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.     

Extensive pectoral muscle necrosis after defibrillation: nonthermal skeletal muscle damage caused by electroporation

A 37-year-old Italian male developed a myocardial infarct with subsequent ventricular fibrillation. He was defibrillated seven times with up to 360 Joules. Thirteen days later the patient died of recurrent myocardial infarct due to thrombotic occlusion of the left circumflex coronary artery. At autopsy, necrosis of the right pectoralis muscle was observed. Electroporation is the pathogenetic mechanism of skeletal muscle damage due to multiple defibrillations with high energy levels. Received: 8 January 1998 Accepted: 15 April 1998     

恒河猴坐姿着陆冲击内耳损伤的观察

为研究机体及各组织器官对冲击力的耐受限值，探讨致伤原因及提出防护措施，利用着陆冲击塔，使实验动物恒河猴的坐姿状态下，进行冲击试验，试验后１ｈ左右处死，作大体解剖观察并取心，肝，脾，肺，颞骨等组织，固定，切片，镜检。同时重点观察了内耳的损伤。结果表明，冲击载荷不大（平台过载值为≤２５Ｇ）时内脏虽然有轻度损伤，但内耳可避免受员，当冲击力加大到一定程度（平台过载值为３０～３５Ｇ）导致内脏中等损伤时，内耳     

成人斯蒂尔病的肝损害

目的；探讨成人斯蒂尔病（adult-onset Stil's disease,AOSD))合并肝损害的发生、表现、治疗和预后。方法；对27例成人斯蒂尔病患者中出现肝损害的13例，根据病情轻重采用中药水剂茵陈蒿汤中味或益肝灵片加服联苯双酯滴丸、强力宁注射液进行治疗。结果：11例（84.6%）肝功能恢复正常，1例好转，1例因急性肝功能衰竭死亡。结论：成人斯蒂尔病患者合并肝损害甚为常见。经中药和西药联合应用合理治疗后多数患者可恢复或好转。应重视和警惕发生危及生命和急性肝功能衰竭。     

双光气对大鼠肺损伤的研究

研究了双光气染毒后不同时间大鼠支气管肺泡灌洗液（ＢＡＬＦ）成分及肺形态学改变。结果表明，双光气染毒后，ＢＡＬＦ成分的变化程度与肺形态改变密切相关ＢＡＬＦ成分分析可作为动物实验中探测双光气所致肺损伤的有力手段。     

镉对肾脏的毒作用

雄性Ｗｉｓｔａｒ大鼠２４只，随机等分为４组，皮下注射不同剂量的ＣｄＭＴ。结果显示镉接触组尿钙和尿蛋白都高于对照组；肾皮质钠泵和钙泵活性低于对照组，体外试验也显示镉能抑制钙泵活性，ＧＳＨ和半胱氨酸对这种抑制有保护作用；肾皮质ＧＳＨ含量低于对照组，ＭＤＡ含量则高于对照组，但肝脏的这两个指标无变化；高剂量组ｃＡＭＰ／ｃＧＭＰ的比值低于对照组。提示脂质过氧化和钙代谢障碍是镉引起肾损害的机理之一。     

新生儿产伤79例分析

目的了解新生儿产伤种类及相关因素.方法用回顾性分析方法对该院23年间分娩造成的新生儿产伤共79例进行分析.结果23年间共分娩25 916例次,分娩造成的新生儿产伤共79例,发生率为3.05‰.产伤类型包括:骨折、臂丛神经损伤、产钳伤、刀伤、面瘫、口底损伤,其中以骨折为最多,计33例,占41.77%,骨折中颅骨骨折所占比例最大,25例(75.76%).与产伤关系最为密切的分娩方式是产钳助产.体重≥2500 g,发生新生儿产伤71例,占89.87%.新生儿产伤Apgar评分≤7分56例,占70.89%.结论正确选择分娩方式,把新生儿产伤降到最低点.     

海生多糖肽对亚急性辐射损伤小鼠的防护作用

目的 研究海生多糖肽对小鼠亚急性辐射损伤的防护作用。方法 给小鼠饲以海生多糖肽制剂，用^60Coγ射线进行全身性亚急性照射，检测外周血白细胞、脾淋巴细胞转化率、红细胞超氧化物歧化酶、丙二醛和过氧化酶含量、精子畸形率、睾丸精母细胞染色体畸变率和肝细胞半胱氨酸蛋白酶-3等指标。结果 海生多糖肽高、低剂量组小鼠的血白细胞数量、脾淋巴细胞转化率、红细胞超氧化物歧化酶值和过氧化酶值均高于照射对照组，红细胞丙二醛值、精子畸形率、睾丸精母细胞染色体畸变率和肝细胞半胱氨酸蛋白酶-3阳性表达率则低于照射对照组，差异有显著性。结论 海生多糖肽对亚急性辐射损伤有良好的防护作用。     

还原型谷胱甘肽和L-NAME对体外培养的脊髓运动神经元的影响

目的 :探讨还原型谷胱甘肽 (GSH)和L NAME对体外培养的脊髓运动神经元的保护作用。方法 :不同浓度的GSH和L NAME作用于脊髓运动神经元 ,3d后计算存活率。并测量存活率高的两组和对照组的免疫细胞化学标本的神经元形态学指标。结果 :GSH 10mmol·L-1和L NAME 1× 10 -3 mol·L-1组存活率最高。两实验组轴突长度、树突总长度、树突分叉点数目和胞体面积高于对照组。结论 :抗氧化剂和NOS抑制剂可以提高脊髓运动神经元的存活率 ,促进神经元生长