感染性休克中血浆cAMP及cGMP含量的变化

环核苷酸特别是cAMP在神经体液传递信息过程中起“第二信使”作用。这些物质的合成和分解受植物神经系统以及多种激素的调节。虽然它们是在细胞内发生作用,但实验资料提示:细胞外cAMP、cGMP的含量可作为反映植物神经功能的指标。感染性休     

大肠杆菌内毒素休克狗和暴发型流脑休克型患儿血浆前列腺素 E 和 F_(2α)含量的变化

大肠杆菌内毒素血症狗血浆PGE和PGF_2a含量显著增高。休克初期血浆PGE增高值与体循环总外周阻力的变化呈负相关。静脉注射654-2对血浆PGE和PGF_2a水平无明显影响。休克型流脑患儿治疗前血浆PGE和PGF_a含量显著增高,康复期降至正常水平。结果提示:PGE可能是引起休克时体循环外周阻力降低的因素之一。     

肾上腺素对培养心肌细胞胞浆游离钙浓度的影响

肾上腺素能增强心肌收缩力,一般认为这与肾上腺素影响钙转运有关,本文采用荧光指示剂Quin-2法测定胞浆游离钙浓度,观察肾上腺素对培养心肌细胞胞浆游离钙浓度的作用。 材料与方法     

为毒素休克大鼠红细胞蛋白激酶C活性的变化

大鼠注射内毒紊后0.5h,红细胞浆蛋白激酶C活性明显降低,细胞膜蛋白激酶C活性显著增高。由正常红细胞浆提纯的蛋白激酶C在体外能增加红细胞膜蛋白区带1、区带2、区带4.2、区带4.5以及区带4.9的~(32)P参入量。结果提示,内毒素休克早期大鼠红细胞蛋白激酶C被激活;激活的蛋白激酶C引起红细胞膜骨架蛋白的磷酸化,进而可能影响红细胞变形性。     

蛋白激酶C对高迁移率蛋白I的磷酸化及其位点分析

纯化的重组人HMGI可被蛋白激酶C（PKC）迅速磷酸化,其化学计量达到2.0～2．5mol／mol,经过蛋白酶水解得到3个磷酸化肽段。磷酸氨基酸分析和氨基酸测序结果表明,该蛋白分子的44和64位的丝氨酸（Ser）是PKC主要的磷酸化位点,其中Ser－64在其第二个DNA结合结构域的C端近旁,而Ser-44则位于第一和第二个DNA结合结构域之间。另外,在75～78位的4个苏氨酸中存在低水平的磷酸化。该结果提示HMGI上PKC的磷酸化位点和CDC2激酶的位点显著不同。后者的位点主要为53和78位的苏氨酸。     

棉酚(-、+、±)对佛波酯和A_(23187)刺激巨噬细胞前列腺素合成的影响

以蛋白激酶C激活剂十四脂酰佛波乙酸酯(PMA)、钙离子载体A_(23187)及花生四烯酸刺激小鼠腹腔巨噬细胞合成花生四烯酸环氧化酶产物PGI_2、TXA_2和PGF_(2α),(-)、(+)及(±)棉酚可显著抑制PMA和A_(23187)刺激的前列腺素合成,而对花生四烯酸刺激的前列腺素合成无明显影响。提示棉酚的左旋体和右旋体均可通过影响花生四烯酸释放而抑制前列腺素合成。     

大肠杆菌内毒素休克狗血液动力学和某些体液因子的变化

大肠杆菌内毒素休克狗平均动脉压变化规律基本一致,心搏出量和体循环总外周阻力变化的差异较大,可将其大致区分为“低排-低阻”、“低排-高阻”和“高排-低阻”三种类型,且绝大多数动物以“低排-低阻”开始和告终。“高排-低阻”代偿最有效,“低排-高阻”次之,低排-低阻”最差,后者实际上是失代偿的表现。体液因子的变化提示,“低排-低阻”型动物胆碱能系统的活动占优势,“低排-高阻”型动物肾上腺素能系统的活动占优势,“高排-低阻”型动物两个系统的活动接近于相对平衡。     

CI-IANGES IN THE PLASMA LEVELS OF PGE, PGF2a AND 6-Keto-PGFla IN CANINE ENDOTOXIC SHOCK

The plasma levels of PGE, PGF2a and 6-keto PGFla in the canine model of endotoxic shock were determined with radioimmunoassay. Following cndotoxin injection, the PGF2a levels were rapidly increased to peak at 5 minutes. There was a negative correlation between the PGE level and the change in total systemic peripheral resistance at early stage of shock. The administration of anisodamine 2 hours after endotoxin injection showed no effect on the changes of PGE and PGF2a levels in the shocked dogs. The plasma levels of PGE and PGF2a in the shocked children with fulminating epidemic menin gococcal meningitis were also markedly elevated dur- ing shock but fell within normal range at convales- sence. After the dogs were given endotoxin the plasma level of 6-keto-PGFla increased slowly during the first hour, reached a peak at 2 hours and re mained high for 12 hours. There was a negative correlation between the 6keto-PGFla level and the blood pressure. The plasma 6keto PGFla level was decreased and the blood pressure improved corres- pondingly with a negative linear correlation as a result of administration of anisodamine 5-10 minutes after endotoxin injection. These results suggested that PGE and PGI2, as one of the humoral factors, might participate at least partially in the endotoxin induced hypotension, and that the inhibition of PGI2 synthesis was considered contributable to certain degree to the antishock effect of anisodamine.