二氮嗪对大鼠脑缺血再灌注细胞凋亡的影响

目的研究二氮嗪开放线粒体ATP敏感性钾通道对大鼠脑缺血再灌注细胞凋亡的影响。方法采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,将20只大鼠随机分成4组,假手术组、缺血组、缺血＋二氮嗪治疗组和缺血＋二氮嚷＋MitoK（ATP）通道特异性抑制剂5-HD组。观察各组凋亡细胞数和凋亡相关蛋白Bcl-2、Bax的变化。结果与缺血组比较,二氮嗪使凋亡细胞数明显减少（83．2±9．04 vs 123．96±13．45）,Bcl-2表达增高（0．17±0．01 vs 0．13±0．01）,Bax表达下降（0．15±0．02 vs 0．20±0．03）,差异具有显著性（P＜0．05）。5-HD能取消这些作用（P＜0．05）。结论局灶性脑缺血再灌注损伤时,二氮嗪能通过上调半暗带区Bcl-2蛋白表达,下调Bax蛋白表达,减少神经元凋亡,对脑缺血损伤起保护作用。     

一种新的单侧听觉气传导持续阻滞大鼠模型

用外耳道外沿皮下缝合法制备了一种新的单侧听觉气传导持续阻滞大鼠模型。它具有制作简便、损伤较小、效果持续的优点。     

栓线法大鼠局灶性脑缺血模型的研究

采用颈部旁侧手术入路，结扎右侧颈总动脉、颈外动脉及其分支后颈内动脉栓线法制作大鼠大脑中动脉闭塞再灌流损伤模型。闭塞成功率９４．１％，动物偏瘫症状评分在缺血２ｈ再灌流３ｄ后趋于稳定，病理改变以尾壳核损害最重。再灌流７ｄ脑梗塞体积为９７．８±９．４ｍｍ３，动物死亡率５９．４％。缺血２ｈ后再灌流先出现过渡灌注，而后呈持续性低灌注。本文模型勿需开颅，缺血效果可靠，对局灶性脑缺血的研究具有实用价值。     

大鼠良性前列腺增生组织中细胞外基质的免疫组化研究

为了研究性激素及细胞外基质在良性前列腺增生(BPH)发生中的相互作用,实验建立大鼠BPH模型,并采用免疫组织化学ABC法对大鼠前列腺组织中的纤维连续蛋白(FN),Ⅳ型胶原蛋白(COL IV)进行表达,发现睾丸素组的前列腺重量明显增加,FN及COL IV强阳性染色率显著高于去势组及对照组(P<0.01,0.05),而且前列腺的重量分别与FN,COL IV表达呈正相关(P<0.05)。提示在大鼠BPH模型中细胞外基质成分增加,增殖的细胞与大量积聚的细胞外基质共同作用导致BPH的发生。     

Strain Difference of Susceptibility to 4-Nitroquinoline 1-Oxide-induced Tongue Carcinoma in Rats

Strain difference of susceptibility to 4-nitroquinoline 1-oxide (4NQO)-induced squamous cell carcinomas of the tongue among Dark-Agouti, Long-Evans, Sprague-Dawley, ACI/Ms, Fischer 344, Donryu and Wistar/Furth rats was surveyed by evaluating the survival times, incidences and sizes of developed tumors as markers of susceptibility. Administration of 4NQO dissolved in drinking water induced squamous cell carcinomas in various sites of the upper digestive tract mucosa of all the experimental male and female rats of the seven strains. Regarding the mean survival times, Wistar/Furth rats survived much longer than any other strain of rats, and Dark-Agouti showed the shortest survival. The incidence of large, mass-type carcinomas of the tongue of Dark-Agouti rats was higher than in any other strain of rats, while that of Wistar/Furth rats was the lowest. Subsequently the mitotic activity and bromodeoxyuridine incorporation in the tongue epithelium of Dark-Agouti and Wistar/Furth rats were estimated after a short-term administration of 4NQO. There was a pronounced difference between the two strains of rats, because the proliferative responses of the tongue epithelium of Dark-Agouti rats to the 4NQO stimulation were much higher than those of Wistar/Furth rats. These results indicated that there are marked differences in the susceptibility to 4NQO-induced tongue carcinoma among the seven strains of rats, and that Dark-Agouti and Wistar/Furth rats could be useful as models of highly and poorly susceptible strains, respectively, for further genetic analysis.     

Mechanisms of pinacidil-induced vasodilatation

The mechanism of the vasodilator effect of pinacidil was examined. Pinacidil (0.1–100 μM) inhibited the increases in cytosolic Ca²⁺ ([Ca²⁺]_i) and muscle tension due to norepinephrine in rat aorta. In contrast, a Ca²⁺ channel blocker, verapamil, inhibited the norepinephrine-stimulated [Ca²⁺]_i more strongly than the contraction. Higher concentrations of pinacidil (3–100 μM) inhibited the verapamil-insensitive portion of the contraction and [Ca²⁺]_i. An inhibitor of ATP-sensitive K⁺ channels, glibenclamide, antagonized the inhibitory effect of low concentrations ( 10 pM) of pinacidol. Pinacidil did not change the contraction induced by Ca²⁺ in vascular smooth muscle permeabilized with Staphylococcus aureus -toxin. Norepinephrine (in the presence of GTP), 12-deoxyphorbol 13-isobutyrate (in the absence of GTP), and treatment with GTP_γS potentiated the contraction of permeabilized smooth muscle induced by the addition of Ca²⁺. Pinacidil (100 μM) inhibited the potentiation due to GTP_γS or noepinephrine but not to phorbol ester. These results suggest that pinacidil has dual effects on vascular smooth muscle contraction. At lower concentrations (>0.1 μM), it decreases [Ca²⁺]_i, possibly by activating ATP-sensitive K+ channels. At higher concentrations (> 3 μM), it may additionally inhibit the receptor-mediated, GTP-binding protein-coupled phosphatidyl inositol turnover.     

不同脑缺血和再灌流过程中大鼠脑组织NO含量的动态变化

采用线栓法制成大鼠大脑中动脉梗塞 ( MCAO)模型 ,依 Hb O2 - NO法测定持续性脑缺血和缺血 /再灌流脑组织内 NO含量的变化 ,以探讨不同脑缺血和再灌流过程中 NO的变化规律及其意义。结果 :缺血 3小时受损脑组织 NO水平即增高 ,再灌流后 NO逐步升高 ,而持续性缺血状态下 NO则表现降低后再升高的变化。虽然两组 NO在 7天时均有明显降低 ,但仍高于缺血前水平。认为持续性脑缺血和缺血 /再灌流情况下 NO的变化规律有所不同 ,与缺血脑组织的缺氧及产生 NO所需底物供应缺乏有关 ,且可能与脑组织的损害密切相关     

大鼠下丘脑弓状核的形态计量研究

为了探讨急性癫痫弓状核形态改变与可复性，我们采用光、电镜技术和形态计量方法对下丘脑弓状核进行了形态定量研究。结果显示：弓状核切面面积为317500±6460um2，神经元胞体和胞核的等效直径分别为12.94±0.34um和8.54±0.43um，暗细胞内线粒体、粗面内质网、高尔基复合体、溶酶体、游离核相体和分泌颗粒的面积分数分别是5.87±1.98％、3.53±0.25％、0.81±0.49％、2.13±0.42％、10.53±0.46％和0.86±0.35％，其面数密度（单位面积为30um2）分别为15.68±1.14um-2、21.29±3.52um-2、10.20±0.42um-2、5.62±067um-2、101.35±7.55um-2和5.22±0.77um-2.本文还对弓状核的形态结构、神经元类型及其功能进行了讨论。     

铁骨晶对大鼠钙代谢、骨密度的影响及临床观察

本实验以铁骨晶（多肽钙），进口脱脂奶粉，活性钙冲剂，贝壳钙为钙源添加于大鼠正常饲料中。观察结果表明：上述４组钙的吸收率分别为６４．４％，６９．１％，５９．９％，５１．６％；钙的储留率分别为８９．８％，９３．３％，８５．２％，７９．０％；钙的存留率分别为４３．６％，４９．０％，３２．４％，２６．８％；股骨指数分别为７．０２×１０（－３），６．４３×１０（－３），６．８４×１０（－３）。６．８８×１０（－３）；折断力（牛顿）分别为６０．５４±１２．５５，４６．８１±９．３２，４３．２６±１６．６２，３８．２４±１０．７９。同时以铁骨晶为钙源对７０例（５～６岁）儿童进行了血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ及生长发育的检测。铁骨晶组的身高，体重，胸围分别比对照组增加。铁骨晶组血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ也均有较好的改善。这表明铁骨晶具有较好的促进钙吸收利用作用，同时能增加骨强度作用。     

The Effect of Quisqualic Acid-Induced Lesions of the Nucleus Basalis Magnocellularis on Latent Inhibition

Latent inhibition (LI) is a reduction in the rate of acquisition of a Pavlovian conditioned response that results from prior nonreinforced preexposure to a conditioned stimulus (CS). LI has been suggested to reflect the operation of mechanisms involved in stimulus selection for subsequent cognitive processing. The present experiment was conducted to assess the effect of bilateral lesions of the nucleus basalis magnocellularis (NBM) on LI employing a conditioned emotional response paradigm. Bilateral lesions of the NBM were produced by administration of 0.12 M quisqualic acid and resulted in decreased cortical acetylcholinesterase staining, as well as a 40% reduction in cortical choline acetyltransferase activity. Following lever press training, preexposed animals received 40 presentations of a 60-s tone CS. Nonpreexposed animals received no tone presentations. Acquisition of conditioned suppression was then assessed over the course of 4 tone-shock (0.6 mA, 0.5 s) pairings. Control, preexposed animals displayed a retarded rate of acquisition in comparison to nonpreexposed controls, thereby demonstrating that the parameters used in the present experiment produced LI. In contrast, lesioned animals preexposed to the CS acquired conditioned suppression as readily as non-preexposed lesioned animals. However, the acquisition of conditioned suppression in both lesioned groups was found to be similar to that displayed in the preexposed control group. This pattern of results was interpreted as being attributable to a lesion-induced impairment in the ability to maintain stimulus processing, rather than a deficit in the ability to filter a stimulus. Copyright © 1996 Elsevier Science Inc.