不同免疫剂治疗扩张型心肌病患儿心功能和临床预后评价

目的观察比较泼尼松联用硫唑嘌呤和大剂量静脉用免疫球蛋白(IVIG)对扩张型心肌病(DCM)患儿心功能及预后的影响。方法将DCM患儿20例分为治疗Ⅰ和Ⅱ组,分别在传统抗心衰治疗基础上加泼尼松联用硫唑嘌呤和大剂量IVIG,治疗1个疗程后评价心功能,检测治疗前后左房横径(LA)、左室舒张期内径(LV)、左室射血分数(LVEF)、心脏指数(CI),并计算其治疗前后变化。所有病例随访1年,计算1年存活率。结果治疗Ⅱ组心功能明显优于治疗Ⅰ组(P均<0.05);两组LA、LV、LVEF和CI治疗后较治疗前均有明显改善(P均<0.05);治疗Ⅰ组各参数变化明显低于治疗Ⅱ组(P均<0.05),其1年存活率明显低于治疗组Ⅱ(P<0.05)。结论泼尼松联用硫唑嘌呤和大剂量IVIG均能改善DCM患儿心功能,但IVIG疗效优于泼尼松联用硫唑嘌呤。     

BIOCHEMICAL CORRECTION IN THE SYNDROME OF HYPERTENSION AND HYPERKALAEMIA BY SEVERE DIETARY SALT RESTRICTION SUGGESTS RENIN-ALDOSTERONE SUPPRESSION CRITICAL IN PATHOPHYSIOLOGY

1. Plasma potassium and chloride concentrations were raised and plasma renin activity, aldosterone, bicarbonate and arterial pH were reduced in two brothers with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome), on unrestricted or moderately restricted sodium diets. 2. These abnormalities were corrected in both patients within 10 days of severe sodium restriction. 3. Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure. 4. Increasing distal tubular sodium delivery by infusion of normal saline increased fractional excretion of potassium when aldosterone had been stimulated by severely restricted sodium diet, but not when aldosterone levels were low on unrestricted sodium diet. 5. These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon's syndrome, leading to volume expansion and suppression of renin and aldosterone. Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities.     

Peak Endocardial Acceleration-Based Clinical Testing of the "BEST" DDDR Pacemaker

The peak endocardial acceleration (PEA, unit g) shows a near correlation with myocardial contractility during the isometric systolic contraction of the heart (dP/dtmax), with sympathetic activity and, thus, with physiological heart rate modulation. The (Biomechanical Endocardial Sorin Transducer (BEST) sensor is incorporated in the tip of a pacing lead and measures PEA directly near the myocardium. In an international study, the lead was implanted with the dual chamber pacemaker Living-1 (Sorin) in 105 patients. The behavior of the PEA signal was tested under conditions of physical and mental stress and during daily life activities by 24-hour recordings of PEA (PEA Holter) at 1 to 2 months and approximately 1 year after implantation. Implantation of the BEST lead was performed without complications in all patients. The sensor functioned properly in the short- and long-term in 98% of patients. Although PEA values differed from patient to patient, the values closely reflected the variations in sympathetic activity due to physical and mental stress in each patient. During exercise and during daily life activities a close correlation between PEA and heart rate was observed among patients with normal sinus rhythm. Peak endocardial acceleration allows a nearly physiological control of the pacing rate.     

1870株致病菌感染概况及敏感性情况

目的了解临床标本中主要致病菌分布及敏感性分析，指导抗生素的选择及合理治疗方法对我院1994～1996年临床分离的1870株细菌的分布及敏感性、耐药性进行分析，1996年与1994年的结果进行比较，并将1995年的结果与北京地区5家教学医院同年的结果进行比较。结果分离菌株主要分布于呼吸道、消化道、泌尿道、血液及骨髓。G＋菌占10.5％，G-菌占89.5％，占明显优势。沙门氏菌对头孢唑啉和哌拉西林的耐药性明显降低（P＜0.01），大肠埃希氏菌对氨苄西林和氟嗪酸的耐药性明显增高（P＜0.01），其余菌株无明显差异。抗生素敏感性覆盖率最高的是复达欣，其次为丁胺卡那，最低者氨苄西林。大肠埃希氏菌、假单胞菌对哌拉西林的耐药率，克雷伯杆菌属对西力欣的耐药率，肠肝菌属对哌拉西林的耐药率均高于北京地区。结论本组资料显示不断监测和分析菌丛的变化及对不同抗生素耐药性出现的频率和耐药谱至关重要。     

老年男性心肌缺血患者心率变异分析（附67例报告）

采用正常搏动ＲＲ间期的标准差（ＳＤ）及心率变异指数（ＨＲＶ ｉｎｄｅｘ）作为指标，分析６７例老年男性心肌缺血患者的心率变异，并与正常老年男性组及正常青壮年男性组进行了对比，发现前组的ＲＲ间期ＳＤ、ＨＲＶｉｎｄｅｘ均明显低于后两组，其结果有显著性差异（Ｐ均〈０．０１）。提示心肌缺血可破坏交感与迷走神经的均衡性，造成心率变异降低。     

左心室舒张(充盈)功能的影响因素

本文用X线电影摄影方法评价了49例左室舒张(充盈)功能的影响因素。冠心病(CAD)组23例,高血压病组12例,正常对照组14例。左室充盈功能或顺应性主要受冠脉病变严重程度的影响。冠脉狭窄程度越重,并有陈旧性心肌梗塞、室壁运动异常、EF下降,则充盈功能受损愈明显。血压、年龄因素对舒张充盈功能的影响较小。在CAD组中,心率与1/3充盈分数呈负相关,与正常化高峰充盈率(NPFR)不相关,而EF则与NPFR相关良好。     

Regulation of local sweating in sleep-deprived exercising humans

Summary Thermoregulatory sweating [total body (m _sw,b), chest (m _sw,c) and thigh (m _sw,t) sweating], body temperatures [oesophageal (T _oes) and mean skin temperature (T _sk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T _air andT _wall at 35° C. Them _sw,c andm _sw,t were measured under local thermal clamp (T _sk,1), set at 35.5° C. After sleep deprivation, neither the levels of body temperatures (T _oes,T _sk) nor the levels ofm _{sw, b},m _{sw, c} orm _{sw, t} differed from control at rest or during exercise steady state. During the transient phase of exercise (whenT _sk andT _sk,1 were unvarying), them _{sw, c} andm _{sw, t} changes were positively correlated with those ofT _oes. The slopes of them _{sw, c} versusT _oes, orm _{sw, t} versusT _oes relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versusT _oes, relationships (m _{sw, c} andm _{sw, t} sweating data pooled which reached 1.05 (SEM 0.14) mg·cm^–2·min^–1°C^–1 and 1.14 (SEM 0.18) mg·cm^–2·min^–1·°C^–1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased theT _oes threshold for the onset of bothm _{sw, c} andm _{sw, t} (+0.3° C,P<0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.     

Heart rate analysis in 24 patients treated with 150 mg amitriptyline per day

Twenty-four patients treated with 150 mg amitriptyline per day for an episode of major depression underwent a standardized heart rate analysis (HRA) before therapy and after 14 days. The battery of cardiovascular reflex tests included the determination of the coefficient of variation (CV) while resting and during deep respiration, a spectral analysis of heart rate, the heart rate response to standing, and the Valsalva manoeuvre. The results of the initial HRA did not differ from a group of 24 normal control subjects matched for age and sex. On day 14 of treatment the patients showed significantly reduced values of heart rate variability in all tests (P<0.0001), probably due to the anticholinergic side effects of amitriptyline. Heart rate increased form 78.1 to 93.6 bpm on average (P<0.0001). Abnormal CV at rest was registered in 96% of the patients; during deep respiration 29% showed abnormal CV results. An abnormal spectral analysis was found in 100% of the cases (low frequency peak: 42%, mid-frequency peak: 100%, high frequency peak: 79%). The heart rate response to standing was abnormal in 75% and the Valsalva test in 33% of the cases. Eighty-eight percent of the patients fulfilled the criteria of a cardiovascular autonomic neuropathy under the conditions of amitriptyline therapy. As yet, the consequences of these changes for the patients have not been sufficiently elucidated.     

苯作业工人白细胞降低者的总估校正现患率

选择乡镇工业苯作业工人４次外周血白细胞计数中的间隔半年的两次数据，应用俘获再俘获法，计算其白细胞降低者的总估校正现患率（ＡＣＰＲ）。结果苯接触组为３６．８ｌ％（２９．１４％～４４．４８％），对照组为１２．７１％（７．２０％～１８．２２％）具有显著差异，其相对危险度为２，９。用常规法求得的４次检出率分别是：苯接触组为２６．３７％，１８．７３％，２７．９３％，３６．７６％；对照组为６。８５％，７．３８％，７．９４％，１５．００％。均在其ＡＣＰＲ之９５％可信限内，可见ＡＣＰＲ计算方法简便、结果准确，值得推广。对于稳定的人群，可用其每年一次的健康监护资料计算ＡＣＰＲ。     

MHPG and heart rate as correlates of nonresponse to drug therapy in panic disorder patients

Little is known about biological predictors of treatment response in panic disorder (PD). In the present study heart rate, blood pressure, plasma cortisol and plasma MHPG were investigated at baseline in a sample of 44 PD patients as possible predictors for nonresponse to treatment. We used a strict definition of nonresponse to find patients who did not respond at all after 12 weeks of treatment with brofaromine or fluvoxamine. Patients were considered nonresponders when they fulfilled two criteria: they did not show a 50% reduction of agoraphobic avoidance and they still experienced panic attacks at endpoint. The variables that differed significantly between the groups were used to predict nonresponse to drug therapy. Using this strict definition of nonresponse, 15 patients (32.6%) were considered nonresponders. These patients were characterised by a higher plasma MHPG concentration and a higher heart rate at baseline. These variables were subsequently used to predict nonresponse.