脓毒血症大鼠心肌II型磷脂酶A_2活性变化及其调控

观察了脓毒血症大鼠心肌ＩＩ型ＰＬＡ２ 活性、蛋白质含量及其ｍ ＲＮＡ 的变化。结果发现, 脓毒血症早期与晚期心肌ＩＩ型ＰＬＡ２ 活性较对照组分别降低２５ ．０ ％ （Ｐ ＜ ０ ．０５）及增高４７．６ ％ （Ｐ ＜ ０ ．０１）,ＩＩ型ＰＬＡ２ 蛋白质含量分别降低２７．０％ 及增高４８ ．０ ％（ 均Ｐ ＜ ０ ．０１）; 心肌ＩＩ型ＰＬＡ２ ｍ ＲＮＡ合成率与含量呈现类似的双相变化, 在脓毒血症早、晚期ｍＲＮＡ 合成率分别降低４５．０％ 和升高７０．０ ％ （均Ｐ ＜ ０ ．０１）,ｍＲＮＡ含量分别降低３４．１ ％ 和增加１５７ ．０％ （均Ｐ＜ ０ ．０１） 。脓毒血症早、晚期心脏ＩＩ型ＰＬＡ２ ｍ ＲＮＡ半衰期无显著变化（Ｐ ＞ ０．０５） 。实验结果表明大鼠脓毒血症发生过程中心肌ＩＩ型ＰＬＡ２ 活性呈现出先下降后升高的变化, 这一变化受其ｍＲＮＡ 转录水平的调节。     

心衰发生的新假说：细胞凋亡可能是慢性压力超负荷导致心衰的机制

心衰发生的新假说：细胞凋亡可能是慢性压力超负荷导致心衰的机制最近,Ｂｉｎｇ在ＪＭｏｌＣｅｌｌＣａｒｄｉｏｌ上的编辑部文章中,提出了一个心衰发病机制的新假说,认为细胞凋亡可能是慢性压力超负荷导致心肌细胞死亡、心功能异常和心衰的重要机制。大量实验表明,压...     

长期口服L－精氨酸可抑制球囊导管诱导的内膜增生

长期口服Ｌ－精氨酸可抑制球囊导管诱导的内膜增生经皮穿刺冠脉腔内血管成形术（ＰＴＣＡ）是近年临床广泛开展的使粥样斑块堵塞的冠脉再通的技术,但术后６个月内有２５％～３５％的患者其再通的冠脉又发生再狭窄。再狭窄的发生机制目前尚未完全阐明,缺乏有效的防治措施...     

内源性一氧化碳在大鼠败血症性休克时 低血压发生机制中的作用

A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. The results showed that BP of sepsis rats,including systolic and diastolic arterial BP,decreased significantly while HO activity and CO content were significantly increased. In contrast,after administration of ZnDPBG,BP of sepsis rats was significantly increased while the HO activity and CO production were significantly decreased. These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock;inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone,and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.     

内源性一氧化碳在大鼠败血症性休克时低血压发生机制中的作用

应用盲肠结扎法制备大鼠败血症休克模型,研究内源性一氧化碳（ＣＯ）在败血症休克时低血压发病中的作用。用血红素加氧酶（ｈｅｍｅｏｘｙｇｅｎａｓｅ,ＨＯ）抑制剂２,４二甘油次卟啉锌（ｚｉｎｃｄｅｕｔｅｒｏｐｏｒｐｈｙｒｉｎ２,４ｂｉｓｇｌｙｃｏｌ,ＺｎＤＰＢＧ）处理大鼠后,观察动物动脉血压,同时测定主动脉平滑肌组织中ＨＯ活性和ＣＯ生成量。结果发现：败血症大鼠动脉收缩压、舒张压降低,同时血管平滑肌ＨＯ活性和ＣＯ生成明显增加。败血症大鼠用ＺｎＤＰＢＧ处理后,动脉血压明显回升,同时ＨＯ活性和ＣＯ生成明显被抑制。实验表明败血症休克时低血压的发生与血管平滑肌细胞ＨＯ活性增加和内源性ＣＯ生成增多明显相关;应用ＨＯ抑制剂阻断ＨＯ活性能导致内源性ＣＯ生成减少,继而使败血症休克时大鼠血压明显回升。实验提示,内源性ＣＯ对血管张力具有重要的调节作用;ＨＯ活性和内源性ＣＯ生成增加是败血症休克时低血压发生的重要机制之一。     

Preliminary investigation of sequence-independent DNA binding proteins in rat skeletal muscle sarcoplasmic reticulum and their function

To observe the binding of plasmid DNA to non-nuclear DNA binding proteins in sar-coplasmic reticulum (SR) and the effects of this binding on SR function, sarcoplasmic reticulum proteins in rat skeletal muscle were isolated by differential centrifuge and sucrose density-gradient centrifuge. The results showed that there are two sequence-independent DNA binding proteins in SR proteins, the molecular weights of which are 83 and 58 ku, respectively. Ca2 uptake and release of SR were remarkably promoted by the binding of plasmid DNA to DNA binding proteins in SR, the mechanism is probably through increasing of Ca2 -ATPase activity in SR and changing of character of Ca2 release channel ryanodine receptors induced by the binding. These results suggest that there exist DNA binding proteins in SR and its binding to DNA may affect Ca2 transport of SR.     

降钙素基因相关肽对血管内膜损伤后内皮细胞功能恢复的影响

在球囊剥脱大鼠主动脉内膜造成的内皮损伤模型上,用ＣＧＲＰ（１０μｇ／ｋｇ／ｄ）治疗后观察血管内皮合成释放ｖＷＦ含量及ｔ－ＰＡ活性的变化。结果表明ＣＧＲＰ能明显降低ｖＷＦ含量和增加ｔ－ＰＡ活性。提示ＣＧＲＰ能减轻内皮损伤反应,在促内皮细胞增殖的同时对内皮某些功能恢复亦有一定的作用     

大鼠高血压相关基因表达蛋白抑制血管平滑肌细胞增殖

大鼠高血压相关基因 ( r HRG- 1 )编码一新细胞内信号传递蛋白 .体外转染 r HRG- 1表达蛋白发现 r HRG- 1表达蛋白能抑制自发性高血压大鼠血管平滑肌细胞内 Raf蛋白 ( Raf- 1 )和丝裂素活化蛋白激酶 ( MAPK)活性 ,抑制抗细胞凋亡基因 ( bcl- 2 )和增殖细胞核抗原 ( PCNA)基因 m RNA表达 ,同时还抑制该细胞 DNA的合成 .r HRG- 1是一正常血压大鼠血管平滑肌细胞内高度表达的基因 ,由此推测在自发性高血压大鼠血管平滑肌细胞内转染 r HRG- 1表达蛋白抑制其细胞 DNA合成的作用可能是抑制细胞内 Raf- 1活性与 MAPK活性及抑制 PCNA和 bcl- 2基因表达的结果     

大鼠骨骼肌肌质网非序列依赖性DNA结合蛋白及其功能的初步研究

应用差速离心法分离大鼠骨骼肌肌质网(SR)膜蛋白,观察质粒DNA与SR上非核DNA结合蛋白的结合及其对SR功能的影响.结果显示:大鼠骨骼肌SR上存在序列非依赖性的DNA结合蛋白,分子量分别为83和58ku,质粒DNA与SR上DNA结合蛋白结合后可明显促进SR的Ca2+摄入与释放能力,其机制可能是通过增强SR上Ca2+-ATPase的活性及影响SR上Ca2+释放通道ryanodine受体的结合引起的.上述结果表明:SR上存在DNA结合蛋白,DNA与之结合后可影响SR的Ca2+转运.     

在体导入NOS基因可抑制球囊扩张术后血管内膜增生

在体导入ＮＯＳ基因可抑制球囊扩张术后血管内膜增生血管平滑肌细胞（ＶＳＭＣ）增生、内膜增厚是球囊扩张术后再狭窄的主要发病机制之一。近年来许多实验表明ＮＯ有抑制培养ＶＳＭＣ增殖的作用;口服ＮＯ前体Ｌ－精氨酸可减轻内皮损伤诱导的血管内膜的增生。Ｌ－精氨酸在...