高血压鼠局部脑梗塞后脑超微结构改变动态观察

本文选用肾血管性高血压鼠(RHR)复制大脑中动脉闭塞(MCAO)模型,其后2h至7d分8次取不同区域脑组织进行透射电镜动态观察超微结构的改变。显示局部脑梗塞后发生全脑性改变,其损害程度和出现时间梗塞区最早,以坏死为主,呈完全不可逆性损害;边缘区稍后,主要是微血管塌陷和微血栓形成及部分脑细胞坏死,呈部分可逆性损害,远隔区和镜区最迟,以内皮和星形细胞水肿为主,呈可逆性损害,认为用RHR复制MCAO,更接近于高血压性脑血管损害基础上发生脑梗塞的临床病理改变,全脑超微结构的动态性改变中微血管损害起着重要作用。     

透明质酸在脑出血和腔隙性脑梗塞中病理作用的探讨

本文对５７例急性脑出血和脑腔梗患者及３５例对照组血清透明质酸（ＨＡ）含量进行了测定，并与相应的临床指标（病程、血压及神经功能缺损评分等）、血液生化指标（血糖、血脂、纤维蛋白原及血液流变学等）和影像学指标进行了相关分析。结果表明：脑出血和脑腔梗组的ＨＡ含量明显高于对照组，腔梗组明显高于出血组（Ｐ＜０．０１）。脑出血组ＨＡ含量与纤维蛋白原含量呈明显负相关，与其它指标无相关性。而脑腔梗组ＨＡ含量与纤维蛋白原及其它指标均无相关性。     

The evolution of today's hospital emergency departments —Current problems and challenges

The announcement of the National Heart Attack Alert Program by the National Heart, Lung and Blood Institute in June of 1991 prompted leaders of the Florida Chapter of the American College of Cardiology to develop a statewide program to reduce the morbidity and mortality from acute myocardial infarctions within Florida. It became apparent that the success of such a program would require the prompt institution of thrombolytic agents or other revascular-ization procedures in appropriate patients. No longer could the decision regarding institution of therapy await discussion by telephone and/or the arrival at the emergency department (ED) of the patient's primary care physician or cardiologist. Efforts to establish appropriate protocols for therapy revealed that many of the 25,000 or more physicians currently staffing the 5,600 or so EDs in this country were moonlighting residents or practitioners from a variety of specialties or subspe-cialties with limited or no formal EM training. Furthermore, it was learned that there were in the entire country only about 800 postgraduate, year-one Council for Graduate Medical Education accredited training positions. There were only 21 such training positions in the entire state of Florida. The reasons for these deficiencies are discussed and a challenge to correct this person power crisis is issued, not principally to the leadership of EM, but to the entire medical profession.     

急性心肌梗塞患者血清唾液酸含量测定

本文测定了５０例正常人，３２例急性心肌梗塞，５４例冠心病无梗塞者血清ＳＡ水平，结果表明，急性心肌梗塞组血清ＳＡ水平与冠心病无梗塞组及正常人相比，具显著性差异，可能与心肌梗塞造成心肌细胞受损所致使细胞表面成份释放入血有关，所以血清ＳＡ测定可提供一新的心肌梗塞诊断依据。     

Short and long term effects of exercise training on the tonic autonomic modulation of heart rate variability after myocardial infarction

We studied the effects of cardiac rehabilitation on the sympathovagalcontrol of heart rate variability in 30 patients after a first,uncomplicated myocardial infarction. Twenty-two patients completed8 weeks of endurance training (trained), while eight decidednot to engage in the rehabilitation programme for logisticalreasons, and were taken as untrained controls. Age, site ofinfarction, ejection fraction, ventricular diameter and stresstest duration were similar in the two groups at baseline. Heartrate variability was evaluated 4 weeks after infarction beforestarting rehabilitation, and repeated 8 weeks and one year laterin both trained and untrained patients. Measures of heart ratevariability, obtained from both time- and frequency- domainanalysis of a 15 min ECG recording in resting conditions, wereas follows: mean RR interval and its standard deviation (RRSD),the mean square successive differences (MSSD), the percent ofRR intervals differing >50 ms from the preceding RR (pNTN50),the low and high frequency components of the autoregressivepower spectrum of the RR intervals and their ratio (LF/HF).At baseline, heart rate variability was similar in trained anduntrained patients. In the short term (8 weeks after infarction),training increased RRSD by 25% (P<0·01), MSSD by 69%(P<0·01), pNN50 by 120% (P<0·01), and reducedLF/HF ratio by 30% (P<0·01). The effects persistedafter one year in trained patients. In untrained patients, theautonomic control of heart rate variability did not change 8weeks after myocardial infarction and was only slightly modifiedby time. Thus, exercise training, performed for 8 weeks aftera myocardial infarction, modifies the sympathovagal controlof heart rate variability toward a persistent increase in parasympathetictone, known to be associated with a better prognosis. This maypartly account for the favourable outcome of patients who undergorehabilitation.     

156例脑梗塞的临床分析

本文报道脑梗塞患者156例,就其发病情况,诱发因素,临床特点,治疗及预防进行了分析讨论。脑梗塞的发病高于脑出血,高血压动脉硬化是发生脑梗塞的主要危险因素。积极预防和治疗高血压有极其重要的意义。脑梗塞的治疗应根据脑水肿的情况进行,不宜普遍首先应用扩血管治疗。本病复发率高,反复发作可引起广泛性脑部损害,其病死率、病残率明显高于首次发病。小剂量阿斯匹林等药物应用对预防复发可能有一定作用。     

Changes of circadian blood pressure patterns and cardiovascular parameters indicate lateralization of sympathetic activation following hemispheric brain infarction

The effects of left- and right-sided hemispheric brain infarction on variability in circadian blood pressure and cardiovascular measures were investigated in 35 patients to test for asymmetry of the sympathetic consequences of stroke. No significant differences regarding age, size of infarction or extent and frequency of damage to the insular cortex could be detected between the two groups. Patients with right-sided infarction showed a significantly reduced circadian blood pressure variability [diastolic: -1% (95% CI -4 to 1) vs -6% (-9 to -2);P < 0.05] and a higher frequency of nocturnal blood pressure increase (47% vs 35%;P < 0.05) as compared with patients with left-sided infarction. Right-sided infarction was also associated with higher serum noradrenaline concentrations [546 pg/ml (95% CI 415–677) vs 405 pg/ml (266–544);P < 0.05], and ECG more frequently showed QT prolongation (53% vs 35%;P < 0.05) and cardiac arrhythmias (67% vs 20%;P < 0.005). However, irrespective of the hemisphere damaged, patients with insular infarction showed the most pronounced changes of these parameters. In addition, two patients with right-sided strokes (13%) involving the insula, but none with a left-sided infarction, developed myocardial infarction. These findings suggest lateralization of sympathetic activation with right-sided dominance for sympathetic effects following hemispheric stroke.Supported by the Friedrich-Schiedel-Stiftung     

Closed cervicocranial trauma, "false aneurysm" of the internal carotid artery and brain infarction

A 17-year-old man developed acute hemiparesis 6 months after a motor cycle accident. In the accident he had a closed trauma on the contralateral side of the head and the neck, with multiple bone fractures. Aortocervical angiography, performed after the infarction, revealed a 2.5 cm long aneurysmatic dilatation in the internal carotid artery, the presumably source of embolic infarction. This and the 24 other cases gathered from the literature support the notion that closed neck trauma may create "false aneurysm" which again may cause neurological deficits.     

Usefulness of different myocardial sampling zones for the postmortem diagnosis of myocardial infarction

Summary The diagnosis of myocardial infarction requires the use of a group of tests that are very efficient, quick and inexpensive. Another important consideration is the choice of myocardial sampling zones, especially in cases of differential diagnosis between a cardiac injury secondary to a trauma or violent asphyxia and others, secondary to myocardial infarction. The aim of this work was to choose, through discriminant analysis, the most useful zones of cardiac tissue for the quantification of free fatty acids and free carnitine and for the performance of the K/Na quotient, as biochemical parameters for the postmortem diagnosis of myocardial infarction. According to the discriminant analysis performed, seven zones of cardiac tissue are necessary to achieve a differential diagnosis among myocardial infarction, other natural deaths, and violent deaths with a 71.9% efficacy. Greater diagnostic efficacy was found (78.1%) for differentiating between natural deaths and violent deaths. Offprint requests to: E. Lachica     

Membrane attack complex of complement and 20 kDa homologous restriction factor (CD59) in myocardial infarction

In order to investigate the mechanism of deposition of the complement membrane attack complex (MAC) in cardiomyocytes in areas of human myocardial infarction, the 20 kDA homologous restriction factor of complement (HRF20; CD59) and complement components (C1q, C3d and MAC) were analysed immunohistochemically using specific antibodies. Myocardial tissues obtained at autopsy from nine patients who died of acute myocardial infarction were fixed in acetone and embedded in paraffin. The ages of the infarcts ranged from about 3.5 h to 12 days. In cases of myocardial infarction of 20 h or less, MAC deposition was shown in the infarcted cardiomyocytes without loss of HRF20. Where the duration was 4 days or more, the cardiomyocytes with MAC deposition in the infarcted areas also showed complete loss of HRF20. Outside the infarcts, HRF20 in the cardiomyocytes was well preserved without MAC deposition. The present study suggests that the initial MAC deposition in dead cardiomyocytes can occur as a result of degradation of plasma-membrane by a mechanism independent of complement-mediated injury to the membrane. Loss of HRF20 from dead cardiomyocytes may not be the initial cause of MAC deposition, but may accelerate the deposition process of MAC in later stages of infarction.