核因子kB在大鼠胃缺血再灌注损伤中的表达及意义

目的研究核因子kB（NF-kB）在大鼠胃缺血再灌注损伤中的表达及意义。方法采用大鼠胃缺血再灌注（gustric ischemia/reperfusion, CI／R）模型（夹闭腹腔动脉30min后再灌注），分别于再灌注0．5、1、3、24h取胃，计算胃黏膜损伤指数。应用免疫组化、Western blot方法检测胃黏膜NF-kB p65。结果大鼠GUR后引起胃黏膜损伤，再灌注1h时损伤最明显，随后降低，24h接近正常。GI／R后胃黏膜NF—kB阳性细胞数和蛋白表达量增多，与胃黏膜损伤变化规律一致。结论NF-kB在大鼠CI／R损伤过程中发挥着重要作用。     

降钙素基因相关肽对犬冠脉流量及冠状动脉的作用

本研究通过整体及离体灌流实验观察到重庆冠脉狭窄时，犬冠脉流量（ＣＢＦ），平均动脉压（ＭＡＰ）明显减小，而心率（ＨＲ）则增加。狭窄３０ｍｉｎ后由冠状动脉注射降钙素基因相关肽（ＣＧＲＰ）０．３μｇ／ｋｇ后，ＣＢＦ、ＭＡＰ和ＨＲ可恢复正常水平。同时，缺血犬的离体冠状动脉对ＣＧＲＰ的反应也出现改变。大冠脉舒张反应明显降低，而小冠脉的舒张反应与正常相比，无明显改变，这可能与缺血后大冠脉的内皮细胞容易损伤有关。同时也提示:急性心肌缺血时，冠脉流量的减少，主要由于小冠状动脉收缩所致。     

‘Ischemic tolerance’ phenomenon detected in various brain regions

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the ‘ischemic tolerance’ phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of ‘ischemic tolerance’.     

老年冠心病患者的动态心电图观察

对97例老年冠心病患者进行动态心电图观察,共检出97例患者缺血性ST段发作347阵,心率减慢时发生缺血48例(49.5％),全程无症状者75例(77.4%),缺血时有无胸痛与ST段下降程度无必然联系。     

Intracerebral distribution of albumin after transient cerebral ischemia: light and electron microscopic immunocytochemical investigation

Summary The blood-brain barrier breaks down following cerebral ischemia, but the exact sequence of events for extravasation of serum proteins and their parenchymal distribution remain uncertain. We studied the distribution of serum albumin in the hippocampus of the gerbil brain using light and electron microscopic immunocytochemical techniques. With light microscopy, there was no reaction for albumin for the first 12 h after unilateral common carotid artery occlusion for 10 min and reperfusion. At 12 h, the reaction was weak and limited to the neuropil in the subiculum-CA1 region (between the subiculum and the medial CA1 region). After 24 h, the reaction became intense in the neuropil and neuronal perikarya in the subiculum-CA1 and medial CA1 regions. The electron microscopic immunocytochemical study of the subiculum-CA1 and medial CA1 regions revealed electron-dense immunoprecipitates in the extracellular space and the peripheral part of the apical dendrites as early as 30 min after reperfusion and in the astrocytic cytoplasm after reperfusion for 1 h. However, immunoprecipitates were not found in the neuronal perikarya until after reperfusion for 24 h. The present study demonstrated prompt appearance of albumin in the extracellular space of the brain parenchyma after re-establishment of cerebral circulation and prompt accumulation in the peripheral part of the dendrites with spreading to neuronal perikarya, likely in the process of degeneration and death.Supported by the grant NS-06663 from the National Institutes of Health, U. S. Public Health Service     

Inhibition of glutamate release in rat hippocampus by kynurenic acid does not protect CA1 cells from forebrain ischemia

We assessed the effect of a broad spectrum glutamatergic receptor antagonist, kynurenic acid (500 mg/kg) on ischemia-induced hippocampal glutamate release and neuronal damage. Kynurenic acid significantly decreased glutamate release during ischemia but had no effect on the hippocampal lesion. Some protection was observed in the cortex and in the striatum. These data suggested that the extracellular accumulation of glutamate during forebrain ischemia does not play a major role in the hippocampus.     

~(99m)Tc-MIBI心肌灌注显像结合门电路心血池显像对高血压患者心肌缺血诊断的评价

本文对40例住院高血压患者作了静息相及负荷相99mTc－MIBI心肌单光子发射计算机断层（SPECT）显像并采用门电路心血池显像（MGBP）评价室壁运动。结果显示：本组病例心肌灌注显像放射性稀疏缺损（MPD）发生率高达87．5％（35／40），其中可逆性（RPD）57．1％；有MPD者在MPD节段室壁运动异常发生率91．4％（32／35），但RPD组与非RPD组间无显著差异。文中对高血压患者心肌缺血及其导致MPD的机制进行了探讨，认为99mTc－MIBI心肌SPECT显像出现MPD是反映高血压患者心肌缺血的敏感方法，MGBP多指标评价室壁运动可揭示绝大多数MPD节段的室壁运动异常。     

血管内支架成形术治疗颅内动脉狭窄

目的:探讨颅内动脉狭窄血管内球囊支架成形术的可行性、安全性及其疗效。方法:17例患者术前3天给予阿司匹林300mg/天和噻氯吡啶250mg/天,6F(Envoy)导引导管放置到颈内动脉远段或椎动脉近颅底段,造影获得工作位,评价血管狭窄程度:狭窄率=(1-狭窄处管径/狭窄远端管径)×100%,微导丝在路途导引下通过颅内动脉狭窄段,向远端直至P2或M2段,确保足够的支撑力。选择支架大小的依据为狭窄远端正常血管的直径,导丝引导下支架通过狭窄部位,造影确定支架位置正确,充盈球囊至5～6大气压,支架释放后造影确认展开良好,回撤球囊,无并发症,操作完毕。随访3～10月。结果:17例患者颅内动脉狭窄处植入支架,技术成功100%,造影显示狭窄由术前(78.3±12.9)%降至术后(6.8±7.3)%,狭窄的动脉管径恢复,短期随访(3～10个月)显示很好临床效果。术中出现一例蛛网膜下腔少量出血(SAH),对症治疗痊愈。6例随访造影未见血管再狭窄。结论:颅内动脉狭窄支架植入增加血管内径,改善血流量,减轻临床症状,是一种安全、可行有效的治疗方法。     

Mental stress-induced myocardial ischemia in coronary artery disease patients with left ventricular dysfunction

Background  Reduced left ventricular ejection fraction (LVEF) is a risk factor for poor outcomes in patients with coronary artery disease (CAD). Mental stress-induced myocardial ischemia (MSIMI) also identifies a subset of CAD patients at increased risk for future cardiovascular events. Susceptibility to MSIMI in patients with CAD and reduced LVEF is unknown. Methods and Results  We enrolled 182 patients (67 women) with a mean age of 64 years and a documented history of CAD in this study. Baseline resting ejection fraction was determined by use of technetium 99m sestamibi gated single photon emission computed tomography. Abnormal LVEF was defined as less than 45% for men and less than 50% for women (based on published norms for our software [Cedars-Sinai Medical Center]). All participants underwent mental stress testing with a public speaking task. Rest/stress myocardial perfusion single photon emission computed tomography was performed via conventional methodology. Images were visually compared for number and severity of perfusion defects by use of a scoring method from 0 to 4. A summed difference score was calculated as the difference between summed stress and rest scores. A score of greater than 3 was considered abnormal. MSIMI developed in 19% of patients with normal LVEF and 31% of those with reduced LVEF. There is no statistically significant difference between the two groups (P=.11). Conclusions  CAD patients with left ventricular dysfunction are equally susceptible to MSIMI as those with normal LVEF. This study was supported by grants HL 070265 and HL 072059 from the National Heart. Lung, and Blood Institute. This material is also the result of work supported by resources and with the use of facilities at the Department of Veterans. Affairs Medical Center, Gainesville, Fla.     

大鼠脑干缺血模型制备及早期超微结构观察

目的:制备脑干缺血动物模型并观察大鼠脑干缺血后早期组织学病理的超微结构。方法:应用两点电凝基底动脉的方法制作鼠脑干缺血动物模型。结果:病理学观察发现脑干缺血2小时即可出现超早期病理变化,并随时间的延长缺血性损害逐渐加重。结论:两点电凝基底动脉后可以造成稳定的脑干缺血,对急性脑干缺血的病理学研究有一定的价值。