促黄体生成素基因免疫对前列腺增生模型鼠生殖内分泌的影响

目的 探讨LH基因免疫对前列腺增生模型鼠生殖内分泌的影响。方法 RT－PCR法从雌性大鼠垂体细胞中RNA扩增大鼠的促黄体素基因（LH）cDNA片段约（461bp）并克隆至T载体，获得重组质粒T－LH，限制酶酶切，酶连接，构建PCDNA3.1(-)/HbsAg/LH，经脂质体转染纯化的重组质粒至COS细胞中，通过肌肉注射构建的PCDNA3.1(-)/HbsAg/LH与前列腺增生大鼠，2个月内给药两次。结果 体外培养COS细胞，发现HBsAg与LH连接物表达较好，肌肉注射前列腺增生模型鼠重组质粒后，模型鼠LH与T的含量明显低于对照组。结论 PCDNA3.1(-)/HbsAg/LH可参与前列腺增生模型鼠生殖内分泌腺的调节。     

六味地黄汤对实验性糖尿病大鼠心、肝、肾组织中过氧化氢酶活性和过氧化脂质含量的影响

用四氧嘧啶诱导雄性Ｗｉｓｔａｒ大鼠为模型进行研究．结果发现，四氧嘧啶大鼠血糖明显升高，且心、肝、肾组织中过氧化氢酶活性较正常组明显降低，过氧化脂质含量在心、肝组织中明显增高，过氧化脂质与过氧化氢酶比值在心、肝、肾组织中均明显高于正常组，表明糖尿病状态下大鼠心、肝、肾组织中均自由基生成增多，氧化损伤加重．经六味地黄汤治疗后，血糖明显下降，但心、肝、肾组织中的过氧化氢酶活性无改变；而心肌中过氧化脂质含量和过氧化脂质与过氧化氢酶比值则明显降低，过氧化脂质含量和过氧化脂质与过氧化氢酶比值在肝、肾组织中无变化，表明六味地黄汤能明显清除心肌中自由基，抑制心肌中脂质过氧化，且此作用并不是通过提高过氧化氢酶活性来达到．     

刺激视上核对大鼠痛阈及电针镇痛的影响

以钾离子透引起的大鼠甩尾反应为痛指标，观察了电和化学刺激视上核（ＳＯＮ）对大鼠痛阈（ＰＴ）和电针（ＥＡ）镇痛的影响。电刺激ＳＯＮ后，ＰＴ明显高于假刺激组（Ｐ＜０．０５～０．００１），电刺激ＳＯＮ后电针足三里，镇痛效应明显提高，并有明显的量效关系。电刺激ＳＯＮ的近旁部位（０．５—１ｍｍ）对ＰＴ及电针镇痛无明显影响。ＳＯＮ内注射Ｌ－谷氨酸（Ｌ－Ｇｌｕ）后痛阈和电针镇痛效应都明显对照组，也有明显的量效关     

Age-related Changes in Excitability and Recurrent Inhibition in the Rat CA1 Hippocampal Region

In hippocampal slices from male Wistar rats aged 1–34 months, we recorded the synaptic field potential responses of the CA1 neurons to stimulation of Schaffer collaterals. Eight electrophysiological indexes were extracted from input/output curves and compared in 11 age groups from 1 to 30 months. Neuronal excitability presented a U-shaped curve of development with a minimum at ˜7–8 months of age. There was a significant continuous increase in neuronal excitability, i.e. a decrease in excitatory postsynaptic potential (EPSP) producing both the threshold and half-maximal population spike from middle age (8–10 months) to senescence (30 months). Synaptic efficiency also increased in old rats to reach a maximum during senescence, i.e. both the current for threshold EPSP and that for half-maximal EPSP reached a minimum in senescence, although the earlier developmental patterns of these two indexes were non-linear. The duration of the field EPSP elicited with maximal stimulation presented an abrupt decay after the first month. Aged animals presented a relatively small maximal population spike. Recurrent inhibition was most prominent on neuronal excitability rather than synaptic strength. Measured as the percentage change in the half-maximal EPSP and half-maximal population spike, recurrent inhibition was found to decrease during the first 7–10 months of life and remained small in later development.     

双氯灭痛药膜体外透皮速率的实验研究

作者选择乙基纤维素、聚乙烯醇等高分子材料制成涂膜剂，用大鼠皮进行双氯灭痛药膜的体外透皮速率测定。结果表明，氮酮与丙二醇可以促进药物渗透。不同的高分子材料可影响药物的扩散与释放，从而影响其透皮速率。与无膜无促透剂处方相比，药物在乙基纤维素中的透皮速率没有增加，在聚乙烯醇膜中的透皮速率有显著增加。     

Presynaptic α2-adrenoceptor-mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats

The present study was designed to investigate the presynaptic alpha 2-adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na-loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na-loaded HT and normotensive control rats (NT-control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na-loaded HT than in NT-control. Yohimbine, a potent alpha 2-adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na-loaded HT compared with NT-control. These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na-loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na-loaded HT could partially depend on impaired presynaptic alpha 2-adrenoceptor-mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt-dependent hypertension.     

IgA肾病大鼠血清IgA-纤维连接蛋白的检测及意义

目的 检测IgA肾病大鼠血清IgA-纤维连接蛋白水平，探讨其在IgA肾小球系膜沉积中的作用。方法 肝叶切除后，尾静脉注射脂多糖，制作IgA肾病大鼠模型。应用ELISA法检测血清IgA-纤维连接蛋白聚合物水平，半定量法对系膜IgA免疫荧光强度评分，二者作相关性分析。结果 IgA肾病时，血清IgA-纤维连接蛋白聚合物水平升高，并与系膜IgA沉积呈正相关。结论 IgA肾病时，血清IgA-纤维连接蛋白聚合物水平是升高的，且可能是导致IgA系膜沉积的原因之一。     

Thrombin Inhibition in discordant xenograft rejection

Abstract: Microvascular thrombosis and the associated platelet and endothelial cell activation are prominent observations in xenograft rejection. This pathological picture could be related to the excessive generation of thrombin in the context of either inflammation or putative inter-species molecular incompatibilities between activated coagulation factors and their natural anticoagulants. Relatively selective thrombin Inhibition with the serine protease inhibitor SDZ MTH 958 (MTH-958) are independent of heparinoids and anti-thrombin III. MTH-958 has been shown to significantly prolong porcine cardiac function during perfusion with human blood in an ex vivo model. The aim of this study was to validate the role of thrombin generation in a rodent model of discordant xenograft rejection in vivo. The effect of thrombin inhibition with MTH-958 was tested in both hyperacute rejection (HAR) and delayed xenograft rejection (DXR) after decomplementation with cobra venom factor (CVF) in normal Lewis (Lew) rats and Intrinsic C6 deficiency In PVG (C6-/PVG) recipient rats. Recipient rats received heterotopic guinea pig cardiac xenografts and were treated with titrated doses of MTH-958 until the time of graft rejection. Plasma samples at selected time points were examined to confirm effective thrombin inhibition, and rejected grafts were analyzed by immunohistology. MTH-958 significantly improved graft survival in HAR albeit the extent of prolongation was not marked, but the agent failed to prolong survival In CVF-treated Lew rats. In C6-/PVG rats receiving MTH-958, a significantly reduced graft survival time was observed when compared with C6-/PVG controls. The grafts from MTH-958-treated animals showed dense deposits of C3, IgM, and IgG with fibrin levels similar to controls. The thrombin antagonist tested could prolong xenograft survival during HAR but had no benefit in DXR. The relative non-specificity of the serine protease inhibitor MTH-958 with the potential activation of alternative pathway of complement via the inhibition of factor I could account for the failure to prolong xenograft survival in DXR. The pathogenetic significance of thrombin generation in this situation remains to be determined by the use of more selective and pharmacologically acceptable I anti-thrombin agents.