脊髓5-HT受体参与电针内关穴对大鼠心脏伤害性感受的调控

目的：观察脊髓水平5-羟色胺（5-HT）受体参与电针（EA）内关穴对大鼠心包内注射缓激肽（BK）诱发心脏伤害性感受的调控作用。方法：雄性SD大鼠随机分为5组：缓激肽（BK）组、BK+EA组、BK+麦角新碱（Methysergide）组、BK+EA+Methysergide组、BK+EA+溶媒（Vehicle）组,每组8只。各组大鼠均行心包内插管,BK组心包内间隔40 min注射0.2 ml BK共3次;BK+EA组心包内注射0.2 ml BK联合电针双侧内关穴;BK+Methysergide组心包内注射0.2 ml BK联合鞘内注射10 μl Methysergide;BK+EA+Methysergide组心包内注射0.2 ml BK联合电针双侧内关穴结合鞘内注射10 μl Methysergide;BK+EA+Vehicle组心包内注射0.2 ml BK联合电针双侧内关穴结合鞘内注射10 μl Vehicle。通过心包内注射BK建立大鼠心脏伤害性感受模型,以背斜方肌肌电（EMG）为痛反应的观测指标。结果：①心包内间隔40 min连续3次注射BK诱发背斜方肌EMG无显著性差异（P>0.05）。②与BK组相比,电针内关穴显著抑制EMG反应（P<0.05）;鞘内注射麦角新碱后,心包内BK诱发的EMG反应无显著性差异（P>0.05）。③与EA+BK组相比,鞘内注射麦角新碱后,部分反转电针内关穴对EMG的抑制作用（P<0.05）;然而,鞘内注射溶媒后,电针内关穴对EMG反应的抑制作用无显著性差异（P>0.05）。结论：脊髓水平的5-HT受体参与电针内关穴对大鼠心脏伤害性感受的抑制调控作用。     

大鼠心脏预处理后产生的内源性保护物质的研究

以外源性腺苷前质硫酸腺嘌呤大鼠心脏预处理和经典缺血预处理建立模型,监测心脏内源性保护物质的变化。方法：采用２５０～３００ｇＳＤ大鼠３２只分成４组,即假手术组（ＳＯ组）、缺血再灌组（Ｉ／Ｒ组）、经典缺血预处理组（ＩＰＣ组）及硫酸腺嘌呤预处理组（ＡＳＰＣ组）。比较各组心肌内源性保护物质的变化。结果：ＩＰＣ组、ＡＳＰＣ组均显示缩小心梗面积、改善心功能的ＩＰＣ效应,同时,肌酸激酶（ＣＫ）、过氧化氢酶（ＣＡＴ）、５”核苷酸酶（５’ＮＴ）、超氧化物歧化酶（ＳＯＤ）活性增强以及一氧化氮（ＮＯ）含量增高,热休克蛋白７０（ＨＳＰ７０）ｍＲＮＡ表达增强。结论：ＣＫ、ＣＡＴ、５’ＮＴ、ＳＯＤ、ＮＯ及ＨＳＰ７０是大鼠腺苷性和缺血性心脏预处理后产生的重要的内源性保护物质。     

留置中心静脉导管加尿激酶心包内灌洗治疗急性结核性心包炎的临床疗效观察

目的：观察留置中心静脉导管引流加尿激酶心包内灌洗治疗急性结核性心包炎的疗效。方法：自1996年1月～2009年5月对我院48例临床确诊为急性结核性心包炎伴中到大量积液的患者（病程均短于1月）,男28例,女20例,年龄14～72岁。随机分为两组,治疗组（常规抗结核、肾上腺糖皮质激素治疗的基础上给予留置中心静脉导管心包引流加心包内尿激酶灌洗治疗）或对照组（常规抗结核、肾上腺糖皮质激素治疗基础上给予留置中心静脉导管引流）。观察并比较两组穿刺并发症（心包内出血、心律失常及感染）,治疗前、后心包膜厚度的变化,拔管时心包积液的残留量,以及通过电话问询及心脏超声随访并发症,随访截止日期为2010年5月。随访期限为11～132个月。结果：治疗组与对照组比较,治疗组治疗1周及2周后心包膜厚度的变化、拔管时积液残留量及发生心包缩窄方面有明显差异（P〈0.05）,穿刺相关并发症方面无明显差异（P〉0.05）。全部治疗组患者给予尿激酶治疗后未见心包内出血及系统性出血并发症。随访期内无一例发生死亡,治疗组及对照组分别有1例（4.2%）及8例（33.3%）发生心包缩窄。结论：留置中心静脉导管加尿激酶灌洗治疗急性结核性心包炎安全、可行,心包积液引流彻底,拔管时间早,心包膜增厚程度显著减轻,心包粘连机会减少,能有效地预防患者心包缩窄的发生。     

人胚心肌纤维中心房特殊颗粒的分布及心钠素的免疫组化研究

收集胚胎标本共24例（经临床证实孕妇无心血管疾病）,用透射电镜观察各胎龄心脏各部位心肌纤维中心特殊颗粒（ASG）分布及含量变化,同时结合免疫组织化学技术对心脏各部位心肌纤维内心钠素的表达进行研究。结果表明,胚第5周时,心肌纤维便有ASG出现,随着胎龄的增长,心房与心耳的颗粒数量逐渐增多。而心室的颗粒数量却逐渐减少,在同一胎龄,心房内的颗粒数量多于心室,心耳ASG多于心房,免疫组织化学的研究结果表明,胚第7周时,心房与心耳内可出现心钠素样免疫反应阳性的心肌细胞,其阳性反应的变化规律与ASG的变化规律一致。心室中未发现阳性反应。     

大鼠中枢和外周组织中脑钠素样物质的分布、特性和作用

本工作首先应用特异性脑钠素放射免疫测定、放射受体分析和免疫组织化学的方法,研究了大鼠中枢神经系统和一些外周组织中脑钠素免疫活性物质的分布、生化特性、受体结合和生物学作用,提出脑钠素可作为一种新的神经递质或循环激素,广泛分布于体内不同组织内,并参与水电介质和心血管活动的调节。     

川芎嗪对缺血心肌的保护及抗氧化作用的实验研究

研究川芎嗪的心肌保护及抗氧化作用机制。在心脏停跳液中加入川芎嗪后对离全兔心脏进行缺血再灌注,然后观察心肌线粒体内丙二醛（ＭＤＡ）含量、超氧化物岐化酶（ＳＯＤ）活性及心肌组织超微结构损伤程度。发现含有川芎嗪的停跳液组丙二醛（ＭＤＡ）含量显著降低,超氧化物岐化酶（ＳＯＤ）活显著升高,观察心肌组织超微结构损伤程度发现较轻,因此,川芎嗪对缺血心肌具有良好的保护脑抗氧化作用。     

AngⅡ诱导的VEGF对食用蛙心包淋巴孔和间皮血窦的影响

血紧张素Ⅱ（angiotensin Ⅱ,AngⅡ）在许多血管性疾病中发挥了重要作用。本文研究AngⅡ对血管内皮细胞生长因子（vascular endothelial growth factor,VEGF）调控蛙心包淋巴孔和心包间皮血窦的影响,选用食用蛙（Rana esculenta）进行本项目研究,应用AngⅡ＋VEGF和VEGF蛙腹膜腔注射,扫描电镜观察和计算机图像处理。正常蛙心包壁层有一些散在分布的心包淋巴孔和少量间皮血窦。VEGF组的淋巴孔直径、分布密度和间皮血窦面积分别是1.50μm、8.25/0.1mm^2和2443.95μm^2/0.1mm^2均高于对照组（P＜0.01）。AngⅡ对VEGF有明显诱导作用,使淋巴孔直径（2.81μm）、分布密度（2882/0.1mm^2）和血窦面积（3866.15μm^2/0.1mm^2）高于VEGF组,两者有显著差异（P＜0.05）。VEGF可使蛙心包淋巴孔开放数量增多,孔径开大,分布密度增高,具有明显调控心包淋巴孔的功能;此外,还能使心包间皮血窦面积增多,进而使心包间皮通透性增加。AngⅡ能促进VEGF的作用,这对于加速心包腔内物质转归,促进心包膜漏出,防止心肌间质水肿有重要作用。结果提示,AngⅡ对VEGF的诱导作用可能是通过增加VEGF基因的表达而实现。     

Ssp dnaB蛋白质内含子介导的重组人脑钠素的制备

脑钠素(BNP)是临床治疗代偿失调性心衰竭的有效药物。将脑钠素与组氨酸标签(His-tag)以及具有自我剪切功能的Ssp dnaB微型蛋白质内含子进行融合表达。表达产物经Ni-Sepharose亲和层析及体外复性处理后,用CM_纤维素对复性产物进行了浓缩,并通过改变CM-纤维素柱内的pH及温度,诱导Ssp dnaB微型蛋白质内含子的剪切作用,使脑钠素从融合蛋白中释放并与载体蛋白(His-DnaB)分离,再经C4反相高效液相色谱法进一步纯化后,从每升培养液中获得了2.8mg纯度达97%的重组人脑钠素。体外活性测定结果表明,重组人脑钠素对兔胸主动脉条具有显著的血管舒张效应,其EC50为1.94×10-6mg/mL。     

间歇性低压低氧方式对发育大鼠心脏缺血/再灌注损伤的影响

本研究旨在探讨两种不同形式的间歇性低压低氧（intermittent hypobaric hypoxia,IHH）对发育大鼠心脏缺血,再灌注损伤的影响。雄性Sprague-Dawley（SD）新生大鼠72只,随机分为三组：对照组、IHH3000in组（IHH3000）、IHH5000m组（IHH5000）。低氧组大鼠出生后立即于低压氧舱分别接受28d、42d和56d（海拔5000m、每天6h：海拔3000m、每天5h）的低压低氧处理。应用Langendorff离体心脏灌流技术,给予心脏缺血（停灌30min）／再灌注（复灌60min）处理,分别在缺血前5min及复灌后l、5、10、20、30、60min记录心功能和冠状动脉流量变化,并测定乳酸脱氢酶（1actate dehydrogenase,LDH）活性。实验结束时测定心脏重量。结果显示：（1）IHH3000组大鼠体重增长与对照组无明显差异;IHH5000组大鼠体重增长明显慢于对照组及IHH3000组大鼠（P〈0．01）。（2）IHH3000组人鼠表现明显的心脏保护效应。与对照组相比较,在心脏停灌,再灌注60min时,心功能（LVDP、±LVdp／drmax）恢复增强（P〈0．05）、LDH活性降低（P〈0．05）、冠状动脉流量增多（P〈0．05）;心脏重量与对照组大鼠无差异;IHH42d处理的大鼠心功能恢复明显好于IHH28d处理的大鼠（P〈0．05）。（3）IHH5000组大鼠表现出明显的心脏损伤效应,各项心功能指标（LVDP、±LVdp／dtmax）的恢复均低于对照组（P〈0．05）,复灌过程中LDH活性明显高于相应对照组（P〈0．05）,右心室重量明显高于对照组大鼠（P〈0．05）。结果表明,适当的IHH增强发育大鼠心脏对缺血,再灌注损伤的抵抗能力;间歇性低氧方式是影响其心脏保护作用的重要因素。     

低温保存诱导大鼠心肌细胞Smac／DIABLO蛋白表达的动态变化

目的：观察大鼠供心不同时程低温保存后线粒体Smac／DIABLO蛋白表达的差异。方法：根据不同的低温保存时程,SD大鼠随机分5组（n=8）。采用Langendorff离体鼠心灌注法停搏大鼠心脏,检测心脏在4℃条件下celsior保存液中分别保存0、3、6、9、12h后,心肌细胞线粒体内超氧化物岐化酶（SOD）活性和丙二醛（MDA）含量的变化。并采用Westom blotting蛋白印迹分析法观察心肌细胞Smac／DIABLO蛋白表达情况,原位末端标记（TUNEL）染色法检测心肌细胞凋亡。结果：①随着低温保存时间的延长,心肌细胞线粒体内SOD活性随之降低,MDA含量随之升高,心肌细胞凋亡指数也逐渐增高。②随着低温保存时间的延长,Smac／DIABLO蛋白表达逐渐增多,至低温保存6h后最为显著,随后又逐渐减弱。结论：随着低温保存时间的延长,可能由于心肌细胞抗氧自由基的能力逐步减弱,致使诱导细胞凋亡的心肌线粒体Smac／DIABLO蛋白表达逐渐增强,心肌细胞凋亡逐渐增多。     

Enhanced accumulation of pericardial fluid adenosine and inosine in patients with coronary artery disease.

Adenosine and inosine are believed to have cardioprotective effects. However, little is known about their possible role in the metabolic autoregulation of human coronaries and in pathologic conditions with supply/demand imbalance of the heart such as coronary artery disease. Since these low molecular weight nucleosides freely diffuse through the monolayer of the visceral pericardium, adenosine and inosine concentrations in pericardial fluid may well reflect the conditions in cardiac interstitium. The pericardial fluid and systemic venous blood adenosine and inosine concentrations were measured in 98 human subjects undergoing heart surgery for coronary artery disease or valvular heart disease. Adenosine and inosine concentrations were measured by HPLC with UV detection. In subjects with coronary artery disease pericardial fluid nucleoside concentrations were significantly higher than in patients with valvular heart disease (adenosine: 1545 (996-3146) nmol/L [median (25th-75th quartiles)] vs. 738 (390-2527) nmol/L, P<0.01; inosine: 658 (321-1331) nmol/L vs. 347 (159-1037) nmol/L, P<0.05), while in both patient groups pericardial fluid nucleoside concentrations were higher by an order of magnitude than in venous plasma. Our results show the enhanced release of adenosine and inosine by the ischemic myocardium as a marker of supply/demand imbalance and support the hypothesis that these cardiac nucleosides may have an important role in the adaptation of coronary blood flow in human coronary artery disease.     

MicroRNA Profiling of Pericardial Fluid Samples from Patients with Heart Failure

Aims

Multicellular organisms maintain vital functions through intercellular communication. Release of extracellular vesicles that carry signals to even distant target organs is one way of accomplishing this communication. MicroRNAs can also be secreted from the cells in exosomes and act as paracrine signalling molecules. In addition, microRNAs have been implicated in the pathogenesis of a large number of diseases, including cardiovascular diseases, and are considered as promising candidate biomarkers due to their relative stability and easy quantification from clinical samples. Pericardial fluid contains hormones secreted by the heart and is known to reflect the cardiac function. In this study, we sought to investigate whether pericardial fluid contains microRNAs and if so, whether they could be used to distinguish between different cardiovascular pathologies and disease stages.

Methods and Results

Pericardial fluid was collected from heart failure patients during open-heart surgery. MicroRNA profiles of altogether 51 patients were measured by quantitative real-time PCR (qPCR) using Exiqon human panels I and II. On the average, 256 microRNAs were detected per sample, and 70 microRNAs out of 742 profiled microRNAs were detected in every sample. The five most abundant microRNAs in pericardial fluid were miR-21-5p, miR-451a, miR-125b-5p, let-7b-5p and miR-16-5p. No specific signatures for cardiovascular pathologies or clinically assessed heart failure stages could be detected from the profiles and, overall, microRNA profiles of the samples were found to be very similar despite the heterogeneity in the study population.

Conclusion

Measured microRNA profiles did not separate the samples according to the clinical features of the patients. However, several previously identified heart failure marker microRNAs were detected. The pericardial fluid microRNA profile appeared to be a result of an active and selective secretory process indicating that microRNAs may act as paracrine signalling factors by mediating the local crosstalk between cardiac cells.     

Intrapericardial angiotensin II stimulates endothelin-1 and atrial natriuretic peptide formation of the in situ dog heart

Angiotensin (AT) II, endothelin (ET)-1, and atrial natriuretic peptide (ANP) play an important role in cardiovascular regulatory processes under physiologic and pathophysiologic conditions. All of these agents are present in the pericardial fluid, and alteration of their pericardial concentrations mirror changes in the myocardial interstitium. Moreover, the composition the pericardial fluid may also reflect the myocardial interaction of these agents. The local myocardial effects of AT II on cardiac ET-1 and ANP production, as well as on cardiovascular function, was studied by intrapericardial (ip) administration of AT II (0.125-1.0 microg/kg) to the in situ dog heart (n = 8). Big ET, ET-1, and ANP [1-28] fragment concentrations were measured by enzyme-linked immunosorbent assay in pericardial infusate samples and in peripheral blood before and after an AT II treatment of 15 mins. Systemic blood pressure (BP), heart rate (HR), and left ventricular contractility (dP/dt) were also recorded. In our studies, the pericardial big ET (but not ET-1) concentration was increased to a maximum value of 139 +/- 28 versus 74 +/- 12 pg/ml (control; P < 0.02) with ip AT II administration, with parallel elevations of the pericardial ANP levels (36.8 +/- 7.2 vs. 24.4 +/- 3.6 ng/ml; P < 0.05). The ip administration of AT II did not influence HR, and it elicited moderate changes in BP (BP(max), +14 +/- 2 mm Hg, P < 0.001; dP/dt(max), +10 +/- 3%, P < 0.02). The plasma levels of big ET, ET-1, and ANP did not change significantly. The results suggest that AT II promotes production of big ET and ANP in the heart. However, no detectable conversion of big ET-1 to ET-1 was observed within 15 mins. The myocardial formation of big ET-1 and ANP occurred, at least in part, independently of the changes in cardiovascular function.     

Cardiac abnormalities in liver cirrhosis.

Cirrhosis is associated with several circulatory abnormalities. A hyperkinetic circulation characterized by increased cardiac output and decreased arterial pressure and peripheral resistance is typical. Despite this hyperkinetic circulation, some patients with alcoholic cirrhosis have subclinical cardiomyopathy with evidence of abnormal ventricular function unmasked by physiologic or pharmacologic stress. Florid congestive alcoholic cardiomyopathy develops in a small percentage, but the concurrent presence of cirrhosis seems to retard the occurrence of overt heart failure. Even nonalcoholic cirrhosis may be associated with latent cardiomyopathy, although overt heart failure is not observed. Tense ascites is associated with some cardiac compromise, and removing or mobilizing ascitic fluid by paracentesis or peritoneovenous shunting results in short-term increases in cardiac output. Cirrhosis also appears to be associated with a decreased risk of major coronary atherosclerosis and an increased risk of bacterial endocarditis. Small hemodynamically insignificant pericardial effusions may be seen in ascitic patients. The release of atrial natriuretic peptide appears to be unimpaired in cirrhosis, although the kidney may be hyporesponsive to its natriuretic effects.     

Presence of immunoreactive atrial natriuretic peptides in pericardial fluid of human subjects with congenital heart diseases

The epicardial release of immunoreactive atrial natriuretic peptides (ir-ANPs) in inside-out perfused rabbit atria has been reported. In order to determine the presence of ir-ANPs in pericardial fluid and to evaluate their biochemical characteristics, we measured the concentration of ir-ANPs in pericardial fluid obtained from the patients with congenital heart diseases during open heart surgery. Serial dilution curves made with the extrats of pericardial fluid using Sep-Pak C18 cartridges were parallel with standard curve. The concentration of ir-ANPs in pericardial fluid was significantly lower than the corresponding plasma concentration. On gel permeation and reverse-phase high performance liquid chromatography, the ir-ANPs in pericardial fluid, plasma and atrial appendage showed both high and low molecular weights. The major peak of ir-ANPs in plasma was observed at the corresponding fraction to the alpha-human ANP and considerable amount of high molecular weight form of ir-ANPs was observed in pericardial fluid. However, the major peak of ir-ANPs in atrial appendage was observed at the corresponding fraction to the rat pro-ANP. The data suggest that ir-ANPs exist both high and low molecular weight forms in pericardial fluid.     

Primary malignant lymphoma of the heart. Antemortem cytologic diagnosis

A case of primary malignant lymphoma of the heart diagnosed cytologically is reported. The patient presented with pericardial tamponade and ventricular arrhythmias and developed rapidly progressive and intractable cardiac failure. Two-dimensional echo-cardiography, which demonstrated the pericardial effusion, showed progressive impairment of the left ventricular contraction. The pericardial fluid contained malignant lymphoid cells. Despite vigorous treatment and chemotherapy, the patient died within 15 days; postmortem examination showed malignant lymphoma confined to the myocardium.     

Assessment and consequences of the constant-volume attribute of the four-chambered heart

The constant-volume hypothesis regarding the four-chambered heart states that total pericardial volume remains invariant throughout the cardiac cycle. Previous canine studies have indicated that the pericardial volume remains constant within 5%; however, this hypothesis has not been validated in humans using state-of-the-art technology. The constant-volume hypothesis has several predictable functional consequences, including a relationship between atrial ejection fraction and chamber equilibrium volumes. Using cardiac magnetic resonance (MR) imaging (MRI), we measured the extent to which the constant-volume attribute of the heart is valid, and we tested the accuracy of the predicted relationship between atrial ejection fraction and chamber equilibrium volumes. Eleven normal volunteers and one volunteer with congenital absence of the pericardium were imaged using a 1.5-T MR scanner. A short-axis cine-loop stack covering the entire heart was acquired. The cardiac cycle was divided into 20 intervals. For each slice and interval, pericardial volumes were measured. The slices were stacked and summed, and total pericardial volume as a function of time was determined for each subject. In the normal subjects, chamber volumes at ventricular end diastole, end systole, and diastasis were measured. Pericardial volume remained invariant within 5 +/- 1% in normal subjects; maximum variation occurred near end systole. In the subject with congenital absence of the pericardium, total heart volume, defined by the epicardial surface, varied by 12%. The predictions of the relationship between atrial ejection fraction and chamber equilibrium volumes were well fit by MRI data. In normal subjects, the four-chambered heart is a constant-volume pump within 5 +/- 1%, and constant-volume-based modeling accurately predicts previously unreported physiological relationships.     

Pericardial and pericardioperitoneal canal relationships to cardiac function in the white sturgeon (Acipenser transmontanus)

Sturgeons are primitive bony fishes and their hearts have structural features found in other primitive fishes. Sturgeons have a pericardioperitoneal canal (PPC), a one-way conduit into the peritoneum. A PPC also occurs in elasmobranchs (sharks and rays) and studies with that group demonstrate that pericardial pressure and pericardial fluid loss via the PPC affect stroke volume. A study of white sturgeon (Acipenser transmontanus) heart function was conducted to test for a comparable PPC and pericardial effects. White sturgeon-elasmobranch heart-function similarities include biphasic ventricular filling, a comparable operational pericardial pressure (-0.03 kPa), and a strongly negative pressure (-0.2 to -0.6 kPa) with complete pericardial fluid withdrawal. Differences include the white sturgeon's relatively smaller atrium and ventricle but a larger conus arteriosus. Although white sturgeon heart size is also smaller, its pericardial volume is disproportionately less (2.4 to 2.7 vs. 3.5 to 5.4 ml kg(-1) in elasmobranchs), meaning it has less scope for increasing stroke volume upon PPC fluid release. These differences may reflect the phylogenetic progression from the less complex operation of the elasmobranch heart, which lacks sympathetic innervation and has a mechanically mediated (PPC) stroke volume, to the condition in the more derived bony fishes which have sympathetic and parasympathetic regulation of both stroke volume and heart rate.     

Primary cardiac lymphoma initially diagnosed by routine cytology. Case report and literature review

A case of primary cardiac lymphoma initially diagnosed by routine cytologic examination of pericardial fluid is presented. In a 64-year-old woman woman who originally presented with chest pain and heart block, the initial clinical impression was ischemic heart disease. However, coronary angiography failed to reveal significant disease. An echocardiogram demonstrated pericardial fluid, which was drained. A small amount was sent for cytologic examination, and the diagnosis of malignant lymphoma, large cell type, was made. Subsequent radiologic examinations revealed an intracardiac mass involving the atrioventricular canal; surgical biopsy confirmed the diagnosis of a large cell lymphoma. While primary malignant lymphoma of the heart is rare, this case highlights the efficacy of routine cytologic examination of an effusion fluid (often drained therapeutically) in establishing the correct diagnosis.     

Management of uraemic pericarditis.

Of 250 patients undergoing haemodialysis from 1967 to 1974 17 presented with uraemic pericarditis. Seven of these patients who had been transferred early enough to peritoneal dialysis treatment were cured without pericardiectomy (mean survival 18 months (range 6-36); no deaths). Only one patient was cured from his pericarditis by "aggressive haemodialysis." In seven out of 10 patients treated with haemodialysis, pericardiectomy finally had to be performed because of pericardial tamponade (postoperative survival 20 months (range 8-36); one death). Two patients died from pericardial tamponade before surgery. In patients with evidence of uraemic pericarditis frequent peritoneal dialysis with high fluid withdrawal is the treatment of choice, but in cardiac tamponade pericardiectomy should follow a preoperative pericardiocentesis with limited fluid aspiration. Of possible significance in the aetiology of pericarditis were the findings that 10 of the 17 patients had hypertension with cardiac enlargement and that 14 presented with evidence of underdialysis, possibly due to the reuse of dialysis components.