冷原子荧光光度法测定痕量汞

本文设计并试制了一套非色散冷原子荧光测汞仪。研究了冷原子荧光光度法测定痕量汞的条件,制定了用还原气化法测定水中痕量汞的分析方法:检出限量为0.04ppb.在5毫升试样中含汞量在5×10~(-10)克——5×10(-8)克范围内,浓度与荧光峰值成直线关系。方法的相对标准误差为4.3％。对于勿需前处理的试样,分析时间为1分钟。     

内皮素、血管紧张素-Ⅱ和心钠素对血管平滑肌和心肌细胞增殖的影响

本工作应用细胞培养、~3H-胸腺嘧啶核苷掺入和C-fos原癌基因斑点杂交等方法,观察到内皮素和血管紧张素-Ⅱ可促进离体培养的血管平滑肌细胞和心肌细胞的DNA合成和增殖;内皮素和血管紧张素-Ⅱ还可刺激血管平滑肌细胞C-fos原癌基因的表达;心钠素可拮抗内皮素和血管紧张素-Ⅱ的上述效应。     

脂质体导向给药治疗缺血性心脏病的可行性研究(Ⅰ)

本工作在离体大鼠心肌细胞、离体灌流大鼠和家兔心脏模型上,对脂质体作为药物载体导向治疗缺血性心脏病的可行性进行了基础研究。结果表明,心肌细胞可通过融合(Fusion)、内吞(Endocytosis)、吸附(Adsorption)和磷脂分子交换(Exchange)四种方式与脂质体相互作用。细胞摄取脂质体的方式主要取决于脂质体的理化性质。缺氧改变了心肌细胞对脂质体的摄取方式并增加其摄取能力。缺血心肌组织对脂质体、尤其对带正电荷脂质体的摄取显著增加。其摄取量按序为缺血-再灌注区>梗塞边缘区>非缺血区>梗塞区。上述实验结果提示:脂质体作为药物载体可将药物输送到缺血心肌组织和心肌细胞内。     

Role of Regulatory Peptide in Pathogenesis of Shock

The present study evaluated the pathogenetic roles of three kinds of regulatory peptide. The results showed that (i) plasma endothelin(ET) level elevated significantly in septic shock rats, persistent intravenous drip of low doses ET caused development of shock state in normal rats and the irreversible outcome of light hemorrhagic shock. Furthermore, i. v. administration of specific ET-antiserum was significantly effective to septic shock rats, (Ⅱ) Plasma calcitonin gene-related peptide (CGRP) increased by 260% in septic shock rats, i. v. drip of low doses CGRP both in early and late sepsis were effective to shock rats, (Ⅱi) An-giotensin-Ⅱ (ANG-Ⅱ) contents of heart and aorta increased dramatically both in early and late septic shock, and inhibiting its increase with Captopril in late sepsis significantly improved the shock state, but results were inverse in early sepsis. It could be concluded that ET was one of the most important factors participating in the pathogenesis of shock, CGRP had a compens     

中枢5-羟色胺在电针镇痛耐受中的作用

给大鼠多次电针,电针镇痛效果逐渐减弱,而产生电针镇痛耐受,并与吗啡镇痛产生交叉耐受。脑室注射5-羟色胺(5-HT)的前体可以翻转电针镇痛耐受。测定电针镇痛耐受的动物脑内5-HT含量和更新率并不降低,5-HT受体的最大结合力也未见下降。多方面的资料表明,机体对内源性释放的5-HT发生耐受,可能是电针镇痛耐受的一个重要原因。     

脂质体导向给药治疗缺血性心脏病的可行性研究(Ⅱ)

在离体大鼠心脏灌流模型上,发现用高[Ca~(2+)](4.5mmol/L)、高[K~+](8.7mmol/L)或自由基发生系统灌流,显著增加心肌对脂质体的摄取。静脉注射与大鼠心肌细胞抗体共价结合的脂质体,显著增强了脂质体趋心肌组织的靶向性。用脂质体携载超氧化物歧化酶(superoxide dismutase,SOD)治疗大鼠心肌缺血-再灌注损伤,其疗效远优于单用SOD治疗。实验结果表明,脂质体作为药物载体治疗缺血性心脏病可能具有临床应用前景。     

001×7阳离子交换树脂溶胀行为的研究

本文用溶胀性能测定仪定量测定了００１×７阳离子交换树脂在水中的溶胀行为、溶胀行为的温度依赖性以及转型过程中溶胀行为的变化，这对了解产品性能及改进工艺提供了科学数据。     

一氧化氮样舒张因子在休克中的变化及意义

本工作观察了大鼠止血带休克、败血症休克和小肠缺血再灌注休克一氧化氮样舒张因子(NO-LRF)的变化及作用。结果表明,休克动物离体主动脉对去甲肾上腺素的反应降低,组织cGMP含量增加。NO合成前体L-精氨酸(L-Arg)或NO合成阻断剂L-硝基精氨酸(L-NNA)、可溶性鸟苷酸环化酶抑制剂亚甲基蓝(MB)分别增强或减弱休克动物主动脉的上述变化,且这些药物的作用不依赖于血管内皮的存在,提示休克时非内皮源的NO-LRF生成增多是血管对收缩物质反应性降低的原因之一。整体实验发现,L-NNA加重晚期休克动物的低血压并恶化预后,而L-Arg延缓休克动物的血压降低,减轻组织损伤,提示NO-LRF对机体有重要的保护作用,休克时非内皮源NO-LRF生成增多可能是机体的适应性代偿反应。     

001×7树脂力学性能的测定

本文用共聚物小球（以下简称白球）力学性能的快速自动测定方法成功地测定了００１×７树脂的表观压缩模量、模量的温度依赖性以及应力松驰性能，以更科学的方法表征了树脂的力学行为。     

Possibility of Targeting Treatment for Ischemic Heart Disease With Liposome (Ⅰ)

This paper reports the basic research on the possibility of using targeting treatment for ischemic heart disease with liposome as drug carrier. Studies have been performed on isolated rat cardiomyocytes, or isolated perfused rat and rabbit hearts. Results show that cardiomyocytes may interact with liposome through fusion, endocytosis, adsorption and molecular exchange of phospholipid. Forms of cellular uptake of liposome depend chiefly on the physicochemical properties of liposomes. Anoxia changes the pattern of liposome uptake by cardiomyocytes and increases uptake of liposomes. Uptake of liposomes, especially of positively charged liposomes by ischemic myocardium is significantly increased. The quantity of increase of liposome uptake is in the following order: ischemia-reperfusion area>peripheral area of the infarct>non-ischemic area>infarcted area. The above results indicate that liposome as drug carrier might promote the delivery of drug into ischemic myocardium and cardiomyocytes.