心先安对充血性心力衰竭患者左室收缩功能的影响及机制的初步探讨

为研究心先安对充血性心力衰竭患者左室收缩功能的影响及其机制,采用超声心动图法对患者治疗前后的左室收缩功能作了评定,并观察了心先安对培养乳鼠心肌细胞内环磷酸腺苷（ｃＡＭＰ） 及乳酸脱氢酶（ＬＤＨ） 漏出的影响。３４ 例病人随机分成２ 组：常规治疗组和心先安治疗组,疗程均为１ 周。治疗后心先安组ＬＶＥＤＤ 缩短（ 从６３ ．９ ±１０ ．５ 到５９ ．０ ±１１ ．６ ｍ ｍ ,Ｐ＜ ０ ．０１） ,ＬＶＥＳＶ 减小（ 从１３９ ．７ ±２９ ．０ 到１１１ ．２ ±２３ ．０ｍｌ,Ｐ＜ ０ ．０５） ,ＬＶＥＦ（ ％ ） 提高（ 从３８ ．９ ±１２ ．３ 到４５ ．７ ±１４ ．５ ,Ｐ＜ ０ ．０１）ＳＶ、ＣＯ、ＣＩ增加（ 分别从６１ ．７ ±２２ ．５到８５ ．１ ±２６ ．３ ｍｌ,从５ ．２ ±１ ．６ 到６ ．６ ±２ ．４１／ｍｉｎ,从２ ．６ ±０ ．４ 到４ ．０ ±１ ．１ １／ｍｉｎ／ｍ２ ,均为Ｐ＜ ０ ．０５） 。常规治疗组治疗前后的改变无统计学显著意义。心先安能增加培养的乳心鼠肌细胞内ｃＡＭＰ 浓度,呈剂量依赖性,并能减少缺氧／ 复氧损伤心肌细胞ＬＤＨ 的漏出,亦呈剂量依赖性。结果显示,心先安能改善心力衰竭患者的左室收缩功能,其机制可能与升高细胞内ｃＡＭＰ?     

不同起搏方式对病窦综合征患者远期效果的影响

为了解不同起搏方式对病窦综合征特别是慢－快综合征患者心功能及房性心律失常的影响，利用超声心动图、体表心电图及Ｈｏｌｔｅｒ检查，对２１１例病窦综合征患者采用自身对照方法进行回顾性分析。结果发现：生理性起搏（ＡＡＩ／ＤＤＤ）组术后左室射血分数（ＬＶＥＦ）、心输出量（ＣＯ）明显增加（ＡＡＩ：５３．５±６．１％ｖｓ４７．２±７．８％，４．９５±０．５７Ｌ／ｍｉｎｖｓ４．２０±０．６２Ｌ／ｍｉｎ；ＤＤＤ：５２．５±６．８％ｖｓ４４．３±０．１％，５．１２±０．７１Ｌ／ｍｉｎｖｓ４．４１±０．３８Ｌ／ｍｉｎ；Ｐ均＜０．０１），左房内径（ＬＡＤ）无明显变化；ＤＤＤ组Ｅ／Ａ比值明显增加（０．９８±０．０９ｖｓ０．８７±０．１５，Ｐ＜０．０１），ＡＡＩ组Ｅ／Ａ比值呈增加趋势（Ｐ＝０．０５７）。房性心律失常发生率明显减少（１５．９％ｖｓ５０％，Ｐ＜０．０１）。非生理性起搏（ＶＶＩ）组术后ＬＶＥＦ、ＣＯ明显下降（４４．１±４．７％ｖｓ４８．３±４．３％，３．７７±０．４２Ｌ／ｍｉｎｖｓ４．１７±０．８５Ｌ／ｍｉｎ，Ｐ均＜０．０１），ＬＡＤ明显增大（３９．２６±２．３７ｍｍｖｓ３６．８１±２．３５ｍｍ，Ｐ＜０．０１），Ｅ／Ａ比值呈?     

214例老年人肺弥散功能测定分析

目的探讨健康老年人和老年ＣＯＰＤ患者肺弥散功能差异和临床应用价值。方法用美国６２００ＡｕｔｏｂｏｘＤＬ型体积描记仪分别测定９７例健康老年人和１１７例ＣＯＰＤ患者的肺弥散功能。结果慢支组与健康组比较肺一氧化碳弥散量（ＤＬＣＯ）差异非常显著（Ｐ＜０．０１）。轻、中、重度肺气肿组与健康组比较ＤＬＣＯ、弥散量／肺泡容积比值（ＤＬＣＯ／ＶＡ）、转送系数（Ｋｃｏ）、弥散时间常数（ＣＯＴ．Ｃ．）相差非常显著（Ｐ＜０．０１）。结论老年人患有慢性呼吸道病变时，肺弥散功能测定是一项较为敏感的指标，常在其他肺功能检查出现异常之前就已有变化。     

腹主动脉结扎大鼠心房纤维化的实验研究

高血压患者有较高心律失常的发生率，房性心律失常可能与左房扩大或心房纤维化有关。为观察压力负荷增高大鼠中心房纤维化的发生情况，将Ｗｉｓｔａｒ大鼠随机分成假手术组和手术组，手术组大鼠行肾上腹主动脉部分结扎。术后４，８，１２周分别测定大鼠颈动脉压及心房胶原容积分数（ＣＶＦ），结果发现：①手术组左室舒张压明显高于假手术组（４，８，１２周分别为１８．５±２．５ｋＰａｖｓ１５．７±１．９ｋＰａ，１８．６±２．７ｋＰａｖｓ１５．３±１．３ｋＰａ，１９．６±３．１ｋＰａｖｓ１５．２±１．９ｋＰａ，Ｐ＜０．０５或０．０１）。②手术组心房ＣＶＦ明显高于假手术组（４，８，１２周左、右房分别比较：４．２３±０．７６％ｖｓ２．９３±０．８７％，４．６５±１．４５％ｖｓ３．１１±１．０７％，５．６２±１．６２％ｖｓ３．２３±１．２８％；３．８８±１．１５％ｖｓ２．５１±０．８４％，４．２４±１．６５％ｖｓ２．５１±０．８４％，５．３４±１．３２％ｖｓ２．３３±１．１４％；Ｐ＜０．０５或０．０１），手术组心房ＣＶＦ有逐渐上升趋势。③左房ＣＶＦ与左室舒张压之间无直线相关关系（ｒ＝０．１６９１，Ｐ＞０．０５）。提示在高血压大鼠模型中存在心房?     

VDD起搏对缓慢性心律失常心力衰竭的血液动力学影响

为了评估ＶＤＤ起搏对缓慢性心律失常心力衰竭的血液动力学影响，对２１例心功能Ⅲ～Ⅳ级的缓慢性心律失常病人安置ＶＤＤ起搏器，并用Ｓｗａｎ－Ｇａｎｚ导管监测起搏前和起搏后３０ｍｉｎ、２４ｈ、４８ｈ、７２ｈ的心输出量（ＣＯ）、心脏指数（ＣＩ）、右房压（ＲＡＰ）、平均肺动脉压（ＭＰＡＰ）和肺毛细血管楔嵌压（ＰＣＷＰ），并记录各时期的心房率（ＡＲ）和心室率（ＶＲ）。结果：ＶＲ在术后即时及各时期显著升高（Ｐ均＜０．０５），ＣＯ、ＣＩ在起搏后３０ｍｉｎ即显著升高〔分别为４．１８±０．８１Ｌ／ｍｉｎｖｓ２．８１±０．９３Ｌ／ｍｉｎ、２．３６±０．６６Ｌ／（ｍｉｎｍ２）ｖｓ１．１８±０．６３Ｌ／（ｍｉｎｍ２），Ｐ均＜０．０５〕，起搏４８ｈ达高峰；ＲＡＰ、ＭＰＡＰ、ＰＣＷＰ在起搏后３０ｍｉｎ无显著改变（Ｐ＞０．０５），但２４ｈ开始显著性下降（分别为１．２８±０．４１ｋＰａｖｓ１．４１±０．３４ｋＰａ、２．６０±０．５１ｋＰａｖｓ３．４０±０．５６ｋＰａ、３．１０±０．５６ｋＰａｖｓ３．５４±０．６８ｋＰａ，Ｐ均＜０．０５），７２ｈ后进一步降低。结果提示ＶＤＤ起搏治疗能显著改善缓慢性心律失常心力衰竭的血液动力学，可作为治疗缓慢性心?     

夜间无创通气在COPD缓解期的康复治疗研究

无创通气对于ＣＯＰＤ患者慢性呼吸功能不全急性加重期有确切的疗效［１、２］。无创通气可改善肺的氧合功能,减少呼吸肌作功。ＣＯＰＤ缓解期治疗,无创通气是治疗措施之一,ＣＯＰＤ往往伴有夜间睡眠障碍。从１９９８年６月到２０００年５月,我们应用无创通气夜间治疗５０例ＣＯＰＤ患者,收到一定疗效。１对象和方法１．１研究对象：１００例ＣＯＰＤ稳定期患者［３］,随机分为两组：夜间无创通气组和对照组各５０例。年龄分别为６４．５±５．６岁、６５．０±６．４岁,男：女为３５：１５、３７：１３。１．２研究方法：１．２．１…     

血液透析对慢性肾衰患者心功能和肺弥散功能的影响及其…

测定２０例慢性肾衰（ＣＲＦ）患者的血透前，后１ｈ的心功能、肺弥散功能变化，发现血透后心排血量（ＣＯ）、心脏指数（ＣＩ），每搏心排血量（ＳＶ）及和母搏指数（ＳＩ）均显著降低，肺一氧化碳弥散量（ＤＬｃｏ）也显著降低，其中ＳＶ、ＳＩ对超滤反应敏感，结果表明，慢性肾衰患者血透后可因左室充盈压降低而导致心功能下降，并有肺弥散功能的损害。     

高频心电图与心率变异在儿科疾病中的联合应用

目的 探讨高主电图（ＨＦＥＣＧ０与心率变异（ＨＲＶ）联合应用小儿心肌炎的辅助诊断意义。方法 对８９例按诊断分４组（Ａ１、Ａ２、Ａ３、Ａ４）进行ＨＦＥＣＧ、短程ＨＲＶ、心肌酶５项检查，并与２１０例正常对照组（Ｂ组）分析。结果 ＨＲＶ时域值在病毒性心肌炎（Ａ１）组，疑似心肌炎（Ａ２）组、呼吸道感染组（Ａ３）稍偏低，ＳＤＮＮ依次为（３３．４±２２．０、３５．８±１５．４、３６．５±１７．５）ｍｓ；Ａ１￣     

经皮冠状动脉腔内成形术对不稳定型心绞痛患者心率变异的影响

应用长程心电图分析系统对１６例不稳定型心绞痛患者（ＵＡＰ组）入院后第２日、经皮冠状动脉腔内成形术（ＲＴＣＡ）后第１，３，３０日以及１４８例健康中、老年人（对照组）２４ｈ心电图进行心率变异（ＨＲＶ）分析。结果：ＵＡＰ组２４ｈ连续正常ＲＲ间期的标准差（ＳＤＮＮ）、２４ｈ内连续５ｍｉｎ节段平均正常ＲＲ间期的标准差（ＳＤＡＮＮｉ）、相邻ＲＲ间期差的均方根（ｒＭＳＳＤ），相邻两个正常心动周期差值大于５０ｍｓ个数占总搏数的百分比（ＰＮＮ５０）、低频功率（ＬＦ）及高频功率（ＨＦ）均明显低于对照组（分别为９２．７±１４．３ｍｓｖｓ１２８．９±１７．８ｍｓ、７８．８±１０．６ｍｓｖｓ１１８．６±１９．１ｍｓ、１９．３±７．７ｍｓｖｓ２９．８±１２．７ｍｓ、３．６±１．７％ｖｓ６．５±５．５％、３１７．２±１４８．３ｍｓ２ｖｓ４７６．５±２８７．３ｍｓ２，Ｐ均＜０．０５），而ＬＦ／ＨＦ高于对照组（３．５±１．３ｖｓ２．４±１．１，Ｐ＜０．０５）。ＰＴＣＡ术后３０天ＵＡＰ患者ＨＲＶ逐渐恢复正常。结果提示ＵＡＰ患者交感神经和迷走神经张力下降，而以后者更明显；ＰＴＣＡ后ＨＲＶ逐渐恢复，说明ＰＴＣＡ能改善ＵＡＰ患者的ＨＲＶ。     

心肌缺血大鼠的心率功率谱变化及其与心脏性猝死关系的研究

采用心率变异（ＨＲＶ）频域指标定量评价心肌缺血大鼠的心脏自主神经功能变化及其与心脏性猝死（ＳＣＤ）的关系。Ｈｏｌｔｅｒ监测仪记录假手术组（２０只）及心肌缺血后存活组（５４只）与ＳＣＤ组（３６只）大鼠的心电信号。结果显示存活组或ＳＣＤ组大鼠于心肌缺血初始１５ｍｉｎ内的低频（ＬＦ）及低频／高频比值（ＬＦ／ＨＦ）较假手术组明显升高〔ＬＦ（ｍｓ２／Ｈｚ）：１９８．８±４１．３或２２６．７±５６．４ｖｓ６５．４±１９．６，Ｐ均＜０．０１；ＬＦ／ＨＦ：４．０８±１．１或５．１２±１．４ｖｓ１．８７±０．７，Ｐ均＜０．０１〕，而且ＳＣＤ组大鼠的ＬＦ与ＬＦ／ＨＦ较存活组增高〔ＬＦ（ｍｓ２／Ｈｚ）：２２６．７±５６．４ｖｓ１９８．８±４１．３，Ｐ均＜０．０５；ＬＦ／ＨＦ：５．１２±１．４ｖｓ４．０８±１．１，Ｐ＜０．０５〕，各组间ＨＦ无明显变化；ＳＣＤ组大鼠于ＳＣＤ发生前１５ｍｉｎ内，心率功率谱动态变化表现为ＬＦ及ＬＦ／ＨＦ随死亡时间的濒临而呈进行性升高（Ｐ＜０．０１及０．０５）。表明大鼠心肌缺血后其交感神经活性明显亢进，ＨＲＶ降低与ＳＣＤ的发生密切相关。     

COPD患者膜弥散和肺血管床容量的变化及支气管扩张剂的影响

目的:探索慢性阻塞性肺疾病(COPD)缓解期不同分级的患者膜弥散功能(Dm)和肺血管床容量(Vc)的变化,以及使用支气管扩张剂后通气功能改善对Dm和Vc的影响。方法:2001年7月至2004年2月COPD缓解期患者95例,分为4组,Ⅰ级8例,Ⅱ级47例,Ⅲ级34例,Ⅳ级6例,正常对照组35例。使用一口气法,测定弥散量(DLCO)、弥散率(KCO即DLCO/VA)、Dm、Vc。58例COPD患者予以做扩张试验,试验阳性和阴性者均再次测定DLCO、KCO、Dm、Vc。将各组间的测定值及扩张前后的结果进行比较。结果:COPD各组患者的Dm、DLCO、Vc及KCO均低于正常对照组,随着级别的增加,降低的程度均加大。COPDⅠ级患者的Vc和KCO显著低于对照组(P<0.05,P<0.01),COPDⅡ级、Ⅲ级及Ⅳ级患者的DLCO、KCO、Dm、Vc均显著低于对照组(P<0.01)。COPD各分级之间除Vc没有显著的差别(P>0.05)外,Dm、DLCO和KCO差异均有显著性(P<0.01)。支气管扩张试验阳性患者扩张试验前后的DLCO、Dm、Vc均无显著的改变(P>0.05)。结论:COPD患者通气功能逐渐恶化导致了弥散量的下降,Dm的持续降低贯穿于整个COPD的早、中、晚期,而Vc的持续下降则发生在COPD的早、中期。支气管扩张剂的使用没有通过通气/血流比的改变对弥散量、Dm、Vc产生影响。     

Membrane and capillary blood components of diffusion capacity of the lung for carbon monoxide in pulmonary sarcoidosis: relation to exercise gas exchange

BACKGROUND: Resting pulmonary diffusing capacity of the lung for carbon monoxide (DLCO) is known to be the best predictor of arterial desaturation during exercise in patients with sarcoidosis. However, the relative contribution of each of the two components of DLCO-alveolar membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc)-remains unclear. STUDY OBJECTIVES: To evaluate which component is responsible for the decrease of resting DLCO in patients with sarcoidosis, and to determine which resting pulmonary function test, including Dm and Vc, is the best predictor of gas exchange abnormalities during submaximal exercise. DESIGN: Prospective analysis of patients referred to our department of respiratory medicine. PATIENTS: Twenty four patients with pulmonary sarcoidosis were separated into two groups according to chest radiographic findings: group 1, stages 2 and 3 (n = 15); group 2, stage 4 (n = 9). All the patients completed pulmonary function tests (flows, volumes, single-breath DLCO, transfer coefficient [Ka], Dm, Vc) and submaximal exercise (two steady-state levels of mild and moderate exercise corresponding respectively to a target oxygen consumption of approximately 10 to 15 mL/min/kg). RESULTS: DLCO was reduced in the two groups (group 1, 63 +/- 16% of predicted; group 2, 64 +/- 16% of predicted). Dm was severely decreased (group 1, 58 +/- 24% of predicted; group 2, 51 +/- 15% of predicted), whereas Vc was unchanged or only mildly decreased (group 1, 81 +/- 18% of predicted; group 2, 85 +/- 28% of predicted). Whatever the group of patients and the exercise level, Dm and DLCO were the strongest predictors (p < 0.001) of gas exchange abnormalities. Ka or volumes were weak predictors, and Vc or flows were not related with exercise gas exchange. CONCLUSIONS: This study demonstrates that a decrease in Dm mostly accounts for resting DLCO reduction, and that Dm as well as DLCO are highly predictive of gas exchange abnormalities at exercise in patients with sarcoidosis.     

慢性阻塞性肺疾病和结缔组织病患者膜弥散与肺血管床容 …

目的 研究慢性阻塞性肺疾病（ＣＯＰＤ）和结缔组织病患者静息及运动后即刻的肺弥散能力（ＤＬ）、肺泡毛细血管膜弥散能力（Ｄｍ）肺泡毛细血管床容量（Ｖｃ）的变化，探讨其对结缔组织病肺改变早期诊断的意义。方法 ＣＯＰＤ组（２０例）及正常对照组２０名，结缔组织病组（２０例）及正常对照组２０名测定静息时不同肺泡气氧分压下的ＤＬ及运动后不同肺泡气氧分压下的ＤＬ，分别按Ｒｏｕｇｈｔｏｎ和Ｆｏｒｓｔｅｒ方法计算静息     

Clinical significance of the measurement of membrane diffusing capacity and pulmonary cappillary blood volume.

The results of 64 membranes diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) estimations were analysed to assess the clinical significance of these measurements. These estimations were performed on 18 healthy subjects, 19 patients with mitral valvular involvement of rheumatic aetiology, 15 patients with chronic bronchitis and emphysema, 8 patients with chronic bronchitis alone, and 4 patients with pulmonary embolism. It was observed that Dm correlated very well with the pulmonary diffusing capacity (DLCO) measured during the inhalation of room air in all the groups of subjects. In patients with rheumatic heart disease, the DLCO was affected little by even large changes in Vc, whereas it ran closely parallel to the Dm in these subjects. In the past Dm has been considered to be an unreliable estimation, varying greatly as a result of small errors in the measurement of DLCO. This appears to be relatively true only in normal subjects having low Vc/Dm ratio. In a majority of diverse clinical conditions where the Vc/Dm ratio is increased, the Dm becomes a more reliable estimation. In these patients the DLCO itself is a good index of the membrane diffusing capacity.     

Lung membrane diffusing capacity, heart failure, and heart transplantation

The pulmonary diffusing capacity for carbon monoxide (DLCO) is reduced in chronic heart failure and remains decreased after heart transplantation. This decrease in DLCO may depend on a permanent alteration after transplantation of one or the other of its components: diffusion of the alveolar capillary membrane or the pulmonary capillary blood volume (Vc). Therefore, we measured DLCO, the membrane conductance, and Vc before and after heart transplantation. At the time of hemodynamic measurements, the Roughton and Forster method of measuring DLCO at varying alveolar oxygen concentrations was used to determine the membrane conductance, Vc, DLCO/alveolar volume (VA), the membrane conductance/VA and thetaVc/VA (theta = carbon monoxide conductance of blood, VA = alveolar volume) in 21 patients with class III to IV heart failure before and after transplantation, and in 21 healthy controls. Transplantation normalized pulmonary capillary pressure and increased cardiac index. DLCO was decreased before transplantation (7.11 vs 10.0 mmol/min/kPa in controls), but DLCO/VA was normal (1.67+/-0.44 vs 1.71+/-0.26 mmol/min/kPa/L in controls). DLCO/VA remained unchanged after transplantation, because the decrease in Vc (82+/-30 vs 65+/-18 ml before and after transplantation) and thetaVc/VA was not compensated by the changes in membrane conductance (11+/-4 vs 12+/-5 mmol/min/kPa before and after transplantation, respectively) and membrane conductance/VA. We conclude that the decrease in DLCO in patients with chronic heart failure is due to a restrictive ventilatory pattern because their DLCO/VA remains normal; the decrease in the membrane conductance is compensated by the increase in Vc. After transplantation, the decrease in Vc due to normalization of pulmonary hemodynamics is not completely compensated for by an increase in membrane conductance. Because the membrane conductances, measured before and after transplantation, are negatively correlated with duration of heart failure, its abnormal pulmonary hemodynamics may have irreversibly altered the alveolar capillary membrane.     

Pulmonary diffusion limitation after prolonged strenuous exercise

To determine the effect of strenuous prolonged exercise on alveolo-capillary membrane diffusing capacity, 11 marathon runners aged 37 +/- 7 years (mean +/- SD) were studied before and during early recovery (28 +/- 14 min) from a marathon race. Lung capillary blood volume (Vc) and the alveolo-capillary diffusing capacity (Dm) were determined in a one-step maneuver by simultaneous measurements of CO and NO lung transfer (DLCO and DLNO, respectively) using the single breath, breath-holding method. After the race, both DLCO and DLNO were significantly decreased in all subjects (-10.9 +/- 4.8%, P less than 10(-4) and -29.0 +/- 11.1%, P less than 10(-4), respectively). The mean value of the derived DmCO decreased by -29.3 +/- 11.1%, whereas Vc had not entirely returned to control resting value. Although these results do not indicate the detailed mechanism involved, interstitial lung fluid was suspected to accumulate, particularly in alveoli, during the race. We concluded that the high overall work load and the extended duration of the exercise both contributed to a transient change in the structure of the alveolo-capillary membrane thereby affecting the diffusing capacity of the alveolo-capillary membrane.     

Effect of alveolar pressure on single-breath CO diffusing capacity at mid-lung volume

The present study examines whether changes in the alveolar pressure (PA) affect the single breath diffusing capacity for carbon monoxide (DLCO) more strongly at mid-lung volume than at total lung capacity (TLC) in normal subjects. DLCO was measured at 60%, 80% and 100% of TLC, while PA was kept at +30, 0, or -30 cm H2O by the subject's effort during the measurement of DLCO at each lung volume. The capillary blood volume (Vc) and the membrane diffusing capacity (Dm) were also determined. DLCO at zero PA was found to be higher at 100% TLC than at lower lung volumes. At PA = +30 cm H2O, DLCO at 100%, 80%, and 60% TLC decreased by 8%, 13%, and 13%, respectively, and the decreases in Vc were 2%, 10%, and 21%, respectively. However, negative PA did not cause any significant changes in DLCO or Vc at any lung volume. Also, Dm did not change at any PA. We conclude that DLCO is more affected by a positive PA at mid-lung volume than at a high lung volume, probably due to a greater decrease in Vc.     

Pulmonary membrane diffusing capacity and capillary blood volume measured during exercise from nitric oxide uptake.

STUDY OBJECTIVES: To validate lung diffusing capacity for nitric oxide (DLNO) as an index of conductance of the alveolar-capillary membrane during exercise, we compared DLNO to lung diffusing capacity for carbon monoxide (DLCO) and pulmonary membrane diffusing capacity for carbon monoxide (DMCO), and compared pulmonary capillary blood volume (Vc) calculated by two methods. SETTING AND PARTICIPANTS: The study was performed at a university medical center involving 12 nonsmoking healthy volunteers (age range, 23 to 79 years). DLCO, DLNO, cardiac output (c), and lung volume were measured simultaneously at rest and during graded ergometer exercise by a rebreathing technique. Pulmonary membrane diffusing capacity and Vc were compared by (1) the classic technique of Roughton and Forster from DLCO measured at two alveolar oxygen tension (PAO(2)) levels, and (2) from DLNO and DLCO assuming negligible erythrocyte resistance to nitric oxide (NO) uptake, ie, DLNO approximately equal to pulmonary membrane diffusing capacity for nitric oxide. RESULTS: In all subjects, DLNO increased linearly from rest to exercise; age, c, and lung volume were the major determinants of DLNO by stepwise regression analysis. The DLNO/DLCO ratio averaged 3.98 +/- 0.38 (+/- SD) and the DLNO/DMCO ratio averaged 2.49 +/- 0.28 irrespective of exercise intensity. Changing PAO(2) did not alter DLNO. Brief exposure to 40 ppm of inhaled NO during 16 s of rebreathing did not alter either DLCO or c. Estimates of pulmonary membrane diffusing capacity and Vc by the two methods showed a strong correlation. CONCLUSION: Results support DLNO as a direct measure of pulmonary membrane diffusing capacity, allowing the estimation of Vc in a single rebreathing maneuver during exercise. The DLNO-DLCO rebreathing technique can be applied clinically in the investigation of pulmonary microvascular regulation.     

Reduction of pulmonary capillary blood volume following cold exposure in patients with Raynaud's phenomenon

In a previous study we induced digital vasospasm with cold pressor stimulus, and an acute decrease in the lung diffusing capacity for carbon monoxide (Dsb) resulted. We hypothesized its cause to be spasm occurring simultaneously in the pulmonary vasculature and the digital arteries. We measured in this study the Dsb, the diffusing capacity of the pulmonary membrane (Dm), and the volume of blood in the pulmonary capillaries (Vc) after cold-induced digital vasospasm in patients with Raynaud's phenomenon. Control subjects showed no significant decrease in Dsb, Dm, or Vc after cold exposure. Eight of 12 subjects with Raynaud's phenomenon had a significant decrease in Dsb 60 min after testing (25.3 +/- 6.6 vs 19.8 +/- 6.1 ml/min/mm Hg, p less than 0.01). The acute decrease in Dsb was due to a significant decrease in Vc (54 +/- 20 vs 39 +/- 10 ml, p less than 0.05), while Dm was unchanged (52 +/- 17 vs 51 +/- 20 ml/min). Four subjects who had a decrease in Dsb after cold challenge had repeated studies later after pretreatment with sublingual nifedipine. The magnitude of change in Dsb was similar to that observed in the untreated state (23.6 +/- 10.6 vs 20.9 +/- 9.6 ml/min/mm Hg). We conclude that digital vasospasm is accompanied by an acute reduction in Vc in both primary and secondary Raynaud's phenomenon and indicates concurrent vasoconstriction within the pulmonary vaculature.     

Lack of improvement of lung diffusing capacity following fluid withdrawal by ultrafiltration in chronic heart failure

OBJECTIVES: We sought to investigate the possibility that lung diffusing capacity reduction observed in chronic heart failure is reversible in the short term. BACKGROUND: Mechanical properties of the lung usually ameliorate with antifailure treatment including drugs, ultrafiltration and heart transplantation, whereas lung diffusion rarely improves. METHODS: We studied the mechanical properties of the lung (pulmonary function tests with determination of alveolar volume, extravascular lung fluids and lung tissue), lung diffusion for carbon monoxide (DLco), including membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc) and pulmonary hemodynamics, in 28 patients with stable chronic heart failure, before a single session of extracorporeal ultrafiltration (3,973 +/- 2200 ml) and four days thereafter. Lung mechanics and diffusion were also evaluated in 18 normal subjects. RESULTS: Vital capacity, forced expiratory volume (1 s) and maximal voluntary ventilation were lower in patients when compared with normal subjects, and increased after ultrafiltration from 2.1 +/- 0.7 to 2.5 +/- 0.7(1)*, 1.7 +/- 0.5 to 2.0 +/- 0.6(1)* and 67 +/- 25 to 79 +/- 26 (1/min)*, respectively (* p < 0.02 vs. pre-ultrafiltration). Post-ultrafiltration alveolar volume was augmented, while lung tissue, body weight (approximately 6 kg), chest X-ray extravascular lung water score and pulmonary vascular pressure were reduced. Heart dimensions (echocardiography) remained unchanged. DLco, Dm and Vc were 29.0 +/- 5.0 ml/min/mm Hg, 47.0 +/- 11.0 ml/min/mm Hg, 102 +/- 20 ml in normal subjects and 17.1 +/- 4.0#, 24.1 +/- 6.5#, 113 +/- 38 and 17.0 +/- 5.0#, 24.8 +/- 7.9#, 100 +/- 39 in patients before and after ultrafiltration, respectively (# = p < 0.01 vs. controls). CONCLUSIONS: In chronic heart failure, ultrafiltration improves volumes and mechanical properties of the lung by reducing lung fluids. Diffusion is unaffected by ultrafiltration, suggesting that, in chronic heart failure, the alveolar-capillary membrane abnormalities are fluid-independent.