Exo-focal postischemic neuronal damage in the rat brain: alteration of [H]forskolin binding using in vitro autoradiography

We studied the alteration of intracellular signal transduction using quantitative autoradiography of the second messenger system in order to clarify the mechanisms of delayed neuronal damage in the remote areas of rat brain after transient focal ischemia. Chronological changes of [³H]forskolin binding sites were measured to demonstrate the striatal-nigral pathway after 90 min of right middle cerebral artery (MCA) occlusion and after such occlusion followed by 3 h, 6 h, 1 day, 3 days, 1 week, 2 weeks and 4 weeks of recirculation. [³H]Forskolin binding sites were found to be markedly decreased in the lateral segment of the caudate putamen supplied by the occluded MCA after 90 min of ischemia with no recirculation. On the contrary, there was no alteration on day 1, but 3 days after ischemic insult, marked reduction of [³H]forskolin binding sites was observed in the ipsilateral substantia nigra which lay outside the ischemic areas. This postischemic delayed phenomenon observed in the substantia nigra developed concurrently with ⁴⁵Ca accumulation, which was detected there in our previous study. The delayed reduction of [³H]forskolin binding sites in the substantia nigra observed in the present study indicates that striatonigral terminal degeneration at presynaptic sites is caused by precedent ischemic damage of the ipsilateral caudate putamen and that exo-focal postischemic neuronal death is caused by a transsynaptic process associated with the ischemic foci.     

老年男性心肌缺血患者心率变异分析（附67例报告）

采用正常搏动ＲＲ间期的标准差（ＳＤ）及心率变异指数（ＨＲＶ ｉｎｄｅｘ）作为指标，分析６７例老年男性心肌缺血患者的心率变异，并与正常老年男性组及正常青壮年男性组进行了对比，发现前组的ＲＲ间期ＳＤ、ＨＲＶｉｎｄｅｘ均明显低于后两组，其结果有显著性差异（Ｐ均〈０．０１）。提示心肌缺血可破坏交感与迷走神经的均衡性，造成心率变异降低。     

Striatal cells containing the Ca2+-binding protein calretinin (protein 10) in ischemia-induced neuronal injury

The present study concerns the vulnerability of striatal interneurons immunopositive for the Ca²⁺-binding protein calretinin to ischemic neuronal injury. An immunohistochemical study was carried out on the striata of rats which had undergone transient middle cerebral artery occlusion. Two weeks after the ischemia, there was a marked reduction in the number of calretinin-positive neurons in the ipsilateral ischemic lesion, although the striatal interneurons positive for parvalbumin, which are a neuronal population distinct from the calretinin-immunoreactive cells in the striatum, were spared in the insulted areas. The present data indicate that the striatal calretinin-positive neurons are less resistant to transient ischemia, suggesting that there may exist vulnerability differences among the striatal interneurons in ischemia-induced neuronal injury.     

NO对兔局灶脑缺血脑水肿和脑梗塞灶的影响

本文在兔MCAO局灶脑缺血模型基础上,利用外源性一氧化氮(NO)前体物质L-精氨酸和NOS抑制剂L-NNA研究NO对脑缺血后脑水肿和脑梗塞的影响。NZW兔42只随机分为7组,每组6只,计对照组、假手术组、MCAO组、MCAO+NS组、MCAO+L-Arg组、MCAO+D-Arg组及MCAO+L-Arg+L-NNA组。结果提示:与单纯MCAO组比较,L-Arg组的脑组织H_2O、Na~+、Ca~(2+)含量明显下降(P<0.01),脑梗塞灶亦明显缩小(P<0.01)。从而显示L-Arg系通过产生NO促使血管舒张而减轻脑水肿和缩小梗塞灶,为临床改进脑缺血的治疗提供依据。     

间断缺血心停搏在冠脉搭桥术中的应用

１９９２～１９９３年间为１８０例冠脉病变的病人施行冠脉搭桥术，全部病人均采用核甙抑制剂利多氟嗪预处理和低温（２８℃）间断缺血心停搏进行术中心肌保护。平均每例病人作冠状动脉端吻合３～４个，每个吻合口用９分钟，主动脉阻断累加时间约２５分钟，体外循环时间９０分钟，术后医院死亡率１．６％（３／１８０），无术后心梗发生。作者认为，冠脉搭桥术的术中心肌保护可采用核甙抑制剂和间断缺血心停搏方法，而不用心肌停搏液。     

温缺血时间与同种心脏瓣膜细胞活性的关系

以１０具脑外伤死亡的健康男性的心脏的６０个同种主动脉、肺动脉瓣叶分为６组进行实验。经不同的温缺血时间灭菌并经过３个月的液氮深低温保存后，通过流式细胞计数测定细胞活性，同时行组织块贴壁培养及电镜观察。结果表明：温缺血时间在１２小时以内，细胞活性为９３．４９±２．３５％，较对照组无明显下降。灭菌２４小时，细胞活性为８９．８２±３．５２％，较对照组明显下降，Ｐ＜０．０１，并且可见形态上改变；冷冻后细胞活性进一步下降，但下降幅度减低，冻存３年后活细胞仍占８０％。结论为：温缺血时间对细胞活性有影响，时间延长与活性的下降成正相关。因此温缺血时间应控制在１２小时以内。     

家兔缺血与再灌流肾内脂质过氧化物含量的变化

本研究发现:家兔缺血60min(未再灌流)肾皮质和髓质内,脂质过氧化物含量均显著降低;缺血60min再灌流15min的肾皮质和髓质内,脂质过氧化物含量均显著增加。实验提示:缺血再灌流贤内氧自由基“爆发性”生成所引发的脂质过氧化可能是肾缺血性损伤的重要机制之一。     

人参总皂甙对不完全性脑缺血后海马CA1区NOS阳性神经元表达的影响

目的探讨人参总皂甙(GS)对不完全性脑缺血及再灌注不同时间后海马CA1区一氧化氮合酶(NOS)的影响及对神经元的保护作用.方法用双侧颈总动脉夹闭加放血的方法制成大鼠不完性脑缺血及再灌注模型,以还原烟酰胺腺嘌呤二核苷酸脱氢酶(NADPH-d)组织化学方法观察缺血及再灌注后海马CA1区NOS阳性神经元变化及GS对其的影响.结果单纯缺血组海马CA1区在缺血30min时NOS阳性细胞数最高(44.5±7.42),为假手术组2倍,再灌注2h、12h、24h、3d后逐渐下降,5d时恢复正常水平(21.12±3.50),缺血再灌注3d、5d时出现神经细胞损伤.GS能抑制缺血30min及再灌注各时程中NOS阳性神经元数量变化,并能预防缺血再灌注后迟发的神经元损害.结论GS对大鼠不完全性脑缺血及再灌注不同时程后海马CA1区NOS的异常表达有抑制作用,对神经元的保护作用.