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。     

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。     

兔心肌细胞核钙转运

本研究在离体家兔心肌细胞核上,观察细胞核钙调节的特征。发现心肌细胞每毫克蛋白质的钱含量较细胞浆高２．６倍,而核总钙含量占细胞总钙含量的１／６。心肌细胞核上存在高新和力的Ｃａ－ＡＴＰａｓｅ,其活性具有Ｃａ＾２＋和ＡＴＰ依赖性,在２．０ｍｍｏｌ／ＬＡＴＰ时,其Ｃａ＾２＋依赖的Ｋａ＝２２６ｎｍｏｌ／Ｌ,Ｖｍａｘ＝３４６０ｎｍｌ／（ｈ．ｍｇ）;在４００ｎｍｏｌ／Ｌ的Ｃａ＾２＋时,其ＡＴＰ依赖的Ｋｍ＝３７６     

缺氧预处理对乳鼠心肌细胞蛋白激酶C活性的影响

在培养的乳鼠心肌细胞缺氧／复氧模型上,观察了缺氧预处理的细胞保护作用及其对细胞蛋白激酶Ｃ活性和蛋白磷酸化的影响。结果表明,ＡＰＣ可减轻心肌细胞的Ｈ／Ｒ损伤;提高细胞存活率,减少细胞脂质过氧化产物生成及细胞内乳酸脱氢酶和蛋白质漏出。模拟ＡＰＣ的短暂缺氧显著激活ＰＫＣ,使心肌细胞内分子量为６６ｋＤ和３１ｋＤ的蛋白条带＾３２Ｐ掺入增加;ＰＫＣ抑制剂Ｈ７完全消除ＡＰＣ对心肌细胞的保护作用,并抑制了短暂缺氧