脑梗死患者纤维蛋白原、D-二聚体、血小板的浓度临床观察

目的探讨纤维蛋白原、血小板、D-二聚体与脑梗死发病有关。方法观察有血栓倾向的疾病、TIA、急性脑梗死患者及正常对照组纤维蛋白原、血小板、D-二聚体的浓度。结果脑梗死急性期的纤维蛋白原、D-二聚体明显高于其他疾病组,血小板明显低于其他疾病组及正常对照组,非腔隙性脑梗死组纤维蛋白原、D-二聚体的浓度明显高于腔隙性脑梗死组,脑梗死各亚组血小板浓度比较无明显差别。结论血小板、FIB、D-二聚体的变化出现在脑梗死之前,它们促进了血栓的形成,纤维蛋白原、D-二聚体的水平可作为评价病情严重程度的指标。     

妇科恶性肿瘤手术前后血浆D-二聚体变化及临床意义

目的:探讨妇科恶性肿瘤手术前后患者血浆D-二聚体动态变化及其临床意义。方法:选择20例妇科恶性肿瘤作为观察组,采用酶联免疫法检测患者术前、术后1小时、24小时、3天、7天的血浆D-二聚体含量,并与对照组比较。结果:术前血浆D-二聚体含量高于对照组(P<0.05),术后24小时、3天血浆D-二聚体水平显著增高,术后7天患者血浆D-二聚体含量与对照组比较(P>0.05)。结论:妇科恶性肿瘤患者术前体内可能处于高凝状态,术后患者体内肿瘤切除,D-二聚体恢复正常水平。因此,D-二聚体作为纤溶系统敏感的指标,动态检测并观察其变化,有助于观察病情变化、治疗效果和预后判断。     

血小板、D-二聚体在感染性休克早期集束化治疗中的临床应用

目的 探讨血小板、D-二聚体在感染性休克早期集束化治疗中的临床应用价值.方法 随机选取成人综合ICU感染性休克患者60例,均予以早期集束化治疗.于集束化治疗前、治疗后6h,入ICU 1、2、3、4、5d,分别检测血小板计数、D-二聚体浓度,并分别记录各时间点急性生理学和慢性健康状况评分系统Ⅱ(APACHE Ⅱ)评分.根据患者28 d转归分为存活组与死亡组,比较两组不同时间点相关指标,并对本组内各时间点相关指标与集束化治疗前进行比较.分别将两组内血小板计数、D-二聚体浓度与APACHEⅡ评分进行相关分析.结果 存活组APACHE Ⅱ评分、D-二聚体随着病情好转下降,死亡组则呈升高趋势;存活组血小板计数随着病情好转逐渐升高,而死亡组则逐渐下降.经Pearson相关分析,APACHEⅡ评分与血小板计数呈负性相关(r=-0.862,P＜0.01),与D-二聚体浓度呈正相关(r=0.445,P＜0.01).结论 血小板计数、D-二聚体浓度可作为感染性休克治疗效果及预后的评价指标,与APACHEⅡ评分结合,能更准确地评估感染性休克病情的严重程度及预后.     

晚期非小细胞肺癌血浆纤维蛋白原、D-二聚体及血小板水平与预后的相关性研究

目的探讨晚期非小细胞肺癌患者血浆纤维蛋白原、D-二聚体水平及血小板计数与其预后的相关性。方法测定112例晚期非小细胞肺癌患者（肺癌组）及30例健康体检者（对照组）血浆纤维蛋白原、D-二聚体水平及血小板计数并进行对比分析。结果肺癌组血浆纤维蛋白原、D-二聚体水平及血小板计数高于对照组（P〈0.05）,肺癌组血浆纤维蛋白原、D-二聚体水平及血小板计数与病理类型、肿瘤大小、TNM分期之间无明显关系。晚期非小细胞肺癌患者血浆纤维蛋白原、D-二聚体水平及血小板计数与生存期呈显著负相关。结论晚期非小细胞肺癌患者血液处于高凝状态,血浆纤维蛋白原、D-二聚体水平及血小板计数与患者的预后密切相关。抗凝治疗对控制晚期非小细胞肺癌患者病情的发展及预后可能有重要的临床意义。     

D-二聚体实验室检查的临床意义分析

目的分析D-二聚体实验室检查的临床意义。方法 360例常见疾病患者,利用乳胶增强免疫投射比浊法检测患者D-二聚体浓度,分析D-二聚体浓度异常情况。结果脑梗死、深静脉血栓形成、肺栓塞患者D-二聚体异常发生率明显高于其他疾病,D-二聚体浓度较其他疾病明显升高,差异有统计学意义(P<0.01);脑梗死、深静脉血栓形成、肺栓塞患者D-二聚体浓度相比差异无统计学意义(P>0.05)。结论通过D-二聚体浓度检测,利于病情判断。通常心脑血管疾病患者D-二聚体浓度升高明显,通过动态观察患者D-二聚体浓度,利于病情预后判断。     

苦参碱对心房颤动犬心房肌I_(KM3)电流的作用

目的探讨正常和持续性心房颤动时犬心房肌M3受体介导IKM3电流的变化及苦参碱对IKM3的作用,为筛选抗心律失常药物作用靶点提供理论和实验依据。方法建立快速心房起搏致心房颤动犬模型,通过膜片钳技术比较犬心房肌正常和模型组电流变化及药物作用的不同。结果持续性心房颤动犬心房肌IKM3电流密度明显增高(实验电压+50mV时,232±81pAvs198±80pA,n=4,P<0.05),苦参碱对IKM3电流有抑制作用,且对正常组抑制作用明显高于模型组。结论M3受体及其介导的IKM3电流可能是治疗房颤的新靶点。     

血栓性疾病和高凝状态患者血浆中D—二聚体测定及其临床意义

用ELISA法测定32例血栓性疾病及高凝状态患者血浆中D-二聚体值的浓度，结果表明弥漫性血管内凝血（DIC）脑梗塞（BI）、急性心肌梗塞（AMI）、深静脉栓塞（DVT）、溶血尿毒综合征（HUS）等明显高干正常。急性早幼粒细胞白血病（APL）伴出血倾向者，D-二聚体值也明显增高，并较其他组更明显，且血小板减少程度与出血范围呈正比。APL伴出血临床尚未达DIC者，测定D-二聚体值增高有助于DIC前状态（preDIC）的诊断。     

血浆D-二聚体水平在乳腺癌诊断及预后中的临床意义

探讨乳腺癌与血浆D-二聚体水平的相关性。对我院收治的乳腺癌及良性乳腺病患者手术前后的血浆D-二聚体水平进行检测,并与健康女性血浆D-二聚体水平进行对比分析。术前乳腺癌组患者的D-二聚体水平及阳性率均明显高于良性乳腺病组及健康组(P<0.05和P<0.01);D-二聚体浓度、阳性率随病变的恶性程度升高而有上升趋势(P<0.05和P<0.01);Ⅰ期、Ⅱ期乳腺癌患者术后D-二聚体改善程度明显高于Ⅲ期乳腺癌患者(P<0.01)。血浆D-二聚体浓度可作为临床上预测乳腺癌患者临床分期及预后的一项重要指标。     

缺血性脑血管病不同抗凝治疗方法血小板表面及血浆内GMP—140和IL—6结果比较

目的：测定缺血性脑血管病患者抗凝前后血小板表面GMP－140分子数、血浆GMP－140、白介素－6（IL－6）含量的变化，进而比较不同药物抗凝效果。方法：用放免法测定80例缺血性脑血管病患者和30例对照组血小板表面GMP－140分子数、血浆GMP－140和IL－6含量，并按缺血性质，临床脑神经功能缺损程度和不同药物治疗前后分组。结果脑血栓形成组和短暂性脑缺血发作组血小板表面及血浆治疗前后分组。结果 脑血栓形成组和短暂性脑缺血发作组血小板表面及血浆GMP－140和IL－6含量均明显高于其对照组；抗凝后均明显低于抗凝前并随时间呈下降趋势；抗凝前与抗凝后第三天血小板及血浆GMP－140含量之间呈正相关（r=0.55,r=0.65,P值均＜0．05）；低分子肝素抗凝稍好于其它方法，联合治疗优于单项治疗（P＜0．05）。结论：缺血性脑血管病患者应用联合治疗效果更好。     

丹参酮Ⅱ-A磺酸钠对家兔心房动作电位及快速起搏所致心房电重构的影响

目的研究丹参酮ⅡA磺酸钠(TSN)对家兔在体心房单相动作电位(AMAP)及短期快速心房起搏时电重构的影响,探讨其防治房颤的可能机制。方法家兔24只,随机分为对照组与TSN组各12只。将电极经颈内静脉置入右心房记录AMAP,观察基础状态下、给药后0.5 h及以600次.m in-1心房快速起搏后0.5 h、8 h AMAP及其频率适应性的变化。结果与起搏前相比对照组AERP200 m s在起搏后0.5h缩短21.2 m s,起博后8h缩短21.6m s(P<0.05),且心房肌的频率适应性丧失。TSN在基础状态下对AMAPA、AMAPD无明显影响,但使AERP200 m s由(105.9±3.8)m s延长至(114.7±7.2)m s(P<0.05)。起搏后TSN组维持原有的心房肌频率适应性。结论快速心房起搏使心房肌的频率适应性丧失而致电重构,TSN能通过抑制L-型钙通道减轻短期快速心房起搏所致电重构。     

蝙蝠葛碱对家兔急性房颤连接蛋白40重构的影响及其机制

目的　观察快速心房起搏所致急性心房颤动 (房颤 )对家兔心房肌组织Ca2 + 含量和连接蛋白 4 0 (Connexin 4 0 ,Cx4 0 )重构的影响以及钙通道阻滞剂蝙蝠葛碱 (DAU)的干预作用 ,并对其作用机制进行探讨。方法　 32只家兔随机分为 3组 :对照组 (n =8)、房颤组 (n =12 )、DAU组 (n =12 )。经颈内静脉将电极置入右心房 ,对照组不予心房起搏 ,另外两组以 6 0 0beat·min-1行快速心房起搏以诱发房颤 ,并且DAU组于快速起搏前 30min按 5mg·kg-1静脉给予DAU ,其余两组则给予等量的生理盐水。用生化方法检测右心耳组织Ca2 + 含量 ,并分别用Westernblot和免疫荧光标记激光共聚焦显微镜检测Cx4 0的含量和分布。结果　房颤组心房组织Ca2 + 含量高于对照组 ,Cx4 0含量低于对照组 (P均 <0 0 1) ,房颤组Cx4 0分布不均一 ;蝙蝠葛碱组Ca2 + 、Cx4 0含量分别低于和高于房颤组 (P均 <0 0 5 ) ,Cx4 0分布不均一的程度较房颤组减轻。结论　快速心房起搏诱发急性房颤可引起家兔心房肌Ca2 + 含量升高、Cx4 0含量降低和分布不均一 ,蝙蝠葛碱能有效抑制Ca2 + 含量升高、减轻Cx4 0重构 ,钙超载可能参与房颤Cx4 0重构。     

高频刺激右心耳引起家兔慢性心房颤动

目的 探讨以高频率起搏刺激右心耳建立家兔慢性心房颤动模型的方法.方法 20只家兔随机分为实验组及对照组,对照组为假手术组.植入起搏电极但不起搏;实验组10只家兔予开胸植入双极电极并予以(800次/min)刺激右心耳30d,4h/d,术后定期监测起搏、心房颤动的发生情况,同时测定起搏前及房颤发生后心房有效不应期(AERP)的变化.结果 实验组均完成了实验,术后第7d,7只(70%),兔发生了房颤,2周时共有8只(80%)发生了房颤并能稳定维持(与对照组比较,P<0.01),30 d时仍示房颤,其余2只兔至30d时仍呈起搏心律;对照组则未发生任何心律失常情况.AERP缩短,AERP频率适应不良,与基础状态相比有显著意义.结论 长期高频率起搏刺激家兔右心耳是建立慢性房颤模型的有效方法.     

Acute hemodynamic, hormonal, and renal effects of neutral endopeptidase inhibition in ovine heart failure.

The effects of neutral endopeptidase inhibition (NEP-I) were studied in 6 conscious sheep with heart failure (HF) induced by rapid ventricular pacing for 7 days. Measurements were performed 1 h before and for 6 h after intravenous (i.v.) bolus administration of vehicle and SCH 39370 (1.25 and 5 mg/kg) on separate days. After the higher dose, an index of serum NEP activity decreased from 0.83 +/- 0.05 to 0.13 +/- 0.07 nmol/ml/min (p less than 0.001) at 1 h and then returned to control levels at 6 h. Plasma atrial natriuretic peptide (ANP) and cyclic GMP rose from 328 +/- 28 and 20.2 +/- 4.3 to a peak of 570 +/- 65 pmol/L (p less than 0.001) and 28.7 +/- 6.3 nmol/L (p less than 0.05) respectively. Natriuresis and diuresis were significant and left atrial pressure (LAP) decreased from 21.9 +/- 1.1 to 20.1 +/- 0.8 mm Hg (p less than 0.05). Despite high endogenous ANP levels in HF, NEP-I further increases both ANP and its "second messenger." Its natriuretic and hemodynamic effects are consistent with enhanced ANP activity in renal and vascular tissues, suggesting that NEP-I may be useful for treating HF.     

Preserved effects of potassium channel blockers in the pacing-induced remodeled canine atrium: a comparison between E4031 and azimilide

This study was designed to evaluate the electrophysiologic effects of E4031 (a pure IKr blocker) and azimilide (AZ: a combined Ikr + IKs blocker) at various stages of atrial electrical remodeling. Twelve dogs underwent continuous rapid atrial pacing (400/min) for 14 days. The electrophysiologic study was performed on the day before as well as after 2, 7, and 14 days of rapid atrial pacing both before and after the administration of either E4031 (n = 6) or AZ (n = 6). In response to rapid atrial pacing, the atrial effective refractory period (ERP), conduction velocity, and wavelength decreased significantly at pacing cycle lengths (PCLs) of 200 and 400 ms (P < 0.05). E4031 prolonged ERP in a reverse use-dependent manner throughout the study period. AZ also prolonged ERP during the 14 days of rapid pacing. ERP prolongation at a PCL of 200 ms was significantly greater with AZ than with E4031 (P < 0.05). The effects of blocking IKr by E4031 and IKr + IKs by AZ were well preserved at various stages of atrial electrical remodeling. However, the effect of prolonging ERP at a shorter PCL was more prominent by AZ than by E4031. Thus, IKs blockade may add a favorable anti-fibrillatory effect to IKr blockade even in the remodeled atrium.     

Electropharmacologic effects of pilsicainide, a pure sodium channel blocker, on the remodeled atrium subjected to chronic rapid pacing.

Clinical experience suggests that sodium channel blockers are effective in converting atrial fibrillation of recent onset but not chronic atrial fibrillation. We investigated changes in the electrophysiologic effects of pilsicainide, a pure sodium channel blocker, on the canine atrium during chronic rapid pacing (400/min). Three pairs of bipolar electrodes were sutured to the right atrial appendage in six dogs. Five days later, rapid atrial pacing was started after baseline measurements of the effective refractory period (ERP), the intra-atrial conduction velocity, the atrial wavelength, and the inducibility of atrial fibrillation. These studies were repeated at 2, 7, and 14 days of pacing, both before and after pilsicainide administration. Before pacing, pilsicainide increased ERP more than it decreased conduction velocity, causing an increase of wavelength, particularly at faster rates. However, this use-dependent prolongation of ERP disappeared after 2 days of pacing. Thus, pilsicainide failed to prolong ERP during chronic pacing, allowing progressive shortening of wavelength in the remodeled atrium. The effect of sodium channel blockers on atrial refractoriness may decline as rapid atrial excitation persists, limiting the usefulness of these agents for the treatment of chronic atrial fibrillation.     

ANP infusion in the treatment of heart failure and comparison with ACE inhibition.

The therapeutic potential of atrial natriuretic peptide (ANP) was assessed in an ovine model of heart failure induced by rapid left ventricular (LV) pacing and compared with the effects of angiotensin converting enzyme (ACE) inhibition. Hemodynamic, hormonal, and metabolic measurements were studied during three 5-day periods of LV pacing. No treatment (control) or a continuous ANP infusion (25 ng/kg/min) was given in random order during the first two periods, while ACE inhibitor was always given during the third period. Baseline measurements immediately prior to the start of each pacing phase showed no significant variation. Significant neurohumoral activation and hemodynamic responses were observed in each pacing phase. During ANP infusion, plasma ANP levels were 3-5-fold higher than those observed in the control or ACE inhibition treatment phases. Compared with control, a natriuresis was observed on the first day, whereas glomerular filtration rate (GFR) tended to be maintained during ANP infusion. The rise in left atrial pressure and plasma aldosterone tended to be blunted. When the two treatment phases were compared, the rise in left atrial pressure during LV pacing was less with ACE inhibition, whereas there was a similar reduction in sodium retention after the initial natriuresis with ANP. By contrast, GFR tended to be maintained better during ANP infusion compared to ACE inhibition. These results suggest that ANP, or a similar "enhancing" analogue, may be useful in the treatment of heart failure, especially if administered early in the development of the disorder.     

冠心病患者血清一氧化氮α-颗粒膜蛋白的含量及临床意义

目的　探讨一氧化氮 (NO)、α 颗粒膜蛋白 (GMP 14 0 )在冠心病 (CHD)发病机制中的作用。方法　采用Griess比色法 ,酶联免疫吸附试验检测了 4 0例冠心病患者 (其中 2 2例不稳定型心绞痛患者 ,18例稳定型心绞痛患者 )血清中NO、GMP 14 0的水平。结果　①冠心病组血清NO水平显著低于正常对照组 (P <0 0 1) ,GMP 14 0水平显著高于正常对照组 (P <0 0 1)。②不稳定型心绞痛组NO水平显著低于稳定型心绞痛组 (P <0 0 1) ,GMP 14 0水平显著高于稳定型心绞痛组 (P <0 0 1)。③冠心病组血清NO与GMP 14 0水平间呈显著负相关 (r =- 0 70 5 ,P <0 0 1)。结论　血清NO、GMP 14 0水平在冠心病的发生、发展中起着重要的作用 ,动态检测患者血清NO、GMP 14 0的水平 ,有助于临床判断病情和观察疗效     

Brain natriuretic peptide reverses the effects of myocardial stunning in rabbit myocardium

We tested the hypothesis that brain natriuretic peptide (BNP) would decrease the effects of myocardial stunning in rabbit hearts. We also examined the mechanisms responsible for these effects. In two groups of anesthetized open-chest rabbits, myocardial stunning was produced by 2 15-min occlusions of the left anterior descending artery separated by 15 min of reperfusion. The treatment group had BNP (10(-3) mol/l) topically applied to the stunned area. Hemodynamic and functional parameters were measured. Coronary flow and O2 extraction were used to determine myocardial O2 consumption. In separate animals, we measured the function of isolated control and simulated ischemia (95% N2/5% CO2, 15 min)-reperfusion ventricular myocytes with BNP or C-type natriuretic peptide (10(-8)-10(-7) mol/l) followed by KT5823 (10(-6) mol/l, cyclic GMP protein kinase inhibitor). In the in vivo control group, baseline delay to contraction was 47+/-4 ms and after stunning it increased to 71+/-10 ms. In the treatment group, baseline delay to contraction was 40+/-7 ms, and after stunning and BNP it did not significantly increase (43+/-6 ms). Neither stunning nor BNP administration affected regional O2 consumption. In control myocytes, BNP (10(-7) mol/l) decreased the percent shortening from 6.7+/-0.4 to 4.5+/-0.2%; after KT5823 administration, the percent shortening increased to 5.4+/-0.5%. In ischemia-reperfusion myocytes, BNP (10(-7) mol/l) decreased the percent shortening less from 5.0+/-0.5 to 3.8+/-0.2%; KT5823 administration did not increase the percent shortening (3.8+/-0.2%). BNP similarly and significantly increased cyclic GMP levels in control and stunned myocytes. The data illustrated that BNP administration reversed the effects of stunning and its mechanism may be independent of the cyclic GMP protein kinase.     

BLUNTED NATRIURETIC RESPONSE TO ENDOGENOUS ATRIAL NATRIURETIC PEPTIDE DURING RAPID CARDIAC PACING IN ANAESTHETIZED DOGS

1. We investigated whether diuresis and natriuresis induced by endogenous atrial natriuretic peptide (ANP) were blunted during rapid cardiac pacing. 2. Changes in plasma ANP, renal function and haemody-namics during rapid cardiac pacing were studied in anaesthetized closed-chest dogs. Dogs were paced via the right ventricle at a rate of 200 b.p.m. (moderate pacing) or 250 b.p.m. (severe pacing) for 180 min. 3. The maximal increases in plasma ANP and urinary excretion of cGMP during severe pacing were four- and three-fold higher, respectively, than those during moderate pacing. Despite the higher concentration of plasma ANP, the maximal increases in urine volume, urinary excretion of sodium and fractional excretion of sodium during severe pacing were similar to those during moderate pacing. Mean arterial pressure and renal vascular resistance were decreased only by severe pacing. The increase in total peripheral resistance during severe pacing was significantly smaller than that during moderate pacing. However, the glomerular filtration rate was kept at basal levels by both moderate and severe pacing. 4. These results suggest that there are certain mechanisms that counteract renal tubular sodium reabsorption induced by endogenous ANP under conditions of severe pacing. The suppression occurs at tubular sites but not at glomerular sites. One of the possibilities for the suppression is the decrease in renal perfusion pressure accompanied by decreases in peritubular capillary hydrostatic pressure.