尿激酶溶栓对急性心肌梗死患者单核细胞组织因子表达的影响

目的 :了解冠心病患者外周循环单核细胞组织因子 (TF)表达与冠心病病情的关系 ;观察溶栓治疗对急性心肌梗死患者单核细胞TF表达的影响。方法 :测定了 2 2例稳定型心绞痛 (SA)患者 ,2 1例不稳定型心绞痛(UA)患者 ,1 5例急性心肌梗死 (AMI)患者用尿激酶溶栓前及溶栓后 ,1 8例健康人外周循环单核细胞组织因子阳性率。单核细胞组织因子阳性率测定用免疫荧光染色及流式细胞术。结果 :SAP组 ,UAP组和AMI组单核细胞TF阳性率高于对照组 ,UAP组和AMI组单核细胞TF阳性率高于SAP组 ,单核细胞TF阳性率与冠心病病情显著相关。急性心肌梗死患者溶栓后 2h单核细胞TF阳性率升高。结论 :外周血单核细胞TF的表达与冠心病病情严重程度密切相关 ;急性心肌梗死患者溶栓治疗后单核细胞TF的表达进一步增强 ,这可能是溶栓后凝血酶活化的原因之一。     

Ethical aspects of withdrawing/withholding renal replacement therapies on patients in acute renal failure in an intensive care unit

The majority of patients being treated for acute renal failure in intensive care units have multiple medical problems. Accordingly, the withdrawal of renal replacement therapies should be considered as part of a general decision about whether to initiate or continue with treatment per se. Several guidelines on withdrawing and withholding therapy have been produced and some common themes emerge: concerns to avoid euthanasia, potential for benefit, patient consent (shared decision‐making), team consensus/decision‐making, and the provision of appropriate palliative care and resource implications. Each of these is considered in turn, although the word limit for this paper does not permit detailed exposition.     

冠状动脉造影正常的急性心肌梗死患者的临床特点

目的：探讨冠状动脉造影（CAG）正常的急性心肌梗死（AMI）患者的发生机制及临床特点。方法：分析2000年6月至2001年10月86例AMI患者的CAG结果及冠心病相关危险因素。结果：86例中CAG正常者8例，年龄（39＋11．4）（25－52）岁；多无心绞痛史、高血压史、糖尿病史、血脂异常史及家族史；以情绪波动、精神压抑、大量吸烟、饮酒史者居多。结论：冠状动脉痉挛、血栓自溶或溶栓治疗后血栓消失是其主要发生机制；冠状动脉正常的AMI患者其貌似正常，实属高危人群，应高度重视。     

青年急性冠脉综合征冠脉造特点及随访

目的:探讨青年急性冠状动脉综合征(ACS)冠状动脉(冠状)造影特点及其与远期心脏事件的关系。方法:比较青年ACS与老年ACS患者冠脉病变程度、范围,并进行心脏事件随访。结果:78例青年ACS患者有冠脉病变74例(94.9％),单支病变46例(58.9％);171例老年ACS患者有冠脉病变166例(97.1％),单支病变41例(23.9％)。平均随访9个月,青年ACS患者发生心脏事件者10例(12.8％),其中心绞痛再入院6例(7.7％);老年ACS患者发生心脏事件者47例(27.5％),其中心绞痛再入院30例(17.5％),两组比较差异有显著性(P<0.05)。结论:ACS患者冠状动脉粥样硬化青年时期之前已经发生,ACS预后与冠脉病变程度和年龄呈正相关。     

Epidemiology of acute diarrhea in children living in Sicily

A longitudinal survey (February 1984 - January 1985) on the incidence of acute diarrhea episodes in a sample of 8,164 children (aged 0–12 years) living in southeastern Sicily was carried out by means of weekly telephone interviews with doctors practising in the territory. The incidence rate was 0.479 (0.472–0.485 95% C.I.) per child per year and the frequency of episodes was significantly higher (p < 0.001) in children aged 0–4 years (0.86). Diarrhea was more frequent in industrial areas than in rural ones, and almost half (45.1%) of the total episodes had a mild course. No death from diarrhea occurred and admission to hospital was reported for 8.4% of all cases.Corresponding author.     

完全性左束支传导阻滞伴快速心房纤颤并急性左心衰竭的抢救

目的总结完全性左束支传导阻滞伴快速心房纤颤并急性左心衰竭的治疗经验,以提高抢救成功率.方法对经抢救治疗的完全性左束支传导阻滞伴快速心房纤颤并急性左心衰竭9例(16次)患者进行治疗方面的回顾分析.结果9例(16次)患者14次抢救成功,成功率87.0%,但复发率较高,预后较差,有5例患者在抢救时或出院后1～2年内猝死.结论该组患者经传统"强心、利尿、扩血管",控制心房纤颤、心室率等治疗是远远不够的.应在未发生肺泡性肺水肿及心源性休克之前,尽早尽快地应用血管扩张剂及联合应用小剂量非洋地黄类正性肌力药物,并维持治疗24～72 h.其中以酚妥拉明加多巴胺和(或)多巴酚丁胺效果可能较佳,血管扩张剂硝酸酯类不及α-受体阻滞剂酚妥拉明疗效明显.     

Intracoronary thrombolysis: Organizational prerequisites,technique, and results

Reestablishing myocardial perfusion during evolving myocardial infarction may limit the ultimate extent of infarction if viable myocardial tissue is present when recanalization of the occluded vessel is achieved. This will result in improved left ventricular function and decreased mortality. In addition to their therapeutic benefits, recanalization procedures have contributed greatly to our knowledge of acute myocardial infarction. It has been demonstrated that myocardial infarction most often occurs after thrombotic occlusion of a coronary artery. This has settled a controversy that has preoccupied cardiologists for decades. Selective intracoronary administration of fibrinolytic agents is followed by recanalization in approximately 80% of cases. Therapeutic failures are attributable to occlusion caused by other factors, to inactivation of streptokinase by high antibody concentrations, and to insufficient concentrations of streptokinase at the thrombus as a results of unfavorable flow conditions. This study is dedicated to Prof. Dr. Med. Horst Schmutzler on the occasion of his 60th birthday.     

Thyroid Hormone in the Treatment of Post-transplant Acute Tubular Necrosis (ATN)

Delayed graft function (DGF) in cadaver kidney transplants is a common problem and is often due to acute tubular necrosis (ATN). DGF in transplants may have a deleterious effect on long-term graft survival. Since thyroid hormone has been shown to hasten recovery from ATN in experimental models, we designed a trial to determine if a defined course of triiodothyronine (T3) would improve the short- or long-term outcome of patients with DGF in cadaveric transplants. A prospective, randomized, placebo controlled, double blind trial of T3 was carried out in patients with DGF in cadaveric renal transplants. End-points were percentage requiring dialysis, percentage recovering function, time to recovery and length of hospital stay. Long-term outcomes were percentage grafts functioning at 1 year and mean serum creatinine at 1 year. Forty-four patients were randomized to receive either T3 or placebo. Three patients were dropped from each group when early biopsies disclosed that DGF was due to rejection. The groups were well matched by age, cold ischemia time of the graft, and percentage reactivity to a random panel of antigens. Baseline thyroid function studies, including T3, reverse T3 (rT3), and thyroid stimulating hormone (TSH) levels, were similar between the two groups and typical of 'euthyroid-sick syndrome'. T3 had no effect on percentage requiring dialysis, time to recovery, percentage recovering function, or length of stay. At 1 year follow-up, graft function was similar in both groups and significantly lower than that seen in patients with good initial function. Thyroid hormone, given early in the course of DGF in cadaver kidney recipients, had no effect on the course of DGF. Long-term graft function is impaired in patients who experience post-transplant DGF compared to those who have good initial function.     

Ischemia independent lesion evolution during focal stroke in rats

Lesion evolution during focal cerebral ischemia may depend on flow restrictions or on accumulation of toxic mediators within the infarct and expansion of these factors to the periinfarct region. So far, the precise contribution of flow dependent versus spreading-mediated impairment of viable periinfarct tissue has not been determined. Therefore, we measured lesion expansion, flow restrictions and glutamate distribution on serial brain sections at different time points after experimental focal ischemia.Permanent focal ischemia was induced by occlusion of the right middle cerebral artery in male rats and the flow reduction was subsequently measured at 1, 12 and 24 h using iodo[¹⁴C]antipyrine autoradiography. Additionally, the necrotic volume was determined on serial brain sections and the glutamate content was measured in tissue samples from adjacent microdissections.Twelve hours after focal ischemia no noteworthy viable areas with blood flow restrictions of 20-40 ml 100 g^− 1 min^− 1 existed but at 24 h the necrotic tissue exceeded the hemodynamically compromised region by 40 ± 21 mm³ (24%). Furthermore, at 12 and 24 h the glutamate content was elevated in areas surrounding the infarct.Relevant flow restrictions are detectable only during early stages of infarct maturation, whereas the propagation of secondary factors may be the predominant mechanism for delayed infarct evolution.     

Central Sensitization Theory of Migraine: Clinical Implications

The clinical science of migraine headache continues to evolve. Theories of the pathophysiology of migraine have progressed from the early vascular basis of migraine to more complex current theories that emphasize the centrality of neuronal dysfunction. The most recently articulated theory of migraine is the central sensitization hypothesis, which proposes that altered processing of sensory input in the brainstem, principally the trigeminal nucleus caudalis, could account for many of the temporal and symptomatic features of migraine, as well as its poor response to triptan therapy when such treatment is initiated hours after the onset of pain. Both preclinical and clinical data support the central sensitization theory. A critical clinical implication of this theory is that drugs that are capable of either aborting or arresting the process of central sensitization, most prominently dihydroergotamine, may have a unique role in the treatment of migraine. An additional, and highly practical, implication is based upon the finding that cutaneous allodynia—pain arising from innocuous stimulation of the skin, as in hair brushing or the application of cosmetics—is an easily identifiable marker of central sensitization. Thus, the presence or absence of cutaneous allodynia can be integrated into the routine clinical assessment of migraine and utilized as a determinant of treatment. Future basic and clinical research on central sensitization is likely to be of ongoing importance to the field.