支气管哮喘大鼠心肌细胞p53表达研究

目的:探讨支气管哮喘心肌损害的机制及法医病理学实践中支气管哮喘猝死者的检测指标。方法:建立大鼠支气管哮喘动物模型,运用免疫组化染色方法观察不同实验条件下大鼠心肌p53表达变化。结果:正常对照组及实验对照组心肌p53呈阴性或弱阳性表达,随着时间的延长无明显的改变;各实验组第2周时心肌p53蛋白阳性面积和积分光密度比正常对照组及实验对照组明显升高(P<0·01),随着时间的延长,阳性表达面积和积分光密度呈增加的趋势,第8周达每实验组的阳性表达最高峰。使用肾上腺素组比使用氨茶碱组各时间段阳性信号面积及积分光密度都明显增加;使用肾上腺素组和使用氨茶碱组各时间段阳性信号面积及积分光密度比不使用药物组明显增加;联合使用肾上腺素氨茶碱组的阳信信号面积及积分光密度比不使用药物组低。结论:支气管哮喘本身对心肌有一定的损害;肾上腺素可加重心肌损害,肾上腺素氨茶碱联合使用对心肌损害较轻;p53免疫组化染色可以作为支气管哮喘猝死的辅助诊断指标。     

SD大鼠支气管哮喘心肌HSP70表达研究

目的 探讨支气管哮喘心肌组织损害机制,为支气管哮喘猝死的法医学诊断提供形态学依据.方法 应用HE和免疫组化染色技术,对大鼠支气管哮喘模型不同药物治疗时心肌HSP70表达规律进行研究.结果 实验组心肌HSP70阳性表达明显高于对照组(P＜0.01),随哮喘时间延续,表达增强,至第八周最强.实验组中根据用药的不同,心肌HSP70表达强弱依次为肾上腺素治疗组＞肾上腺素 氨茶碱治疗组＞不使用药物治疗组＞氨茶碱治疗组.结论 支气管哮喘SD大鼠心肌损害机制与哮喘时心肌的缺血、缺氧密切相关.某些支气管哮喘治疗药物的使用可加重心肌细胞的损害,如肾上腺素的使用.HSP70免疫组化染色对支气管哮喘诱发的猝死的法医学诊断有一定的帮助.     

生长激素对大鼠心肌缺血/再灌注后心肌细胞凋亡及凋亡相关基因Caspase-3 Cleaved caspase-3蛋白表达的影响

目的 研究生长激素(Growth hormone, GH)对大鼠心肌缺血/再灌注(ischemia reperfusion,I/R) 后心肌细胞凋亡及相关基因Caspase-3、Cleaved caspase-3蛋白表达的影响.方法 24只大鼠随机分为三组,假手术组(sham-operated group,n=8,仅手术24 h)、心肌缺血/再灌注(I/R)组(n=8)、GH组(n=8),后两组均缺血30 min,再灌注24 h,GH组于建立模型前7 d每天给予人重组生长激素(reconbination human growth hormone,rhGH)针剂皮下注射(1 U/kg体质量),其他二组等量生理盐水注射.以TUNEL法检测心肌细胞凋亡情况, DAB免疫组化法检测心肌细胞Caspase-3、Cleaved caspase-3蛋白表达并进行心肌组织病理学检查.结果 大鼠心肌I/R 24 h后心肌细胞凋亡指数明显上升(对照于假手术组,P<0.05),心肌细胞Caspase-3、Cleaved caspase-3蛋白表达呈阳性染色指数明显升高(P<0.05),心肌病理检查见心肌缺血区呈大小不一的坏死灶,缺血心肌间有炎症细胞浸润,心肌排列不整齐(HE染色),而GH组心肌细胞凋亡率及心肌细胞Caspase-3、Cleaved caspase-3蛋白表达呈阳性染色指数明显好于I/R组(P<0.05),心肌细胞炎症细胞也明显减少,坏死灶也少于I/R组.结论 GH可以减少心肌I/R后心肌细胞凋亡及细胞Caspase-3、Cleaved caspase-3染色阳性指数,说明GH对I/R后的心肌具有保护作用.     

应激性心肌损伤发病机制的实验研究

目的 探讨应激性心肌损伤的发病机制.方法 30只雄性Wistar大鼠按随机数字表法分成正常对照组、制动后冰泳应激组(每日制动6h,第13日开始制动后冰泳5 min)、内毒素组[腹腔注射脂多糖(LPS)10 mg/kg]3组,每组10只.取心肌组织,光镜下观察心肌组织病理变化;电镜下观察心肌超微结构;用酶联免疫吸附试验(ELISA)检测血清心肌肌钙蛋白Ⅰ(cTnI)含量;用原位末端缺刻标记法(TUNEL)检测心肌细胞凋亡并计算凋亡指数;用免疫组化法检测心肌组织天冬氨酸特异性半胱氨酸蛋白酶(caspase-8和caspase-3)的表达;并分析caspase与细胞凋亡指数的相关性.结果 与正常对照组相比,制动冰泳应激组和内毒素应激组在光镜和电镜下均有不同程度的心肌细胞损伤表现,血清cTnI含量(μg/L)均明显增加(0.63±0.12、0.74±0.08比0.53±0.03,P＜0.05和P＜0.01);心肌细胞凋亡指数有不同程度增加[(7.91±1.71 )％、(12.94±2.00)％比0],心肌组织中caspase-8和caspase-3表达增加(caspase-8灰度值:126.65±3.13、114.82±8.67比156.99±9.66; caspase-3灰度值:130.20±2.96、108.58±5.72比160.51±5.25,均P＜0.01),且内毒素应激组各指标均明显高于制动冰泳应激组(P＜0.05或P＜0.01).相关分析显示,制动冰泳应激组中caspase-8、caspase-3与细胞凋亡指数呈显著正相关(r=0.914,P1=0.002;r2=0.929,P2=0.001);内毒素应激组中caspase-8、caspase-3与细胞凋亡指数呈显著正相关(r1=0.956,P1 =0.000;r2=0.916,P2=0.001).结论 应激可能通过增加caspase-8和caspase-3蛋白的表达诱导大鼠心肌细胞凋亡,从而导致心肌损伤.     

促红细胞生成素对大剂量异丙肾上腺素所致心肌损伤及细胞凋亡的作用

目的观察促红细胞生成素（erythropoietin，EPO）对异丙肾上腺素（isoproterenol，ISO）引起大鼠心肌损伤及心肌细胞凋亡相关基因表达的影响。方法将雄性Sprague—Dawley（SD）大鼠分为3组：对照组、ISO组和EPO治疗组，检测血肌酸激酶、肌酸激酶同工酶水平及心肌caspase-3、iNOS的蛋白表达变化。结果EPO治疗组心肌酶水平及caspase-3、iNOS的蛋白表达均较ISO组明显减低。结论促红细胞生成素可以显著减轻异丙肾上腺素引起的心肌损伤，抑制caspase-3、iNOS蛋白表达。     

胰岛素受体在糖尿病大鼠心肌组织中的表达

目的 通过研究胰岛素受体（insulin receptor，IR）在链脲佐菌素诱导的糖尿病大鼠模型中心肌组织中的表达，探讨IR与糖尿病性心肌病发病机制的关系。方法 成年Sprague—Dawley雄性大鼠20只，成实验组和对照组。实验组用链脲佐菌素诱导产生糖尿病模型，4周后对各组大鼠心肌进行IR免疫组织化学染色，观察IR在糖尿病大鼠和正常大鼠左心室心肌细胞中的表达差异。结果 发现糖尿病大鼠中心肌间质纤维增生，心肌间微血管壁增厚，IR表达阳性心肌细胞的数目为（9．42±2．32）个／mm^2及其光密度均为（66．58±6．32）较正常对照组减少（t分别：17．24、8．75，P均〈0．05）。结论 糖尿病心肌病可作为一种特异性的病变发展为心肌自主神经系统的紊乱和冠脉血流储备的障碍。IR表达阳性心肌细胞减少可能会造成心肌糖代谢的损害与心力衰竭的发生。     

复苏早期应用氨茶碱对心肌超微结构的影响

目的研究心搏骤停大鼠心肺复苏早期应用氨茶碱对复苏成功率、血液流变学、心功能及大鼠心肌超微结构的影响。方法选60只SD大鼠,随机分为3组:手术对照组(A组),肾上腺素治疗组(B组)和肾上腺素+氨茶碱治疗组(C组),各20只。分别于窒息前、自主循环恢复时及自主循环恢复30min后进行血流动力学及心功能测定,电镜观察心肌超微结构的变化。结果比较自主循环恢复时间,C组明显少于B组(P<0.05)。C组中有75%自主循环恢复,30min存活率为70%,B组分别为60%(P>0.05)和55%(P>0.05)。C组自主循环恢复时及自主循环恢复30min后的LVSP、dp/dtmax、经LVSP校正后的dp/dt和-dp/dt均明显高于B组(P<0.05)。A组心肌细胞超微结构正常,C组复苏后心肌超微结构略有部分改变,线粒体轻度肿胀及少量空泡形成。B组复苏后心肌细胞部分损害,心肌细胞肌丝排列不整齐,线粒体明显肿胀及空泡化,损害程度比C组严重。结论在复苏早期应用腺苷受体拮抗剂氨茶碱提高了复苏成功率,并且改善了心脏功能,减少了对心肌细胞超微结构的破坏,因此,氨茶碱可作为肾上腺素的增补剂。     

N-乙酰半胱氨酸对急性肺损伤大鼠肺组织水通道蛋白-1表达的影响

目的:观察N-乙酰半胱氨酸(NAC)对急性肺损伤大鼠肺组织水通道蛋白-1(AQP-1)表达的影响,进一步探讨NAC对急性肺损伤肺组织的保护作用.方法:应用脂多糖诱导大鼠急性肺损伤模型,然后应用NAC进行干预.实验设对照组、模型组、NAC组,在肺损伤模型成功造模后24 h处死大鼠,取左叶肺组织.采用免疫组化染色,检测NAC对急性肺损伤大鼠肺组织中AQP-1的表达.利用HPIAS-2000图像分析系统测定AQP-1在以上各组中表达的平均光密度和平均阳性面积率.结果:对照组肺组织表达高水平AQP-1.模型组肺组织呈浅黄色染色,AQP-1表达较低.NAC组肺组织表达高水平AQP-1.对照组与模型组之间AQP-1的平均光密度及阳性面积率差异有显著性(P＜0.01),对照组与NAC组之间AQP-1的平均光密度及阳性面积率差异无显著性(P＞0.05).结论:NAC能使急性肺损伤组织中AQP-1呈高表达,对急性肺损伤组织有重要的保护作用.     

钙离子拮抗剂对大鼠心肌梗死后心肌细胞凋亡的影响

目的探索钙离子拮抗剂对缺血后心肌细胞凋亡的影响.方法结扎大鼠冠状动脉(冠脉)造成心肌梗死;实验组动物冠脉结扎前和术后3 h分别经口腔内滴注和腹腔注射钙离子拮抗剂Adalat 1 mg/kg和0.4 mg/kg,缺血对照组给安慰剂;正常对照组行假手术不结扎冠脉,给安慰剂.术后6 h测定左室功能,并取心脏标本作原位缺口末端标记法(TUNEL)原位细胞凋亡和Fas、Bcl-2蛋白免疫组织化学(组化)染色,高倍镜下计算细胞凋亡指数.结果实验组和缺血对照组的左室收缩压、左室舒张末压和压力改变速度(dp/dt)无显著差异,3个指标分别为76.7±7.5/8.0±6.1 mm Hg比74.9±11.1/11.6±8.3 mm Hg,P>0.05;(777.3±128.6)mm Hg/s比(761.8±136.4)mm Hg/s,P>0.05;但均低于正常对照组[94.9±7.5/2.8±3.2 mm Hg,P<0.001;(1 131.5±112.8)mm Hg/s,P<0.001];实验组和缺血对照组心肌缺血区TUNEL染色阳性,实验组心肌细胞凋亡指数显著低于缺血对照组(0.201±0.053比0.261±0.045,P<0.05),在缺血周边的心肌区Fas和Bcl-2蛋白免疫组化染色阳性,而正常对照组3种染色均阴性.结论缺血可诱导心肌细胞凋亡及Fas和Bcl-2基因的表达;钙离子拮抗剂具有抑制心肌细胞凋亡的作用.     

罗格列酮对糖尿病大鼠肺炎性病变的影响

目的 现察过氧化物酶体增殖体活化受体-r(PPAR-r)激动剂罗格列酮对链脲菌素诱导的糖尿病大鼠肺部炎性病变的影响.方法 30只10周龄SD大鼠随机分为正常对照组(C组,雌雄各5只)、糖尿病模型组(D组,雌雄各5只)、糖尿病罗格列酮处理组(DR组,雌雄各5只),采用链脲菌素诱导建立10周糖尿病大鼠模型.其中糖尿病罗格列酮处理组用马来酸罗格列酮1mg.kg-1.d-1灌胃治疗,对照组及糖尿病模型组用同体积0.9%氯化钠注射液代替.模型建立10周后,全部大鼠于氯胺酮35mg/kg和苯巴比妥50mg/kg腹腔内注射麻醉处死,并取肺组织.光学显微镜下现察肺组织炎症程度、检测杯状细胞的分布,免疫组织化学方法检测肺组织TNF-α表达的阳性面积百分比与平均积分光密度值(I0D).结果 ①肺部炎症观察:大多数正常对照组大鼠肺组织内未见炎症细胞.糖尿病模型组可见片状炎症细胞聚集,局部肺泡结构消失.罗格列酮处理组糖尿病大鼠肺组织炎症明显比模型组轻;②杯状细胞观察:在AB/PAS染色下,正常对照组大鼠各级气管上皮内均未见杯状细胞出现,糖尿病模型组在一级或二级支气管内出现较多的杯状细胞.罗格列酮处理组糖尿病大鼠在一级或二级支气管内也出现杯状细胞,但数量明显少于糖尿病模型组;③TNF-α的表达TNF-α主要表达于气管、血管周围的成纤维细胞内,糖尿病模型组、罗格列酮处理组还可见巨噬细胞胞浆内阳性表达.正常对照组肺组织阳性表达较其余两组弱,罗格列酮处理组阳性面积百分比及平均积分光密度值介于正常对照组和糖尿病模型组之间[其中阳性面积百分比(%)C:D:DR组为9.07±4.17vs23.75±5.66vs12.21±1.50(F=54.5,P<0.05;平均光密度C:D:DR组为0.60±0.03vs0.73±0.08vs0.66±0.04(F=22.73.P<0.05)],差异有统计学意义.结论 高血糖能引起肺部炎症及组织结构的破坏.罗格列酮能够保护糖尿病大鼠肺组织,该作用独立于降血糖之外. 内阳性表达.正常对照组肺组织阳性表达较其余两组弱,罗格列酮处理组阳性面积百分比及平均积分光密度值介于正常对照组和糖尿病模型组之间[其中阳性面积百分比(%)C:D:DR组为9.07±4.17vs23.75±5.66vs12.21±1.50(F=54.5,P<0.05;平均光密度C:D:DR组为0.60±0.03vs0.73±0.08vs0.66±0.04( =22.73.P<0.05)],差异有统计学意义.结论 高血糖能引起肺部炎症及组织结构的破坏.罗格列酮能够保护糖尿病大鼠肺组织,该作用独立于降血糖之外. 内阳性表达.正常对照组肺组织阳性表达较其余两组弱,罗格列酮处理组阳性面积百分比及平均积分光密度值介于正常对照组和糖尿病模型组之间[其中阳性面积百分比(%)C:D:DR组为9.07±4.17vs23.75±5.66vs12.21±1.50(F=54.5,P<0.05;平均光密度C:D:DR组为0.60±0.03vs0.73±0.08vs0.66±0.04( =22.73.P<0.05)],差异有统计学意义.结论 高血糖能引起肺部炎症及组织结构的破坏.罗格列酮能够保护糖尿病大鼠肺组织,该作用独立于降血糖之外. 内阳性表达.正常对照组肺组织阳性表达较其余两组弱,罗格列酮处理组阳性面积百分比及平均积分光密度值介于正常对照组和糖尿病模型组之间[其中阳性面积百分比(%)C:D:DR组为9.07±4.17vs23.75±5.     

Budesonide/formoterol decreases expression of vascular endothelial growth factor (VEGF) and VEGF receptor 1 within airway remodelling in asthma

INTRODUCTION: Angiogenesis and microvascular remodelling may play a vital role in the chronic inflammatory process within asthma. One of the most important factors involved in angiogenesis is vascular endothelial growth factor (VEGF). In this study we hypothesised that an increased expression of VEGF may be involved in airway remodelling in asthma patients. To this end, we compared the histology and expression levels of VEGF and one of its receptors (VEGFR1) in bronchial tissues of patients with asthma compared with control patients. We also investigated the effect of treatment with budesonide/formoterol (Symbicort(R); AstraZeneca, Lund, Sweden) in the relationship between VEGF and airway remodelling. METHODS: Bronchial tissues were obtained from patients attending the West China Hospital from April to November 2006. Thirteen patients were diagnosed with moderate asthma and 10 others were treated as control. Histological and immunohistochemical comparisons between asthmatic and control patients were made at baseline, and (for asthmatic subjects) following 6 months of treatment with budesonide/formoterol. RESULTS: Compared with control patients, asthmatic patients had significantly decreased respiratory parameters, including forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV(1)) (% predictive). Furthermore, patients with asthma had submucosal gland hyperplasia, increased smooth muscle mass, increased subepithelial fibrosis and neovascularisation. Asthmatic patients also exhibited increased expression of VEGF and VEGFR1 within epithelial cells. The increased expression of VEGF and its receptor correlated well with airway remodelling, airflow obstruction and airway hyper-responsiveness. After treatment with budesonide/formoterol for 6 months, the expression of VEGF and VEGFR1 was decreased, with correlatory decreased airway remodelling in patients with asthma. CONCLUSION: The increased expression of VEGF and VEGFR(1) in asthmatic patients is accompanied by an increased number and size of blood vessels in asthmatic airways, as well as airway remodelling. Budesonide/formoterol therapy for 6 months can decrease the expression of VEGF and VEGFR(1) alongside airway remodelling in asthma. The inhibition of VEGF and its receptor may be a good therapeutic strategy for asthma.     

放松疗法改善哮喘儿童的心身症状

背景放松疗法可减轻成人哮喘患者的不良情绪反应,降低哮喘发作次数,但缺乏对于哮喘儿童作用的评估数据.目的探讨放松疗法对学龄哮喘患儿的焦虑、抑郁和咳嗽、气喘等症状的影响.设计以诊断为依据,随机对照研究.单位中南大学湘雅二医院儿科和中南大学精神卫生研究所.对象2001-01/2004-01中山市博爱医院儿科就诊的1 438名哮喘患儿中筛选出符合标准578例,再随机抽取64例作为研究对象,随机分配到实验组31例,对照组33例.干预在两组药物治疗相同的基础上,实验组每晚睡前给予放松治疗,持续4周.治疗前后评估两组患儿的焦虑、抑郁症状,治疗期间评估哮喘症状、记录计算哮喘控制参数.主要观察指标焦虑和抑郁评分,日间和夜间哮喘症状记分、无哮喘症状的天数、哮喘发作与加重次数等指标.结果治疗前两组焦虑和抑郁症状评分无统计学差异(P＞0.05),两组患儿的焦虑和抑郁评分在治疗结束时均明显降低(P均＜0.01),但实验组较对照组下降更明显,差异具有统计学显著性(P均＜0.01).日间哮喘症状记分,夜间哮喘症状记分,无哮喘症状的天数比率,≥1次哮喘发作的比率,两组比较差异均有显著性意义(P＜0.05～0.01).结论放松疗法可以减轻学龄哮喘患儿的不良情绪反应,并改善多项哮喘控制参数,是一种较好的辅助治疗手段.     

Rhinovirus-induced basic fibroblast growth factor release mediates airway remodeling features

ABSTRACT: BACKGROUND: Human rhinoviruses, major precipitants of asthma exacerbations, induce lower airway inflammation and mediate angiogenesis. The purpose of this study was to assess the possibility that rhinoviruses may also contribute to the fibrotic component of airway remodeling. METHODS: Levels of basic fibroblast growth factor (bFGF) mRNA and protein were measured following rhinovirus infection of bronchial epithelial cells. The profibrotic effect of epithelial products was assessed by DNA synthesis and matrix metalloproteinase activity assays. Moreover, epithelial cells were exposed to supernatants from cultured peripheral blood mononuclear cells, obtained from healthy donors or atopic asthmatic subjects and subsequently infected by rhinovirus and bFGF release was estimated. bFGF was also measured in respiratory secretions from atopic asthmatic patients before and during rhinovirus-induced asthma exacerbations. RESULTS: Rhinovirus epithelial infection stimulated mRNA expression and release of bFGF, the latter being positively correlated with cell death under conditions promoting rhinovirus-induced cytotoxicity. Supernatants from infected cultures induced lung fibroblast proliferation, which was inhibited by anti-bFGF antibody, and demonstrated increased matrix metalloproteinase activity. Rhinovirus-mediated bFGF release was significantly higher in an in vitro simulation of atopic asthmatic environment and, importantly, during rhinovirus-associated asthma exacerbations. CONCLUSIONS: Rhinovirus infection induces bFGF release by airway epithelium, and stimulates stroma cell proliferation contributing to airway remodeling in asthma. Repeated rhinovirus infections may promote asthma persistence, particularly in the context of atopy; prevention of such infections may influence the natural history of asthma.     

Use of metaiodobenzylguanidine for assessing status of ends of myocardial sympathetic nerves in myocardium of patients with bronchial asthma

AIM: To evaluate sympathetic nervous system activity of the heart in patients with bronchial asthma (BA) given beta-adrenomimetics (BAM). MATERIAL AND METHODS: 27 patients with moderate BA (13 patients in an acute phase and 14 patients in remission) treated with BAM and 13 healthy people were examined by using 123I-metaiodobenzylguanidine (MIBG) myocardial planar scintigraphy and estimating the washout rate, early (15-min) and late (240-min) uptake; single-photon emission computed tomography; assessment of MIBG distribution in the left ventricular myocardium, catecholamine excretion with urine. RESULTS: It was found that the MIBG washout rate was significantly higher in asthmatic patients especially in the acute period. The cardiac MIBG uptake was significantly lower in the group of patients with impaired cardiac sympathetic activity. More inhomogeneous myocardial MIBG uptake also occurred in the asthmatic group. Norepinephrine and epinephrine excretion was significantly higher in patients with bronchial asthma and cathecholamine and MIBG excretions correlated. CONCLUSION: Cardiac functional sympathetic activity impairment in asthmatic patients was shown by increased MIBG washout rate and reduced myocardial MIBG uptake, more inhomogeneous substance distribution in the left ventricular myocardium and higher catecholamine excretion levels reflecting sympathetic nervous activity intensification.     

哮喘患者外周血单个核细胞表面共刺激分子检测及意义

目的探讨共刺激分子在哮喘发病免疫学机制中的作用。方法选取28例哮喘患者和15名对照者,采用三色标记的流式细胞术检测哮喘患者外周血单个核细胞表面共刺激分子的表达水平。结果与对照组相比,哮喘患者T细胞各亚群所占比例及B细胞、单核细胞占外周血单个核细胞的比例差异未见显著性,但CD4/CD8明显高于对照组(P<0.05)。CD4和CD8阳性T细胞表达的CD28及CTLA-4分子在两组间差异无显著性。哮喘组单核细胞(CD14阳性)CD80表达水平低于对照组(P<0.05)。而B细胞(CD19阳性)表面表达的CD86低于对照组(P<0.05)。结论哮喘患者体内存在的T淋巴细胞功能紊乱可能与T淋巴细胞活化过程中共刺激信号的异常有关。     

A concept analysis of self-management of asthma in children

Asthma is a chronic disease commonly seen in children. It is absolutely essential for a child who suffers from the disease, and his/her family members, to learn how to perform self-management to minimize the rate of asthmatic deterioration, attack episodes, and the risk of mortality. Literature review indicates that there is no consistency of definition and terminology as far as the concept of "self-management" is concerned. This study, therefore, adopts the concept analysis proposed by Walker & Avant, by searching seven health-related databases via systematic review methodology. From the results of the concept analysis it can be concluded that there are three definitive features of self-management among asthmatic children: 1) the learning and performance process factors determined reciprocally by cognition, physiology, behavior, and environment, 2) the prevention and management of sudden asthma attacks, 3) the normalization of the patient's life with proper control of the asthmatic condition and a reduction of asthma attacks. On the basis of this concept analysis, the authors expect to develop a theoretical framework and related research to build up an asthma knowledge base for future care of children with asthma.     

Sudden asthma death: etiology and prevention

The duration of the last lethal asthma attack in children was short and their asthma deaths were unexpected and abrupt in many cases by the annual reports of the committee on asthma death in children of the Japanese Society of Pediatric Allergy and Clinical Immunology. In adult asthma death, sudden death type died in three hours 29.3%, unstable sudden aggravation type 16.2% and status asthmatics was only 21.2% by the national wide study in Japan. The severity of asthma prior to asthma death; in children mild was 26%, moderate 30%, severe 43% and in adult, mild was 9.3%, moderate 41.4% and severe 49.2%. Asthma deaths during sports were also discussed. In adolescent and young adult, asthma was one of the main causes of sudden death. Prevention of sudden asthma death was discussed.     

心肌肌动蛋白在青壮年猝死综合征患者死因诊断中的应用

目的 :探讨心肌细胞内肌动蛋白在青壮年猝死综合征死因诊断方面的价值。方法 :应用免疫组化LSAB法对 16例青壮年猝死综合征病例进行心肌细胞内肌动蛋白的研究 ,并以 15例冠心病猝死病例和 15例非心性死亡病例分别作阴性和阳性对照。结果 :16例青壮年猝死综合征病例中 ,有 13例心肌细胞内肌动蛋白明显缺失 ,2例轻度缺失 ,1例无缺失。 15例冠心病猝死阴性对照组心肌细胞内肌动蛋白均明显缺失。 15例非心性死亡阳性对照组心肌细胞内肌动蛋白均无缺失。结论 :心肌细胞内肌动蛋白免疫组化检测可作为青壮年猝死综合征死因诊断的指标。