急性冠脉综合征中妊娠相关蛋白-A与斑块不稳定性

目的探讨妊娠相关蛋白-A(PAPP-A)在急性冠脉综合征(ACS)中的变化及其与斑块不稳定性的关系。方法26例冠脉正常者作为对照组,稳定性心绞痛(SA)组22例,ACS组40例,包括不稳定性心绞痛(UA)20例、急性心肌梗死(AMI)20例。定量检测外周血PAPP-A、C-反应蛋白(CRP)、肌酸激酶MB同工酶(CK-MB)。对所有冠脉造影显示狭窄≥30%的病变进行影像学分析。结果ACS中PAPP-A含量(13·19±4·04)mIU/L明显高于SA(5·47±3·00)mIU/L(P<0·01)及对照组(5·09±2·19)mIU/L(P<0·01);并且与CRP(r=0·62P<0·01)、复杂性狭窄的数量(r=0·45P<0·05)有显著的正相关。结论PAPP-A在ACS患者外周血中明显升高,可能与斑块的不稳定性有关,对ACS的危险度分层可能具有一定的价值。     

山莨菪碱和无创面罩正压通气治疗急性呼吸窘迫综合征的临床观察

目的比较山莨菪碱联合无创正压面罩通气（654-2＋NIPPV）和传统机械通气（CMV）治疗急性呼吸窘迫综合征（ARDS）的临床效果，评估山莨菪碱联合无创正压通气在ARDS治疗中的作用。方法将各种原因所致ARDS患者42例随机分为654-2＋NIPPV组（21例）和CMV组（21例），在给予病因治疗同时分别实施654-2＋NIPPV和CMV。观察分析两组患者在治疗过程中动脉血气变化、并发症的发生率及治疗效果。结果654-2＋NIPPV组有8例（38．1％）治疗失败转为气管插管实行CMV，其中6例（28．6％）死亡。CMV组死亡7例（33．3％），两组病死率无显著差异（P〉0.05）。两组治疗有效的患者在分别接受654-2＋NIPPV和CMV治疗后1h和6h动脉血气有相似的显著改善。654-2＋NIPPV组患者机械通气时间和住院时间短于CMV组（P〈0.05）。654-2＋NIPPV组的并发症发生率低于CMV组（P〈0.05）。结论在经过选择的ARDS患者中，应用654-2＋NIPPV治疗的临床效果与CMV相似。实施654-2＋NIPPV可缩短机械通气和住院时间，减少并发症。654-2＋NIPPV可作为经过选择的ARDS患者首选的通气支持治疗手段。     

SARS胸部影像表现与评价(附75例分析)

目的：回顾分析75例严重急性呼吸综合症(SARS)病例，探讨该病影像学表现及其与临床治疗有关的问题。方法：全部75例患者均行胸片检查，一般隔日行影像追踪复查。结果：胸部X线表现为肺实质渗出病灶为主，肺内网状改变及肺门片块影较少。影像表现与临床病程有一定关系。结论：胸部影像表现以肺实质渗出病灶较常见。胸片检查是进行本病诊断和评估病程及疗效的重要方法。     

心率变异性与心肌梗塞范围关系的研究

报道７２例急性心肌梗塞患者的心率变异性（ＨＲＶ）值与心肌梗塞范围的关系，并与１２０例正常人的ＨＲＶ值进行对比，结果发现，心肌梗塞急性期ＨＲＶ值明显降低，与正常组对比有显著统计学意义，但ＨＲＶ值降低与心肌梗塞部位、范围无关，可能主要为心肌梗塞引起的应激反应所造成的体液及神经调节改变所致。     

烧伤患者急性期反应物的变化及其临床意义

用环状免疫单扩散法观察了２７例烧伤患者伤后４６天以内血清急性期反应物前白蛋白、铜蓝蛋白、α＿１酸性糖蛋白、α＿１抗胰蛋白酶、转铁蛋白、Ｃ反应蛋白、纤维连接蛋白、补体成分Ｃ＿４、Ｃ＿（３ｃ）、触珠蛋白的变化趋势、试图探讨它们与病情发生、发展规律之间的关系。结果：Ｃ反应蛋白、α＿１酸性糖蛋白和α＿１抗胰蛋白酶在所有患者都升高，提示烧伤后组织损伤逐渐加重及伴发炎症、感染的存在；白蛋白、铜蓝蛋白、转铁蛋白和纤维连接蛋白在伤后均明显降低，提示伤后的分解代谢增加、贫血及网状内皮系统功能降低与之有关；触珠蛋白伤后明显降低且死亡组更明显，提示其作为具有过氧化物酶活性的保护作用降低是促进死亡的原因之一；伤后补体Ｃ＿４、Ｃ＿（３ｃ）在存活组升高而死亡组明显降低，因而可能被用于对患者病情和预后的判断。总之，观测急性期反应蛋白的变化规律，有助于及时发现患者病情的变化，以便临床及时采取相应措施。     

急非淋白血病完全缓解后巩固治疗的对照研究

目的探讨急非淋白血病完全缓解后巩固治疗与缓解期的关系。方法对３０例坚持与未坚持完全缓解后巩固化疗的急非淋患者（每组１５例）进行对照研究。比较两组患者的完全缓解期。结果两组患者入院时情况、治疗及达完全缓解时间经统计学处理无明显差异（Ｐ＞０．０５）；而坚持巩固化疗组平均持续完全缓解期（１９．８ｍｏ）明显长于对照组（８．４ｍｏ），统计学具有显著差异（Ｐ＜０．０１）。结论急非淋白血病达完全缓解后，坚持骨髓抑制性治疗对延长完全缓解期以达长期生存目的具有重要意义。     

5名电离辐射事故患者外周血T细胞T细胞抗原受体、T细胞分化抗原决定簇－3效应的研究

文中报道了５名事故性急性骨髓型放射病患者照后２．５和３．５年外周血Ｔ淋巴细胞Ｔ细胞受体（ＴＣＲ）基因，ＴＣＲ、Ｔ细胞分化抗原决定簇－３（ＣＤ_３）表达与ＴＣＲ／ＣＤ_３复合物功能的辐射效应．发现５名患者于照后２．５年，２名（５．２Ｇｙ和２．４Ｇｙ，５５岁）于照后３．５年外周血Ｔ细胞应答抗ＣＤ３单抗刺激而增殖的能力尚未完全恢复；经同时用ＩＬ－２和抗ＣＤ_３单抗刺激，增殖能力比单用抗ＣＤ_３单抗刺激有所增强；后２名的外周血ＴＣＲ、ＣＤ_３阳性细胞百分率一直低于正常对照和其他患者；并见一患者出现ＤＮＡ重排杂交带型．本文并从ＴＣＲ／ＣＤ_３在介导Ｔ细胞抗原刺激反应中的作用，电离辐射对ＴＣＲ／ＣＤ_３复合物的影响，后果和意义等方面进行了讨论．     

Acute heart failure and acute renal failure in Kawasaki disease

Acute renal failure and acute heart failure are rare in Kawasaki disease. We experienced two patients with Kawasaki disease who presented acute renal failure and acute heart failure. These two patients gave us an important insight into the understanding of water balance and fluid therapy in Kawasaki disease. One patient showed acute prerenal failure due to fluid exudation from the intravascular to the extravascular space, and subsequent acute heart failure. The other patient showed acute heart failure caused by fluid infusion for the treatment of dehydration. It is suggested that acute renal failure could be caused by a fluid shift from the intravascular to the extravascular space in Kawasaki disease. It is also demonstrated that the reserve of cardiac function could be decreased in patients with Kawasaki disease due to myocarditis even with normal echocardiography and chest X-rays.     

潘南金在急性心肌梗死治疗中的作用

目的探讨潘南金在急性心肌梗死(AMI)治疗中改善恶性心律失常及心功能的作用。方法将患者随机分为潘南金组及对照组各40例,在AMI常规治疗基础上,潘南金组予潘南金注射液40mL加入5%葡萄糖注射液500mL中静脉点滴,1次/d;同时加服片剂2片/次,3次/d。对照组则予极化液静点,1次/d。2组均在CCU监护1周后转入普通病房,共治疗3～4周。结果恶性心律失常发生率潘南金组为25%,对照组为65%,2组比较P<0.01。出院时心功能NYHA分级改善2级以上者,潘南金组为58%,对照组为45%,2组比较P<0.05。结论对AMI患者尽早应用潘南金治疗,可明显降低恶性心律失常发生率和改善心功能,且不良反应少,可列为常规用药。     

Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: Evidence for loss of compartmentalization of contrast media

The purpose of this study was to characterize the contrast caused by a susceptibility MRI contrast agents, on spin echo T₂-weighted imaging of reperfused myocardial infarction. Our interest in this model focused on the expected requirement that such agents be compartmentalized in the tissue to cause signal loss on spin echo images, a condition which may not be present in reperfused infarcted myocardium. Accordingly, nine rats were subjected to 2 h of left coronary artery occlusion followed by 3 ± 0.5 h of reperfusion prior to administration of contrast media. Three sets of MR images were acquired: (a) baseline axial images at the midventricle, both T₁-weighted (TR/TE = 300/20) and T₂-weighted (TR/TE = 1500/60); (b) T₁-weighted images after administering a T₁-enhancing agent, Gd-DTPA-BMA (0.2 mmol/kg), to document that contrast media is delivered to the reperfused infarction; and (c) T₂-weighted images after administering the susceptibility agent, Dy-DTPA-BMA (1.0 mmol/kg). Gadolinium-enhanced T₁ images depicted reperfused infarction as regions with greatly enhanced signal intensity compared with unin-farcted myocardium, indicating that contrast agent was delivered to the infarcted zone. Dysprosium-enhanced T₁ images depicted the injury as a region of persistent signal intensity relative to depletion of signal in normal myocardium, consistent with failure of the contrast agent to cause signal loss. Similar infarction sizes were observed for unenhanced T₂-weighted images (33 ± 5%), gadolinium-enhanced T₁ weighted images (36 ± 5%) and postmortem staining (30 ± 6%); strong correlations (r > 0.9) were noted in comparisons of these data. Dysprosium-enhanced images exhibited a smaller region of differential signal presumed to be infarction (20 ± 5%, P < 0.05) and weak correlations (r < 0.75) with the other measurements. We conclude that the smaller infarction depicted on dysprosium-enhanced images is a subregion of the true infarction in which myocardial necrosis is sufficiently advanced that the agent is homogeneously distributed throughout all tissue compartments, preventing T₂*-dependent phase loss on spin echo images.