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脂质体导向给药治疗缺血性心脏病的可行性研究(Ⅰ) 总被引:2,自引:0,他引:2
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。 相似文献
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Role of Regulatory Peptide in Pathogenesis of Shock 总被引:1,自引:0,他引:1
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 相似文献
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一氧化氮样舒张因子在休克中的变化及意义 总被引:1,自引:0,他引:1
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。 相似文献
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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. 相似文献
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Results from a systematic experiment on isolated perfused rat heart and isolated myc-cytes of adult rat showed that the mechanism of calcium influx during myocardial ischemia-reperfusion is due to the development of intracellular sodium overload during ischemic pe-riod, on reperfusion, the high intracellular Na~+ content activated the reverse direction ofNa~+-Ca~(2+) exchange over myocardial sarcolemma (SL), thus a large quantity of extracellularCa~(2+) fluxed over the SL to the intracellular space, forming a condition of intracellular Ca~(2+)overload, which leads to irreversible damage of the myocardium. 相似文献
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