Lipoprotein lipase in relation to inflammatory activity in rheumatoid arthritis

Objective. To evaluate the impact of chronic inflammation on lipoprotein lipase (LPL) levels and triglyceride metabolism in patients with rheumatoid arthritis (RA). Design. Plasma levels of LPL activity and mass before and after heparin were determined in post-menopausal women with active RA and in controls. The results were related to lipid levels and inflammatory variables. The LPL activity and mass together with triglyceride levels were also measured before and 6 h after an oral fat load. Setting. The study was performed on in- and out-patients at a University Rheumatology clinic. The controls came from the same reference area. Subjects. Altogether 17 consecutive post-menopausal female patients with RA and 16 age and sex matched controls were enrolled for the initial determination of LPL. Fifteen of the patients and 15 of the controls agreed to take part in the fat load. Of these, one patient and one control were excluded. Main outcome measures. LPL determination: basal levels and post-heparin levels of LPL activity and mass. Correlations between LPL and blood lipids (cholesterol, triglycerides), lipoprotein levels (high density lipoprotein, HDL; low density lipoprotein, LDL), erythrocyte sedimentation rate (ESR) acute phase proteins (orosomucoid, haptoglobin, fibrinogen mass) and cytokines (tumour necrosis factor α, TNF-α; interleukin 1β, IL-1β; and interleukin-6, IL-6). Fat tolerance test: LPL activity, mass and triglyceride levels before and 6 h after a per oral fat load. Results. Pre-heparin LPL mass (P<0.01) and activity (P<0.01) were significantly lower in the rheumatoid patients. Pre-heparin LPL mass showed no correlation to the lipid levels, but an inverse correlation to several inflammatory parameters; it was significant for orosomucoid (r_s=?0.63, P<0.05) and C-reactive protein (CRP) (r_s=?0.54, P<0.05) and close to significant for haptoglobin (r_s=?0.48, P=0.087) and IL-6 (r_s=?0.52, P=0.061). Six hours after a lipid load the LPL activity and mass were significantly lower in RA (P<0.05 and P<0.01, respectively) but the triglyceride level was not significantly different compared to controls. Conclusion. An inverse relationship exists between inflammatory status and pre-heparin LPL mass. Pre-heparin LPL mass reflects mainly the inactive monomeric fraction of LPL. This has been shown to hinder the uptake of remnant lipoprotein particles through competition with lipoprotein bound dimeric LPL for the LDL receptor-related protein (LRP receptor) on hepatocytes and macrophages in culture. A decrease of the level of monomeric LPL in plasma may thus be beneficial for remnant catabolism. The same mechanism may on the other hand increase macrophage uptake of lipids. This may not affect global lipid metabolism but may be important in driving the atherosclerotic process in the vessel wall.     

Chrome congestive heart failure: Non-invasive measurement of cardiac output by a carbon dioxide rebreathing method at rest and during exercise

Cardiac output was measured in 11 patients undergoing routinecardiac catheterization using a carbon dioxide rebreathing techniqueand compared with cardiac output measured by direct Fick andthermodilution. The carbon dioxide rebreathing technique gaveconsistently lower values for cardiac output than the othertwo methods (mean difference –0·73, 95% CI –0·95to–0·511. min^–1 with the direct Fick and–0·72. 95% CI –1·19 to –0·261.min^–1 with thermodilution). The direct Fick and thermodilutionmethods gave similar results (mean dtfference –0·08,95% CI –0·32 to 0·16a. min^–1). Cardiacoutput was also measured in 10 healthy subjects at rest andduring two steady-state levels of exercise using the carbondioxide rebreathing technique. Measurements were made in triplicateon 3 separate days. The technique gave reproducible resultsbetween replicates at rest (coefficient of variation 91%) andbecame more reproducible on exercise (coefficients of variation56% and 54% respectively at each exercise level). There wasa good correlation between cardiac output and oxygen consumption(r=0·98 The carbon dioxide rebreathing technique is afeasible non-invasive way of measuring cardiac output. It tendsto underestimate cardiac output at rest but is reproducibleand becomes more so on exercise which is where it should beof most value.     

Bilocular atrial malignant mesenchymoma causing mitral and localized pulmonary vein flow obstruction: diagnosis by transoesophageal echocardiography.

Cardiac malignant mesenchymoma is an extremely rare malignancy with poor prognosis. We report a patient presenting with a history and clinical findings typical of mitral stenosis. Transthoracic echocardiography showed a mass on the thickened posterior mitral leaflet. Transoesophageal echocardiography revealed two tumoural masses: one on the atrial side of the posterior mitral leaflet causing mitral obstruction, the other arising in the region of the right lower pulmonary vein orifice and obstructing inflow through this vein.     

间置空肠贲门再造术在抗返流性食管炎上的应用

作者对１５例贲门癌患者行根治术同时，采用食管残胃间插入带蒂空肠并附加贲门再造术，通过ＳＰＥＣＴ胃食管返流指数测定、食管下端ｐＨ检测及返流症状评定方法，并与单纯食管胃套叠吻合术进行随机对比分析，证明该术式具有单向住屏障作用，能有效地预防返流性食管炎的发生。     

超声心动图诊断原发性心脏肿瘤

目的：探讨原发性心脏肿瘤超声心动图(ECG)特征。方法：利用ECG检查42例心脏肿瘤。其中粘液瘤38例，恶性肉瘤2例，均经手术病理证实。横纹肌瘤2例，经随访证实。结果：ECG对38例粘液瘤，2例横纹肌瘤全部做出正确诊断。2例恶性肿瘤提示相应部位占位病变。粘液瘤多发生在左房，有明确的瘤蒂，肿瘤回声稀疏，活动度大。恶性肿瘤回声较强、无蒂，活动度小。横纹肌瘤多发生在室壁心肌内，呈结节状，与正常心肌间有明确的界限。结论：ECG对原发心脏肿瘤的诊断具有重要意义，可初步区分良、恶性肿瘤。     

心脏创伤35例报告

本文报告心脏创伤３５例。年龄最小７岁，最大６８岁，其中包括心脏刺伤患者１０例，心肌挫伤患者２５例，死亡５例。作者强调快速确定诊断，紧急剖胸心包切开减压和心脏修补止血是心脏刺伤救治成功的关键。同时，对心肌挫伤的临床表现、早期诊断和及时处理等问题进行了讨论。     

Cystic brain stem necrosis in a premature infant after prolonged bradycardia

Summary A case is described of symmetrical cavitating brain stem necrosis produced by cardiac arrest in a premature infant. Two months after birth this 25-week gestational age infant suffered a prolonged episode of bradycardia. She was resuscitated and then died 3 weeks later. The autopsy revealed striking bilateral cavitation of the brain stem tegmentum extending in a columnar fashion from the upper portion of the spinal cord to the hypothalamus. The findings in this case are identical to the brain stem injury experimentally produced by complete cardiac arrest in the rhesus monkey.     

Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat.

AIMS: Severe sustained bradycardia may cause acute and possibly chronic congestive heart failure (CHF). The aim of this study was to investigate acute and chronic effects of complete heart block (CHB) on cardiac function, morphology, and creatine (Cr) metabolism. METHODS AND RESULTS: CHB was induced in male Sprague-Dawley rats (approximately 250 g, n = 11) by means of electrocautery applied to the region of AV node and were compared with controls (n = 15). The rats were investigated at 1, 3, and 12 weeks after CHB induction with transthoracic echocardiography. Invasive haemodynamic assessment of left and right ventricular pressures was performed at 12 weeks. After the sacrifice, the hearts were freeze-clamped for analysis of myocardial Cr, and high energy phosphometabolites. The efficacy of operative procedure was 54%. The peri-operative mortality rate was 20%. Heart rate (HR) decreased by approximately 50% (P < 0.01) while stroke volume (SV) increased 2.5 times (P < 0.01) in the CHB rats. Cardiac index remained unchanged. The rats with CHB grew normally and were in no apparent distress. Filling pressures in left and right ventricles were normal. The CHB rats developed marked cardiomegaly with biventricular dilatation and eccentric left ventricular hypertrophy (P < 0.01). There was no change in the myocardial content of Cr and high energy phosphometabolites. CONCLUSION: Rats with CHB are compensating for reduction in HR with increased SV without haemodynamic and biochemical characteristics of CHF. This model may be useful to study the effects of CHB and bradycardia on myocardial structure, function, electrophysiology, and metabolism as well as for studies of cell therapy for reparation of AV conductance.     

质疑Frank—Starling心脏定律

心脏收缩释放的能量（作功）是心肌纤维长度（心室舒张末期容积，EDV）的函数，即Frank—Star一1ing（FS）心脏作功定律，被誉为心脏生理学中的“经典”理论。对此，笔者从各种不同角度进行了探讨：首先分析了Frank伸展离体心肌和Starling及其同事使用心肺制备做的实验与动物生理实际的差异，以及人们在实验中观测到的增加心肌前负荷引起收缩力增强的现象（FS现象），认为：①在正常生理条件下的动物体内，来自心脏以外的、如同心肺制备中那样人工控制心室充盈压力升高、引起EDV增加的那种血液的重力动力是不存在的。②另一方面，人为地增加前负荷，那是改变了心肌收缩时的外环境条件。③由此而激发出的FS现象，是心脏适应其外环境条件变化所作出的反应。④此种心肌收缩力增强的反应，需通过心肌细胞内部与收缩过程发生有关的心肌兴奋一收缩和化学一力学偶联等一系列生化机制（不恒定因素）方能得以实现。⑤根据他们实验中观测到的FS现象，在逻辑上不能得出前负荷这一心肌收缩时的外环境条件变化调控其作功的推论。换言之，所有的在实验中被激发出来的FS现象，都不足以成为支持FS心脏定律的证据。然后，引用国内外公认的计算心脏每搏射血作功（w）的生物物理学公式“w=P×（EDV—ESV）”，证明了w和EDV之间没有函数关系。根据心脏作功的医用物理学和生物数学的基本原理，笔者认为Frank—Starling心脏定律表达的不是心脏作功的规律。