for 3H-yohimbine. These results indicate that human platelet alpha 2-adrenoceptors levels are related to blood pressure values. Moreover, up-regulation in orthostatic hypotension and lack of down-regulation in essential hypertension suggest that only sustained abnormal plasma noradrenaline levels could allow the development of alpha 2-adrenoceptors regulatory mechanisms. These variations can represent tentative compensatory mechanisms for normalization of blood pressure levels.     

Effect of ACE inhibitors and beta-blockers on homocysteine levels in essential hypertension

Recent studies have shown that antihypertensive drugs like diuretics increase plasma homocysteine (Hcy) levels. However, the effect of other antihypertensive drugs on plasma Hcy levels has not been tested extensively. The aim of present study was to investigate the effect of antihypertensive therapy (AHT) on Hcy levels in essential hypertensive subjects. A case-control study of 273 patients with essential hypertension (EH) and 103 normotensive controls was undertaken. Plasma Hcy levels were measured before and after 6 weeks of AHT. The genotyping of MTHFR C677T polymorphism was performed by polymerase chain reaction-restriction fragment length polymorphism. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers significantly decreased and hydrochlorothiazides significantly increased the plasma Hcy levels in hypertensive patients (P<0.05). No significant association between MTHFR C677T genotypes and changes in Hcy levels in response to antihypertensive was observed in EH patients. The decrease in Hcy induced by beta-blockers and ACE inhibitors observed in our study may be due to the improvement of endothelial function along with improved renal function. Thus, our results suggest that ACE inhibitors and beta-blockers may provide additional beneficial therapeutic effects to the EH patients by decreasing Hcy levels.     

Platelet aggregation in relationship to plasma catecholamines in patients with hypertension.

Plasma catecholamine concentration and platelet aggregation were studied in 22 patients with uncomplicated primary hypertension and 13 age-matched normotensive, healthy subjects at rest and in some during isometric handgrip exercise. The effect of norepinephrine (NE) infusion upon platelet aggregation was also examined. Plasma catecholamine concentration was slightly higher in the hypertensive than the normotensive group, but the difference was not significant. However, platelet aggregation to ADP was significantly greater in the hypertensive than the normotensive subjects. Exercise increased significantly both catecholamines and aggregation in both groups. Platelet aggregation was correlated with age (r = 0.62, P less than 0.01) and plasma NE (r = -0.34, P less than 0.05 for the total group of subjects). The infusion of NE increased significantly plasma NE and platelet aggregation and there was an inverse correlation between NE increase and threshold decrease (r = -0.69, P less than 0.05). Thus, plasma catecholamines and important determinants of platelet aggregation. However, in our study, uncomplicated primary hypertension was not associated with abnormal plasma catecholamine concentration. It is likely that the observed abnormal platelet aggregability to ADP represents a secondary phenomenon, possibly related to more advanced atherosclerotic vascular changes in hypertensive than normotensive subjects.     

The role of plasma substance P and catecholamines in hypertension]

In the present study, the contents of plasma substance P (SP) and noradrenaline (NA) and adrenaline (AD) in human normotensive subjects and patients with essential hypertension as well as Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were measured. The results showed that: (1) The levels of plasma SP in both hypertensive subjects were lower than that in both normotensive subjects. (2) The concentration of plasma NA and AD were significantly higher in patients with essential hypertension than that in normotensive subjects. (3) The levels of plasma SP increased and the concentrations of NA and AD decreased after antihypertensive drug treatment. These results suggest that both plasma SP and catecholamines were involved in essential hypertensive pathogenesis.     

Treatment of hypertension with captopril: preservation of regional blood flow and reduced platelet aggregation

The BP of 12 patients with essential hypertension was controlled with captopril over a period of three months. Cerebral blood flow, muscle blood flow (anterior tibialis muscle), platelet aggregation and platelet thromboxane A2 release were measured during a baseline drug-free period, and measurements repeated during the treatment phase on achieving BP control, after one and three months. Cerebral blood flow rose during the early phase of treatment and then dropped to baseline levels during chronic therapy. Muscle blood flow, both at rest and following maximal exercise, was unaffected by captopril therapy. Platelet aggregation was diminished during therapy, and this finding was paralleled by a reduction in platelet thromboxane A2 generation. Control of hypertension with maintenance of regional blood flow and beneficial changes in platelet function during treatment with captopril may improve the overall risk profile of hypertensive patients. Inhibition of platelet aggregation and thromboxane A2 release may contribute to the antihypertensive action of captopril and the maintenance of regional blood flow.