新活素在重症病毒性心肌炎心力衰竭中的作用

目的 观察新活素在重症病毒性心肌炎心力衰竭中的疗效及安全性.方法 选取2010年1月至2013年12月在我科诊断的重症病毒性心肌炎患者27例,分为新活素组和对照组,新活素组在强心、利尿、扩血管基础上加用新活素治疗,观察两组患者脑利钠肽（BNP）、肌钙蛋白（cTnT）、肌酸激酶同工酶（CK-MB）、心脏彩超改变情况并比较两组的疗效.结果 新活素组能明显降低BNP [（203.1±39.8）vs.（1185.5±48.3） pg/ml]、cTnT [（13.5±9.8）vs.（24.8±13.2） μg/L]、CK-MB [（32.9±10.7）vs.（195.3 ±48.2） U/L],改善左室射血分数[（59.2±9.2）％vs.（38.1±8.8）％],并且疗效优于对照组（P＜0.05）,没有出现明显不良反应.结论 新活素对重症病毒性心肌炎心力衰竭是一个有效安全的治疗措施.     

心衰患者血浆脑钠肽水平的变化及其临床意义探讨

目的探讨慢性心衰患者血浆脑钠肽（BNP）变化的临床意义。方法采用荧光免疫分析法对328例慢性心衰患者及50例健康对照者进行血浆BNP水平的测定,同时以彩色多普勒超声心电动仪测定慢性心衰患者左心室舒张末期内径（LVEDD）、左心室收缩末期内径（LVESD）、左心室射血分数（LVEF）,并与血浆BNP含量作相关性分析。结果慢性心衰组患者血浆BNP水平明显高于健康对照者（P〈0．01）,且不同心功能患者之间的血浆BNP含量亦存在显著差异（P〈0．01）：慢性心衰组患者血浆BNP水平与LVEF、LVESD、LVEDD呈现良好的相关性（r分别为-0．61、0．55和0．59,P均〈0．01）。结论BNP是反映慢性心衰患者心室功能的灵敏指标。     

血浆脑钠素水平与心衰患者左心功能关系的临床研究

为探讨血浆脑钠素(BNP)水平与心力衰竭患者临床心功能变化之间的关系,本文采用IRMA法测定患者血浆BNP水平,同时采用NYHA心功能分级和超声心动图检查评定患者左心功能。结果表明,随着心功能恶化,血浆BNP水平呈上升趋势。各级心功能间均有显著性差异(P<0.05)。经抗心衰药物综合治疗后,BNP水平降低(P<0.01)。BNP水平与左心室射血分数(LVEF)、左心室短轴缩短率(△D%)呈负相关;与左室收缩末内径(LVDS)、左室舒张末内径(LVDd)呈正相关。总之,在患者心力衰竭的进展中其血浆中BNP水平与心衰程度密切相关,测定患者血浆BNP水平是监测心衰程度的有效手段之一。     

血浆脑钠素水平与心衰患者左心功能关系的探讨

目的:为探讨血浆脑钠素(BNP)水平与心力衰竭患者临床心功能变化之间的关系。方法:本文采用IRMA测定患者血浆BNP水平,同时采用NYHA心功能分级和超声心动图检查评定患者左心功能。结果:随着心功能恶化,血浆BNP水平呈上升趋势。各级心功能间差异均有显著性临床意义(P<0.05)。经抗心衰药物综合治疗后,BNP水平降低(P<0.01)。BNP水平与左心室射血分数(LVEF)、左心室短轴缩短率(D%,D即leftventriclefractionshortening)呈负相关;与左室收缩末内径(LVSd)、左室舒张末内径(LVDd)呈正相关。结论:在患者心力衰竭的进展中其血浆中BNP水平与心衰程度密切相关,测定患者血浆BNP水平是监测心衰程度的有效手段之一。     

急性冠脉综合征患者血浆脑钠素水平变化及临床意义

目的探讨急性冠脉综合征(acute coronary syndrome,ACS)患者血浆脑钠素(brain natriuret-ic peptide,BNP)水平的变化规律及对诊断急性冠脉综合征的临床意义.方法采用酶联免疫吸附法测定ACS患者和对照组血浆BNP浓度,将55例ACS患者分为急性心肌梗死组(acute myocardial infarction,AMI组,n=25),不稳定型心绞痛组(unstable angina,UA组,n=30),分别测定症状发作6 h及24h的BNP,并和30例正常健康体检者(对照组)作比较.结果①症状发作6 h内,BNP含量AMI组(60.10±17.10)μg/L和UA组(34.80±14.80)μg/L,均显著高于对照组(10.60±1.70)μg/L(P《0.01).②症状发作24h,AMI组BNP(154.00±18.60)μg/L,UA组BNP(70.31±23.30)μr/L,显著高于正常对照组(10.54±1.80,P《0.01).结论血浆BNP水平升高与ACS有显著关系,并认为血浆BUN水平升高可作为ACS的早期诊断的有效指标.     

血清CA125水平在心力衰竭患者心功能分级中的应用价值

目的 探讨血清CA125(糖类抗原125)与BNP(B型脑利钠肽)水平在心力衰竭患者心功能分级中的变化及其临床意义.方法 收集118例我院2011年1月至2011年12月住院且诊断为心力衰竭患者数据进行回顾性统计学分析.结果 与健康对照组比较,NYHA Ⅱ(纽约心脏病协会心功能分级)、NYHA Ⅲ、NYHA ⅣV、心血管疾病无合并心力衰竭组四组血清CA125、BNP水平均显著高于健康对照组(P＜0.01),且血清CA125与BNP水平升高与NYHA分级呈正相关.不同病因(冠心病、风湿性心脏病、高血压性心脏病、扩张型心肌病、心脏瓣膜疾病)组血清CA125、BNP水平两两比较扩张型心肌病组血清CA125水平显著高于高血压性心脏病组(P＜0.05),而BNP水平在不同病因组中无统计学差异.左心室扩大组血清CA125水平显著高于正常左心室组(P＜0.01);而LVEF水平显著低于正常左心室组(P＜0.01).NYHA分级有胸腔积液、心包积液、房颤组血清CA125水平均高于无上述体征组,且差异具有统计学意义(P＜0.01).血清CA125与BNP呈显著正相关(P＜0.01);血清CA125与LVEF(左室射血分数)呈显著负相关(P＜0.01).结论 结合血清CA125、BNP、LVEF等指标可判断HF严重程度,并为NYHA分级提供实验室辅助依据.血清CA125、BNP、LVEF等指标作为临床实验室指标,综合病因、症状、体征和其他非创伤性指标可有效监控HF的发生与发展.     

原发性高血压患者血浆脑钠素含量及其临床意义

目的 探讨原发性高血压（EH）患者血浆脑钠素含量及其临床意义。方法 采用免疫放射分析法测定122例EH患者和36例对照组血浆BNP浓度；用心脏彩色多普勒超声诊断仪器测定左室质量指数（LVMI）。结果 EH患者BNP浓度显著高于对照组（P〈0．01），且EH伴LVH者BNP浓度明显高于EH无LVH者，差异有非常显著性（P〈0．01）；EH患者不同分级间、不同病程、不同年龄和不同性别问的血浆BNP浓度比较，差异无显著性（P〉0．05）。结论 EH患者血浆BNP水平明显升高．且与LVH密切相关；BNP浓度的测定可望成为EH患者LVH的一项诊断指标。     

脑利钠肽水平联合肺动脉CT评估老年心力衰竭患者预后的价值

目的:研究脑利钠肽（BNP）水平联合肺动脉电子计算机断层扫描（CT）评估老年心力衰竭（HF）患者预后的价值。 方法:选取100例HF患者,根据5年随访的患者生存情况将其分为存活组（n=54）和死亡组（n=46）。检测并比较两组血清 BNP 水平;回顾肺动脉CT 结果,比较右肺动脉直径（RPAD）、室间隔厚度（IVST）、升主动脉直径（AA）、降主动脉直径 （PA）、左肺动脉直径（LPAD）以及主肺动脉直径（MPAD）。结果:与死亡组比较,存活组血清BNP水平、RPAD、LPAD显著 降低,IVST显著升高,差异有统计学意义（P<0.05）;血清BNP水平与RPAD、LPAD呈正相关,与IVST呈负相关,差异均具 有统计学意义（P<0.05）;与单一指标评估相比,BNP水平联合肺动脉CT评估的灵敏度、特异性、准确度、阳性预测值、阴性 预测值、ROC曲线下面积显著升高（P<0.05）。结论:BNP水平联合肺动脉CT评估老年HF患者预后的特异性、灵敏度以 及准确度更高,具有较高的临床参考价值。     

慢性CHF患者BNP与AT-Ⅱ及ALD水平的探讨

目的：探讨慢性充血性心力衰竭患者血中脑利钠肽（BNP）与血管紧张素-Ⅱ（AT-Ⅱ）及醛固酮（ALD）的水平,并进行相关性分析,以提示其在充血性心力衰竭（CHF）发展中的临床意义和价值。方法：使用美国博适公司生产的Triage Meter Plus型免疫荧光定量心衰快速检测仪,检测全血BNP水平。采用放射免疫分析（RIA）受试者血浆AT-Ⅱ、ALD含量。结果：CHF组BNP、AT-Ⅱ、ALD均显著高于对照组,且BNP与AT-Ⅱ、ALD水平呈正相关（P〈0.05）,治疗后血中水平均下降与治疗前差异有显著性（P〈0.01）。结论：同步监测BNP、AT-Ⅱ、ALD有助于早期发现CHF,判断病情及预后。     

雷米普利对充血性心力衰竭患者血循环内皮细胞及脑钠素的影响

目的探讨充血性心力衰竭(CHF)时血循环内皮细胞计数(CEC)、血浆脑钠素(BNP)、血浆内皮素-1(ET-1)及6-酮-前列腺素F1α(6-Keto-PGF1α)水平的变化及雷米普利的干预效应.方法25例CHF患者服用雷米普利两周,并检测用药前后自身外周血循环CEC数量、BNP、ET-1及6-Keto-PGF1α的含量,20例健康体检者为对照组.结果CHF患者CEC数量、血浆ET-1及BNP水平明显增高,6-K-PGF1α明显降低(P均＜0.01).雷米普利治疗可使CEC数量、血浆ET-1及BNP水平明显降低及6-Keto-PGF1α含量显著增加(P＜0.01).结论心力衰竭时存在血管内皮细胞受损,而雷米普利具有保护血管内皮细胞及改善心脏功能的作用.     

急性心肌缺氧对乳鼠心肌细胞脑钠尿肽表达的影响及其作用机制

目的: 观察急性缺氧损伤对乳鼠心肌细胞脑钠尿肽(BNP)表达水平的影响并探讨其可能作用机制。方法: 原代乳鼠心肌细胞缺氧、无糖、无血清培养以模拟心肌缺血损伤,利用CCK-8法测细胞存活率、ELISA法测白细胞介素-6(IL-6)和BNP的表达;以IL-6直接干预体外培养的心肌细胞, 采用RT-PCR、Western blotting和ELISA方法观察BNP、转化生长因子β₁(TGF-β₁)、Smad2 mRNA的转录和蛋白的表达。结果: 缺氧显著上调IL-6和BNP的表达,且两者呈线性正相关;IL-6直接干预可剂量和时间依赖性地上调心肌细胞BNP的mRNA和蛋白表达水平,同时TGF-β₁和Smad2的表达水平亦增加;而针对TGF-β₁的中和抗体能够部分地抑制由IL-6引起的BNP表达增加。结论: 急性心肌缺氧可直接上调BNP的表达水平,这种调节效应与TGF-β₁/Smad2信号通路上调有关。     

Cellular orientation of atrial natriuretic peptide in the human brain

Many peptide hormones and neurotransmitters have been detected in human neuronal tissue. The localisation of atrial natriuretic peptide (ANP) in the human brain was considered to be both interesting and relevant to the understanding of neurochemistry and brain water–electrolyte homeostasis. This vasoactive peptide hormone has been localised in rat and frog neuronal tissue. In the present study, we report the immunohistochemical localisation of ANP in autopsy samples of human brain tissue employing the avidin–biotin–peroxidase complex technique, using an antibody against a 28 amino acid fragment of human ANP. The most intense staining of immunoreactive ANP was detected in the neurones of preoptic, supraoptic and paraventricular nuclei of the hypothalamus, epithelial cells of the choroid plexus and ventricular ependymal lining cells. Immunoreactive neurones were also observed in the median eminence, lamina terminalis, infundibular and ventromedial nuclei of the hypothalamus, and in neurones of the brain stem, thalamic neurones and some neurones of the caudate nucleus. The network of ANP cells in numerous hypothalamic centres may regulate the salt and water balance in the body through a hypothalamic neuro-endocrine control system. ANP in the brain may also modulate cerebral fluid homeostasis by autocrine and paracrine mechanisms.     

利钠肽结构、受体的生理和病理作用

Five natriuretic peptides (NP) have been identified: A- type, B- type, C- type, D-type and V - type. AU of them have tinged- structures. The actions of the natriuretic peptides are modulated through their cognate receptors, which are named as NPR- A, NPR- B and NPR- C. The receptors are in-volved in the cGMP- dependent signaling cascades, which take part in many different physiological regulation,such as diureses, vasedilatation, depressing blood pressure, improving immunity, promoting development of bone, regulating nerve system and so on. At present, AhT and BNP have become a marker in diagnostic some cardiovascular diseases.     

Expression and glucocorticoid regulation of natriuretic peptide clearance receptor (NPR-C) mRNA in rat brain and choroid plexus

The natriuretic peptide clearance receptor (NPR-C) binds atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide with high affinity. This receptor lacks an intracellular guanylate cyclase domain, and is believed to exert biological actions by sequestration of released natriuretic peptides and/or inhibition of adenylate cyclase. The present report summarizes the first detailed mapping of NPR-C mRNA in rat brain. In situ hybridization analysis revealed high levels of NPR-C mRNA expression in frontal and retrosplenial granular cortices, medial preoptic nucleus, ventral cochlear nucleus and choroid plexus. NPR-C mRNA expression was also observed in deep layers of neocortex and limbic cortex, posterior cortical amygdala, ventral subiculum, amygdalohippocampal area, and dentate gyrus. Positive hybridization signal was observed in both anterior and intermediate lobes of the pituitary gland. Regulatory studies indicated that expression of NPR-C mRNA was increased in the medial preoptic nucleus of adrenalectomized rats, suggesting negative glucocorticoid regulation. No changes in NPR-C mRNA expression were observed in frontal cortex or choroid plexus. These results suggest a role for the NPR-C in modulation of natriuretic peptide availability and/or adenylate cyclase activity in a subset of central natriuretic peptide circuits concerned with cortical, olfactory and neuroendocrine functions. Response of the NPR-C gene to changes in circulating hormones suggests the capacity for glucocorticoid modulation of natriuretic peptide action at the receptor level.     

病毒性心肌炎小鼠心肌细胞线粒体DNA缺失的定量分析

目的：探讨线粒体DNA(mtDNA)缺失在病毒性心肌炎(VMC)发病机制中的作用。 方法： 50只BALB/c小鼠随机分为2组，实验组(40只) 腹腔注射内含CVB3(TCID50＝108)的Eagle液制备VMC小鼠模型，另10只为对照组。分别于病毒感染后第3、11和24 d行在体心功能和心肌细胞mtDNA3867缺失率测定，并用Spearman法对mtDNA3867缺失率及心功能测值行相关分析。 结果： 实验组小鼠病毒感染后第3 d心肌细胞mtDNA3867缺失率比对照组高8.3倍［(0.01970±0.00118)% vs (0.00211±0.00032)%，P＜0.05］，同时可见其-dp/dtmax亦显著高于对照组(P＜0.05)；病毒感染后第11 d时，mtDNA3867缺失率比对照组高14.6倍［(0.03292±0.00308)% vs (0.00211±0.00032)%，P＜0.05］，心脏的收缩(LVPSP、+dp/dtmax)和舒张功能(-dp/dtmax)亦有更显著损伤(均P＜0.05)；病毒感染后第24 d时，mtDNA3867缺失率仍显著高于对照组，比后者高11.5倍，其心功能亦未恢复正常。相关分析显示，mtDNA3867缺失率与LVPSP和+dp/dtmax呈显著负相关，与-dp/dtmax呈显著正相关，相关系数分别为－0.66、－0.79和0.80(均P＜0.05)。 结论： mtDNA3867缺失可能是VMC发病的病理生理机制之一。     

Diagnosis and presentation of fatal myocarditis

The clinical presentation of myocarditis is highly variable, and histopathology is thus considered to be the cornerstone of diagnosis. We studied how accurately myocarditis was diagnosed in a series of routine autopsies and how fatal myocarditis presents clinically. All death certificates with myocarditis recorded as the underlying cause of death in Finland in 1970 to 1998 were collected retrospectively (N = 639). All cases with cardiac autopsy samples and clinical data available (n = 142; median age, 51 years) were included in this study. The cardiac samples were reexamined for the presence of myocarditis by 3 experienced independent pathologists using the Dallas criteria. The clinical data were evaluated for the presenting signs and symptoms of myocarditis. Histopathologic reanalysis showed that only 32% of the 142 subjects met the Dallas criteria for myocarditis (75% of pediatric and 28% of adult patients, P = .001). Clinicians had suspected myocarditis in only one third of the hospitalized Dallas-positive patients. Dallas-positive patients presented more often with features of myocardial infarction (26% versus 9%, P = .026) or heart failure (35% versus 10%, P = .001) than Dallas-negative subjects. The signs and symptoms of infectious disease were also more common in Dallas-positive patients (61% versus 23%, P < .001). In contrast, Dallas-negative subjects died suddenly or were found dead more frequently (68% versus 39%, P = .004). The most evident cause of death in the Dallas-negative subjects was ischemic heart disease (n = 78, 55% of all cases). Our study provides evidence that myocarditis is overdiagnosed on routine autopsies, particularly in patients who have died suddenly or are found dead. Fatal myocarditis appears to present equally often as heart failure, sudden death, or mimicking myocardial infarction.     

Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure

Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations were measured in patients with dialysis-dependent chronic renal failure and in patients with coronary artery disease exhibiting normal or elevated left ventricular end-diastolic pressure (LVEDP) (n = 30 each). Blood samples were obtained from the arterial line of the arteriovenous shunt before, 2 h after the beginning of, and at the end of hemodialysis in patients with chronic renal failure. In patients with coronary artery disease arterial blood samples were collected during cardiac catheterization. BNP and ANP concentrations were determined by radioimmunoassay after Sep Pak C₁₈ extraction. BNP and ANP concentrations decreased significantly (P < 0.001) during hemodialysis (BNP: 192.1 ± 24.9, 178.6 ± 23.0, 167.2 ± 21.8 pg/ml; ANP: 240.2 ± 28.7, 166.7 ± 21.3, 133.0 ± 15.5 pg/ml). The decrease in BNP plasma concentrations, however, was less marked than that in ANP plasma levels (BNP 13.5 ± 1.8%, ANP 40.2 ± 3.5%; P < 0.001). Plasma BNP and ANP concentrations were 10.7 ± 1.0 and 60.3 ± 4. 0 pg/ml in patients with normal LVEDP and 31.7 ± 3.6 and 118.3 ± 9.4 pg/ml in patients with elevated LVEDP. These data demonstrate that BNP and ANP levels are strongly elevated in patients with dialysis-dependent chronic renal failure compared to patients with normal LVEDP (BNP 15.6-fold, ANP 2.2-fold, after hemodialysis; P < 0.001 or elevated LVEDP (BNP 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that the elevation in BNP concentrations was more pronounced than that in ANP plasma concentrations. The present results provide support that other factors than volume overload, for example, decreased renal clearance, are also involved in the elevationin BNP and ANP plasma levels in chronic renal failure. The stronger elevation in BNP concentrations in patients with chronic renal failure and in patients with elevated LVEDP and the less pronounced decrease during hemodialysis suggest a different regulation of BNP and ANP plasma concentrations.[/ p]Abbreviations ANP atrial natriuretic peptide - BNP brain natriuretic peptide - LVEDP left ventricular end-diastolic pressure Correspondence to: C. Haug