急性心肌梗死、不稳定型心绞痛及糖尿病患者血浆脑钠素氨基末端前体水平的临床研究

目的 :血浆脑钠素氨基末端前体 [N -terminalpro -brainnatriureticpeptide ,NT - proBNP(1- 76 ) ) ]和脑钠素 (brainnatriureticpeptide ,BNP)来自于同一前体 ,前者水平升高比后者更能反应左室功能不全的程度。本文旨在研究冠心病急性心肌梗死、不稳定型心绞痛以及糖尿病患者血浆NT -ProBNP(1- 76 )水平的变化 ,以探讨NT -ProBNP(1- 76 )在上述疾病过程中的意义。方法 :清晨空腹抽血 ,分离血浆 ,采用放射免疫分析检测血浆NT -ProBNP(1- 76 )含量。结果 :健康人血浆NT - proBNP(1- 76 )含量为 (36 0 8± 5 7 3)pg/ml,不同性别间无明显差异。急性心肌梗死和不稳定型心绞痛患者血浆NT - proBNP(1- 76 )水平分别为 (5 5 4 1± 195 9)和 (5 2 5 7± 199 1)pg/ml,明显高于健康人 (均为P <0 0 1) ,并且急性心肌梗死患者在PTCA术后 12h血浆NT - proBNP(1- 76 )水平较术前明显升高 (P <0 .0 5 )。 2型糖尿病患者血浆NT -proBNP(1- 76 )含量也明显高于健康对照组 (5 5 2 6± 14 1 9pg/mlvs 36 0 8± 5 7 3,P <0 0 1)。 结论 :急性心肌梗死、不稳定型心绞痛以及 2糖尿病患者血浆NT -proBNP(1- 76 )含量明显升高 ,提示NT - proBNP(1- 76 )可作为上述疾病重要诊断指标之一。     

低氧性肺动脉高压发病机理与防治研究现状

肺原性心脏病是常见病．在我国85％的肺心病由慢性阻塞性肺疾患发展而来，其中肺动脉高压是肺心病的关键发病学环节，而低氧又是形成肺动脉高压的重要因素，因此，阐明低氧性肺动脉高压CHPH)的发病机制及寻找有效的防治方法一直是人们研究的热点之一。     

二维斑点追踪技术评估阻塞性睡眠呼吸暂停综合征患者的右心室收缩功能

目的探究二维斑点追踪技术评估阻塞性睡眠呼吸暂停综合征患者的右心室收缩功能。方法 40例阻塞性睡眠呼吸暂停综合征患者分为伴肺动脉高压(PH)组和未伴PH组(每组20例),另组为30例正常体检者。均给予二维斑点追踪技术进行右心室收缩功能评估。结果阻塞性睡眠呼吸暂停综合征患者在右室舒张末内径、右室收缩末内径、室间隔厚度、右室后壁厚度、射血分数上与健康体检者存在显著差异(P 0. 05),阻塞性睡眠呼吸暂停综合征伴PH组在右室舒张末内径、右室收缩末内径、室间隔厚度、右室后壁厚度上均比其它二组高(P 0. 05),在射血分数上显著比其它两组低(P 0. 05)。结论将二维斑点追踪技术应用于阻塞性睡眠呼吸暂停综合征患者时,能评估右心室结构和功能,值得应用与推广。     

慢性肺心病患者PAC-1、CD62p的变化及临床意义

目的：探讨慢性肺心病患者血小板膜糖蛋白PAC-1、CD62p的变化及其临床意义。方法：用三色全血流式细胞术测定加例慢性肺心病患者外周血中血小板PAC-1、CD62p的表达水平，并与30例健康对照者比较。用超声心动图检测慢性肺心病患者肺动脉收缩压。结果：慢性肺心病组PAC-1、CD62p的表达均明显高于正常对照组（均P〈0．001），并与肺动脉收缩压呈正相关。慢性肺心病患者PAC-1的变化与CD62p之间有显著的正相关（r=0．73；P〈0．001）。结论：慢性肺心病患者血小板明显活化，其活化程度与肺动脉高压关系密切。     

老年肺心病患者血浆VIP水平的观察

老年肺心病是临床上的常见病、多发病。为了了解老年肺心病患者血浆ＶＩＰ水平 ,我们对 6 0例临床上明确诊断的老年肺心病患者进行了血浆ＶＩＰ水平的观察 ,并就临床价值作初步探讨 ,现将结果报告如下。材料和方法一、对象 :(一 )正常对照组 :35例 (男 2 1 ,女 1 4 ) ,年龄 5 6～ 76岁 ,平均 6 5 7岁。均为我院医务科进行健康体检合格的老年人 ,均无心、肝、肺、肾等重要脏器疾患。肝、肾功能试验正常 ,胸部Ｘ线、心电图正常。(二 )老年肺心病组 :6 0例 (男 4 2 ,女 1 8) ,年龄 6 0～ 85岁 ,平均 6 8 4岁。均为我院从 2 0 0 0年 1 0月～ 2 …     

慢性肺心病患者脑利钠肽前体检测意义探讨

目的 探讨慢性肺源性心脏病(chronic cot pulmonlale,CCP)患者血清脑钠肽前体(pro-BNP)检测的临床意义.方法 测定50例老年慢性肺心痛患者血清pro-BNP水平,并与肺动脉压(PASP),右室内径(RDvd),左心室射血分数(LVEF)及动脉血氧分压(PaO2)等进行相关回归分析.结果 慢性肺心痛患者血清pro-BNP水平与肺动脉压,右室内径成正相关,与LVEF水平及PaO2水平呈负相关.结论 慢性肺源性心脏痛患者血清pro-BNP水平升高,可能与缺氧、肺动脉高压(PAH)及LVEF等因素有关:对肺心痛合并左心功能不全的鉴别可提供依据.     

婴儿重症肺炎合并心力衰竭时血浆TNF—α与CGRP水平变化的研究

目的　探讨肿瘤坏死因子 -α(TNF -α)与降钙素基因相关肽 (CGRP)在婴儿重症肺炎并急性充血性心力衰竭时的动态变化及其临床意义 .方法　对 2 2例肺炎并心衰、16例轻型肺炎患儿及 16例正常同龄儿童的血浆TNF -α与CGRP水平进行同期动态观察 .结果　心衰急性期血浆TNF -α较缓解期显著增高 (p <0 .0 1) ,并明显高于轻型肺炎组与对照组 (p <0 .0 1) .急性期血浆CGRP水平较缓解期及对照组均显著降低 (p <0 .0 1) ;心衰缓解期与轻型肺炎组和对照组间血浆TNF -α、CGRP水平变化无差异 (p >0 .0 5 ) .急性期血浆TNF -α含量变化与CGRP水平呈显著负相关 (t=0 .4 7,p <0 .0 5 ) .结论　TNF -α与CGRP在肺炎合并心衰的发生中起重要作用 ,TNF -α参与了肺水肿及心肌功能减退的病理过程 ,CGRP可能对肺血管及心肌有保护作用 ;动态监测血浆TNF -α及CGRP水平变化对判断病情及预后有重要临床意义     

磷脂酶A2活性与慢性常压低氧性肺动脉高压关系的研究

目的:研究磷脂酶A₂(PLA₂)活性及其相关炎症介质在大鼠慢性常压低氧性肺动脉高压形成中的作用。方法:29只健康SD大鼠随机分为正常对照组、单纯低氧组和低氧加白藜芦醇苷(PD)组。右心导管法检测大鼠肺动脉压力(mPAP),观察右室/左室+室间隔比值(R/L+S)、血浆和肺匀浆中PLA₂、血栓素B₂(TXB₂)、6-酮-前列腺素F_1α(6-k-PGF_1α)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平的变化。结果:低氧3周后大鼠mPAP、R/L+S、血浆及肺匀浆中PLA₂活性、TXB₂、MDA含量显著升高;6-k-PGF_1α、SOD水平下降。用PD预处理后可减轻上述变化。结论:PLA₂通过相关炎症介质及与自由基的相互作用在慢性低氧性肺动脉高压的形成中起着重要的介导作用。     

红花注射液对慢性低O2高CO2肺动脉高压大鼠COX-2 mRNA和蛋白表达的影响

目的：探讨红花注射液对慢性低O₂高CO₂肺动脉高压大鼠环氧酶-2(COX-2)基因表达的影响。方法: 将SD大鼠分为正常对照组、慢性低O₂高CO₂组、慢性低O₂高CO₂+红花注射液组。用原位杂交、电镜、放射免疫测定等方法,观察各组大鼠肺动脉平均压（mPAP）、肺细小动脉显微结构、肺动脉COX-2基因及蛋白表达、血浆和肺匀浆血栓素B₂(TXB₂)和6-酮-前列腺素(6-keto-PGF_1α)含量的变化。结果: ①慢性低O₂高CO₂组mPAP显著高于正常组,红花注射液组的mPAP显著低于慢性低O₂高CO₂组,3组间平均颈动脉压(mCAP)无显著差异。②慢性低O₂高CO₂组与正常对照组组相比血浆和肺匀浆TXB₂浓度、TXB₂/6-Keto-PGF_1α比值显著增高,6-Keto-PGF_1α浓度显著下降;红花注射液组与慢性低O₂高CO₂组相比血浆和肺匀浆TXB₂浓度、TXB₂/6-Keto-PGF_1α显著下降,6-Keto-PGF_1α显著升高。③光镜下慢性低O₂高CO₂组与正常组相比,肺细小动脉管壁面积/管总面积(WA/TA)和肺细小动脉中膜厚度(PAMT)均显著增高;电镜下显示肺细小动脉中膜平滑肌细胞增生,纤维细胞增多,肺泡II型上皮细胞微绒毛脱落;红花注射液组WA/TA和PAMT显著降低;肺细小动脉中膜平滑肌细胞增生减轻,纤维细胞少,胶原纤维减少,肺泡II型上皮细胞微绒毛丰富、结构清楚。④红花注射液组与慢性低O₂高CO₂组相比,COX-2基因与蛋白表达明显增强,而COX-1表达无明显变化。结论: 肺动脉COX-2基因表达增强可能是红花注射液减轻慢性低O₂高CO₂性肺动脉高压和肺血管结构重建的重要机制之一。     

三七总皂甙对慢性低氧性肺动脉高压大鼠的防治作用

目的:探讨三七总皂甙(PNS)对慢性常压低氧性肺动脉高压大鼠的防治效果及其机制。方法: 将雄性SD大鼠随机分为:正常对照组(C组)、单纯低氧组(H组)、低氧+PNS组(HT组)。进行血流动力学、红细胞比积(Hct)、透射电镜和有关生化指标检测。结果:(1)H组平均肺动脉压(mPAP)、平均右室压(RVMP)和Hct显著高于C组而HT组显著低于H组;(2)H组血浆、肺匀浆一氧化氮(NO₂^-/NO₃^-)含量、一氧化氮合酶(NOS)活性及血浆总超氧化物歧化酶(T-SOD)、铜/锌超氧化物歧化酶(Cu/ZnSOD)活性显著低于C组, HT组显著高于H组,但HT组血浆、肺匀浆NO₂^-/NO₃^-、NOS仍显著低于C组;(3) HT组肺小动脉内皮细胞损伤显著轻于H组 。结论: 三七总皂甙可抑制大鼠慢性低氧性肺动脉高压的形成,其机制可能与其调节NO含量、抗氧自由基损伤、减轻细胞损伤和降低红细胞比积有关。     

慢性阻塞性肺病患者血浆内皮素水平与肺血流动力学的关系

本文报告采用放射免疫方法测定慢性阻塞性病２４例（ＣＯＰＤ）患者体静脉，肺动脉，体动脉血的血浆ＥＴ－１水平，并与１６例正常对照组作了比较，ＣＯＰＤ患者尚进行了肺动脉压力直接测定，结果表明，ＣＯＰＤ患者ＥＴ－１水平显著高于正常组（Ｐ〈０．００１），肺动脉高压（ＰＡＨ）组ＥＴ－１水平显著高于ＰＡＨ组（Ｐ〈０．０５）。本文还分参与ＣＯＰＤ患者血浆ＥＴ－１水平的升高在ＰＡＨ形成可能是参与发病的因素之定。血浆     

Regional cardiac expression and concentration of natriuretic peptides in patients with severe chronic heart failure

The purpose of this study was to examine the regional cardiac mRNA expression and concentration of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) in relation to the circulating peptide concentrations in patients with chronic heart failure (CHF). The myocardial mRNA levels and peptide concentrations of BNP and ANP were analysed in seven different regions of the heart from patients undergoing cardiac transplantation. Autopsy samples from individuals without known cardiovascular disease were used as controls. The plasma levels of natriuretic peptides and their N‐terminal propeptides, Nt‐proBNP and Nt‐proANP, were measured in the CHF patients and healthy volunteers. In the autopsy specimens, the atrial regions appeared to contain the highest peptide levels for BNP as well as ANP, the atrioventricular ratio being 12–262 and 72–637‐fold, respectively. In the CHF patients there was a relative shift towards the ventricle for BNP, reducing the atrioventricular ratio to 6–16‐fold. The circulating concentrations of BNP/Nt‐proBNP in the CHF patients correlated closely to the BNP mRNA expression in most myocardial regions including the left ventricle (r=0.72, P < 0.001). For circulating concentrations of ANP/Nt‐proANP, such correlation were limited to the left atrium free wall (r=0.66, P < 0.002). Thus, of the two natriuretic peptides, BNP/Nt‐proBNP may be a better reflector of left ventricular overload.     

Circulating endothelin-1 concentrations in patients with chronic hypoxia.

AIMS--To evaluate the behavior of plasma endothelin-1 in patients with chronic hypoxia. METHODS--Fifteen male patients (mean age 52.1 +/- 3.1 years) with mild chronic obstructive pulmonary disease (COPD) were studied. Twelve healthy men (mean age 48.3 +/- 5.4 years) served as controls. Both patients and controls underwent standard pulmonary function tests, echocardiographic evaluation, and arterial blood gas evaluation. Blood samples for endothelin-1 assay were taken from a previously incannulated antecubital vein after 60 minutes of rest in the supine position. Endothelin-1 was measured by radioimmunoassay after extraction from plasma. RESULTS--Patients with chronic hypoxia had lower PaO2 values (66.1 +/- 6.2 mmHg) than controls (83.8 +/- 2.7 mmHg) but PaCO2 values were similar (38.1 +/- 2.5 v 36.7 +/- 3.1 mmHg, respectively). Arterial pulmonary pressure, therefore, was higher in patients (18.1 +/- 3.7 mmHg) than in controls (10.4 +/- 2.7 mmHg) as were circulating endothelin-1 concentrations (1.22 +/- 0.36 v 0.57 +/- 0.1 pg/ml). Furthermore, plasma endothelin-1 concentrations were negatively correlated with PaO2 and directly correlated with pulmonary pressure levels. No significant correlations were found in controls. CONCLUSIONS--These results show a clear relation between chronic hypoxia and circulating endothelin-1 concentrations. Therefore, chronic hypoxia may be regarded as an important stimulus for endothelin-1 release and as one of the main contributors to increased vasoconstriction in the vascular pulmonary bed which often accompanies lung disease.     

Increased Oxidative Stress and Altered Levels of Antioxidants in Chronic Obstructive Pulmonary Disease

An imbalance between oxidative stress and antioxidative capacity has been proposed to play an important role in the development and progression of chronic obstructive pulmonary disease. We carried out a study to assess the systemic oxidant-antioxidant status in patients with chronic obstructive pulmonary disease (COPD) and relate it to the severity of disease. We measured a wide range of parameters of oxidant-antioxidant balance in leukocytes, plasma and red cells of 82 patients with COPD and 22 healthy non-smoking controls (HNC). Lung function was measured by spirometry. Staging of COPD was done as per the recommended guidelines. Red cell antioxidative enzyme activities were altered, with glutathione peroxidase (GSH-Px) having lower, superoxide dismutase (SOD) having greater and catalase having similar activity in patients as compared to HNC. In plasma, ferric reducing antioxidant power (FRAP) and total protein sulfhydryls were lower and GSH-Px, lipid peroxides measured as MDA-TBA products, and protein carbonyls were higher in the patients as compared to HNC. Plasma total nitrates and nitrites (NO_x) were similar in the two groups. Superoxide anion (O₂^•−) release from leukocytes upon stimulation with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) and total blood glutathione were also higher in patients as compared to HNC. Plasma FRAP had a positive whereas total blood glutathione had a significant negative correlation with the severity of airways obstruction (FEV₁% predicted). Further, comparisons between clinical stages of severity of COPD revealed significant differences in plasma FRAP and total blood glutathione. Our observations suggest there is a systemic oxidant-antioxidant imbalance in the patients with COPD.     

Increased release of transforming growth factor (TGF)-beta1, TGF-beta2, and chemoattractant mediators in pneumonia.

Transforming growth factor-beta (TGF-beta), interleukin-8 (IL-8), and leukotrienes are potent neutrophil chemoattractants that are released in several lung diseases. There is limited information about the release of TGF-beta in bronchoalveolar lavage fluid (BALF) of patients with pneumonia. Furthermore, it is not clear if TGF-beta is differentially expressed in different lung diseases. The aim of our study was to compare the concentrations of TGF-beta1 and TGF-beta2 in the BALF of patients with pneumonia and other lung diseases. Furthermore, correlation of the TGF-beta levels with the concentration of chemoattractant mediators as well as with indicators of macrophage and granulocyte activation should be investigated. Patients with pneumonia, interstitial lung disease (ILD), or chronic obstructive pulmonary diseases (COPD) were included. Patients with ischemic heart disease without pulmonary involvement served as controls. The concentrations of TGF-beta1 and TGF-beta2, of the chemoattractant cytokine IL-8, of leukotriene B4, and of the leukotrienes C4, D4, and E4 were measured. Neutrophil elastase and granulocyte content (PMN) were used as markers for granulocyte activation, and neopterin was used as a marker for the activation of macrophages. Significantly elevated levels of TGF-beta1 (mean = 0.216 ng/ml, p < 0.01) were found in patients with microbiologically positive pneumonia but not in patients with ILD or COPD. A significant (p < 0.001) correlation was found between the TGF-beta1 concentrations and the IL-8 levels and the percentage of granulocytes (r = 0.76, and r = 0.44, respectively). Elevated TGF-beta2 concentrations were measured in the BALF of patients with pneumonia (mean = 1.4 ng/ml, p < 0.01) and with ILD. Pneumonia was also associated with increased concentrations of leukotrienes C4, D4, and E4 (mean = 91.61 pg/ml, p < 0.05) and leukotriene B4 (mean = 203.9 pg/ml, p < 0.01), significantly elevated levels of PMN elastase (mean = 2958.26 ng/ml, p < 0.01), and neopterin (mean = 0.42 nmol/L). Our results strongly suggest that different lung diseases do differ with regard to the released cytokines. TGF-beta1 probably plays a key role in regulation of pulmonary inflammation, particularly in pneumonia.     

Measurement of right ventricular ejection fraction with krypton-81m in chronic obstructive pulmonary disease

Thirty patients with chronic obstructive pulmonary disease (COPD) and 15 healthy volunteers have been studied to assess the value of measuring right ventricular ejection fraction (RVEF) at rest with a perfusion of krypton-81m (81mKr). With this perfusion, equilibrium RVEF can be measured in a 30 degrees right anterior oblique projection, avoiding a superimposition of cardiac cavities. The average RVEF of the patients with COPD was significantly lower than that of the normal patients (36.3 +/- 9.3% vs 52.6 +/- 3.9%; p less than 0.001). An inverse linear relation was found between mean pulmonary artery pressure (Ppa) and RVEF (r = -0.543; p less than 0.01). The RVEF in a group of 15 patients with COPD and pulmonary hypertension (Ppa greater than 20 mmHg), averaged 30.4 +/- 7.26%, which was significantly lower than that of the other 15 COPD patients with normal Ppa, whose RVEF averaged 42.3 +/- 7.1% (p less than 0.01). Taking a RVEF value less than or equal to 35% as an indicator of pulmonary hypertension, the sensitivity was 80% and specificity was 75%, the predictive value for a positive test was 75%, and for a negative test was 80%. A positive but weak correlation was found between RVEF and PaO2 (r = 0.52; p less than 0.01), SaO2 (r = 0.41; p less than 0.05) and the forced expiratory volume in one second (FEV1) (r = 0.40; p less than 0.05). No correlation was found between RVEF and prior history of right cardiac insufficiency, PaCO2, pH, the ratio FEV1/vital capacity, ECG signs of cor pulmonale and left ventricular ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

慢性心衰患者血浆BNP、cTnI和CRP联检的临床意义

目的：探讨联检血浆B钠尿肽（BNP）、肌钙蛋白I（cTnI）和C反应蛋白（CRP）水平对慢性心力衰竭（CHF）患者疗效观察及预后评估的临床意义。方法：选取50名健康体检者作为对照,45例CHF患者,分别动态监测其血浆BNP、cTnI和CRP水平。结果：CHF患者血浆BNP、cTnI和CRP水平明显高于对照组（P〈0.01）,且与CHF程度、疗效、预后的评估有关（P〈0.01）。结论：血浆BNP、cTnI和CRP在CHF患者中明显升高,且升高幅度与病情的严重性相一致,对疗效观察和病情转归有实际的临床价值。     

Genetics of humoral and cytokine activation in heart failure and its importance for risk stratification of patients

The study objective is to prove an association among plasma concentration of big endothelin and endothelin-1, other clinical parameters and two frequent polymorphisms - G8002A and -3A/-4A - in the endothelin-1 (EDN-1) coding gene (6p21-23), and among plasma concentration of TNF alpha and gene polymorphisms TNF alpha -308 A/G, -238 A/G, TNF beta Ncol and 3'TACE (tumour necrosis factor alpha converting enzyme) in patients with chronic heart failure (CHF). The second objective is to find an association between polymorphisms G8002A and -3A/4A EDN-1 with diabetes mellitus (DM), peripheral artery disease (PAD) and myocardial infarction (MI) in patients with chronic heart failure (CHF). The study population included 266 patients with symptomatic CHF and proven dysfunction of the left ventricle (LV). Genotyping and plasma concentrations of humoral substances were examined in 224 patients with ejection fraction (EF) below 40%. No associations between plasma concentrations of endothelin-1 and big endothelin and polymorphisms G8002A (p=0.87, p=0.81) and -3A/-4A (p=0.871, p=0.749) in the gene coding endothelin-1 were found. No associations were observed between plasma concentration of TNF alpha and genotypes in four polymorphisms in TNF alpha, beta and TACE genes. A significant correlation was seen between plasma concentration of big endothelin and pulmonary congestion. Patients with ischemic heart disease (IHD) and previous MI showed a difference in the distribution of genotype G8002A for endothelin-1: allele G 0.718 and A 0.282 vs those without MI: allele G 0.882 and A 0.118, (p<0.05). Patients with IHD and DM had allele G in 0.67 and A 0.33, while those without DM had allele G in 0.790 and A in 0.209 (p<0.03). Patients with IHD and concomitant PAD had allele G in 0.718 and A in 0.282 vs those without PAD allele G in 0.882 and A in 0.118 (p<0.0004). Patients with dilative cardiomyopathy (DCMP) showed no differences in genotype G8002A and presence of DM or PAD. It might be speculated that in the case of endothelin-1 and TNF alpha in CHF the genetic determination is not important, and plasma concentrations are influenced more by the disease severity. Ischemics with previous MI, concomitant DM or PAD showed more frequently allele A and less often allele G than those without these diseases. A genotype with allele A is associated with higher risk of concomitant diseases.     

Changes in atrial natriuretic factor during preload reduction with nitroglycerin in patients with congestive heart failure

Nine patients with congestive heart failure, New York Heart Association class II-III, were evaluated with right heart catheterization. Plasma atrial natriuretic factor (ANF) was determined in blood samples from the pulmonary artery simultaneously with recordings of right atrial, pulmonary arterial, pulmonary capillary wedge and systemic arterial pressures and heart rate during preload reduction with 0.5 mg nitroglycerin sublingually. Basal plasma ANF levels were higher in patients with congestive heart failure compared to normal controls, and correlated to right atrial, pulmonary arterial, and pulmonary capillary wedge pressures. After nitroglycerin all patients had reductions in right atrial, pulmonary arterial, and pulmonary capillary wedge pressures and a simultaneous decrease in plasma ANF concentrations, reaching lowest values after 10 min. Central pressures and plasma ANF rose to baseline values within 30 min. After nitroglycerin plasma ANF concentrations correlated to pulmonary arterial and pulmonary capillary wedge pressures, while changes in plasma ANF correlated to changes in right atrial and pulmonary arterial pressures. These results provide further evidence that ANF is released by a pressure-sensitive mechanism and demonstrates that ANF secretion in relation to central pressure variations is preserved in patients with congestive heart failure and that the response is rapid.     

Histometric research on cor pulmonale in chronic nonspecific lung diseases

Micrometric parameters of lungs and the right ventricle myocardium under the pulmonary heart compensation and decompensation were studied. Correlative and information analysis of parameters at various stages of the pulmonary heart formation in chronic non-specific pulmonary diseases in 14 patients dying at the age of 48 to 80 years is performed. Morphometric analysis allowed to distinguish micrometric signs of the pulmonary heart compensation and decompensation. Information analysis of the pulmonary heart parameters established the thickness of cardiomyocytes and transversal diameter of their nuclei to be the most informative indexes. Correlation analysis revealed the enhancement of the parameters links, in proportion with the development of the pulmonary heart decompensation. The changes observed reflect a structural-functional myocardium restructuring and indicate an energy deficiency of the right ventricle cardiomyocytes.