儿茶酚胺类药物对脓毒性休克大鼠心肌的影响

目的 :利用生化指标和形态学方法研究儿茶酚胺类药物对脓毒性休克大鼠心脏的影响与机制。方法 :用盲肠结扎穿孔术 (CL P)制成大鼠的脓毒性休克模型。采用多巴酚丁胺 (DB)、去甲肾上腺素 (NE)及两者最小剂量联合应用以纠正血压。动物随机分为假手术对照组、CL P对照组、CL P+DB组、CL P+NE组、CL P+DB+NE组 ,每组各 8只大鼠。心肌损害程度应用血清心肌钙蛋白 I(c Tn I)和肌酸激酶 (CK)浓度来表达 ,用光镜与电镜检查心肌组织形态学变化。结果 :脓毒性休克大鼠 c Tn I升高 (P<0 .0 5 ) ,儿茶酚胺类药物浓度不影响 c Tn I的水平 ;但 CK总量水平在儿茶酚胺治疗组升高 (P均 <0 .0 5 ) ;心肌组织形态学检查与 c Tn I的结果相符合。结论 :脓毒性休克心肌损害由缺血引起 ,没有明确的证据显示儿茶酚胺类药物能加重心肌损害。     

精-甘-天冬-丝氨酸对脓毒性休克大鼠心肌肌浆网钙转运的影响(英文)

目的:探讨一种人工合成的纤维蛋白原降解肽片段RGDS对脓毒性休克大鼠心肌肌浆网钙转运功能的影响。方法:大鼠盲肠结扎穿孔术后4h和14h分两次尾静脉注射RGDS 5μmol·kg~(-1)。制备大鼠心肌肌浆网(SR)膜;测定SR Ca~(2 )摄取和[~3H]ryanodine受体结合功能。结果:RGDS组大鼠心肌SR摄Ca~(2 )率及摄Ca~(2 )量分别较休克组提高104％(P<0.01)和12％(P<0.05),而心肌SR钙释放通道-[~3H]ryanodine受体结合B_(max)和K_d值没有明显变化。同时RGDS还可以减轻休克大鼠心肌组织钙聚积。结论:RGDS提高休克大鼠心肌SR Ca~(2 )摄取功能,维持心肌细胞钙稳态,具有心肌保护作用。     

降钙素基因相关肽（CGRP）在败血症休克中的作用

为探讨调节肽CGRP在休克中的发病学意义,本工作在结扎大鼠盲肠加穿孔的败血症休克模型上,观察了CGRP的变化及外源性CGRP对败血症休克过程的影响。结果发现,败血症休克时,血浆中CGRP显著增加(14.3±4.0 vs 5.5±1.8 Pg/ml,P<0.01)。在休克早期、晚期运用CGRP治疗(5μg/kg CGRP ⅳ)都能明显改善动物的低血压状态(分别是14.8±0.8,15.5±0.9 vs休克组10.3±1.6kPa,P<0.05),减轻心肌组织病理损伤,减少血浆中酶(LDH,CD)的漏出。同时,也可抑制休克动物血浆中AGT-Ⅱ含量的增加,提高血浆6-kcto-PGF_1α/TXB_2的比值(早期:69.1±5.3,晚期:65.8±4.1 vs休克组51.0±4.7%,P<0.05)。结果提示,CGRP可能参与败血症休克的代偿调节,适当应用CGRP治疗败血症休克是有益的。     

Clinical and experimental studies on the role of platelet-activating factor (PAF) in the pathogenesis of septic DIC

Various toxic factors induced by endotoxin (Et) are thought to be deeply involved in the pathogenesis of severe infections. In this study, particular attention was paid to the role of the platelet-activating factor (PAF) in these conditions, and clinical and experimental studies were conducted on the relationship between PAF and the changes observed in the general parameters after surgical infections. In the clinical study, changes in the PAF concentration in the blood of seven patients with disseminated intravascular coagulation (DIC), five of whom were septic and two non-septic, were monitored by gas/mass spectrometry. The mean PAF level in the septic DIC group tended to be higher than that in the non-septic DIC group. Moreover, in the septic DIC group, the relationship between the increase in the PAF level and platelet count was analyzed with the lapse of time and we surmised a negative correlation between these parameters.Experimentally, we also investigated the role of PAF in Et shock and the effect of an anti-PAF agent and protease inhibitor. The Et-induced fall in blood pressure was similarly prevented by both the anti-PAF agent and protease inhibitor. However, the decrease in the platelet count was more significantly inhibited by the anti-PAF agent than by the protease inhibitor, whereas the parameters of the blood coagulation/fibrinolysis system were more affected by the protease inhibitor than by the anti-PAF agent.     

Septic shock: a goal-directed therapy using volume loading, dobutamine and/or norepinephrine

In patients with septic shock and acute respiratory failure, norepinephrine (NE) alone or in combination with dobutamine was used. The aim of therapy was to obtain or maintain Cl greater than or equal to 4.5 l.min-1.m-2, SVR greater than or equal to 700-800 dyn.s.cm-5 and oxygen delivery (Do2) greater than or equal to 550 ml.min-1.m-2. Twenty-three patients (58 +/- 3 years) were studied. Initially patients were given intravenous fluid resuscitation to obtain optimal cardiac filling pressures. Eleven patients were considered to be in hyperdynamic septic shock (cardiac index (CI) greater than 4.5 l.min-1.m-2, SVR less than or equal to 600 dyn.s.cm-5 and oliguria) and were given NE as a single agent (0.9 +/- 0.2 micrograms kg-1.min-1). The other 12 patients had Cl less than 3.5 l.min-1.m-2 and were given a combination of dobutamine (12 +/- 0.09 micrograms.kg-1.min-1) and NE (1.1 +/- 0.2 micrograms.kg-1.min-1). The latter drug was added since systemic vascular resistance (SVR) was less than 600 and oliguria persisted while on dobutamine. In all patients, during NE infusion SVR was greater than 700 dyn.s.cm-5, Cl greater than or equal to 4.5 l.min-1.m-2 and Do2 greater than 550 ml.min-1.m-2. Urine flow was significantly increased during NE infusion, and only four patients remained oliguric. Anion gap and oxygen consumption were not modified. A complete resolution of septic shock was seen in 16 out of 23 patients (70%). Hospital mortality was 56%.     

急性胆道感染休克病人麻醉处理（附54例报告）

报道54例急性胆道感染休克病人的麻醉处理，其中硬膜外麻醉26例；静脉复合全麻25例；中药麻醉1例，局麻加强化麻醉1例，神经安定镇痛麻醉1例，并就术前准备，术中管理和麻醉的选择进行了初步讨论。     

一氧化氮检测在新生儿败血症中的应用

为探讨一氧化氮（ＮＯ）在新生儿败血症中的作用，测定了２０例新生儿败血症外周血亚硝酸／硝酸根离子（ＮＯ２＾－／ＮＯ３＾－）水平。结果表明：新生儿败血症外周血ＮＯ２＾－／ＮＯ３＾－水平与肿瘤坏死因子水平密切相关（Ｐ＜０．０５）。８例外周血ＮＯ２＾－／ＮＯ３＾－水平高于２００μｍｏｌ／Ｌ者，６例发生休克；其余１２例ＮＯ２＾－／ＮＯ３＾－水平低于此标准者，无一例发生休克，差别显著（Ｐ＜０．０５）。本文显示     

Effects of α1-acid glycoprotein in different rodent models of shock

Summary— It was the aim of the present study to investigate the effects of the acute phase protein α₁-acid glycoprotein in different models of shock. The human plasma preparation used was without effect on mortality in lipopolysaccharide-injected mice when administered in two different doses (1 or 0.33 g/kg iv) and according to different treatment schedules. The same preparation significantly increased survival rate (48 h) in rats with septic peritonitis. This effect was seen when α₁-acid glycoprotein (200 mg/kg iv) was given 15 min prior to and 24 h after cecal puncture. All other dose regimes tested were without significant effect on survival rate. A hemorrhagic/hypovolemic shock model (including a defined trauma) in rats resuscitated with 200 mg/kg α₁-acid glycoprotein resulted in significantly higher values of mean arterial blood pressure, cardiac output and stroke volume when compared to corresponding values obtained after resuscitation with Ringer's solution or 200 mg/kg albumin iv (free of α₁-acid glycoprotein; placebo formulation). Taking all other possible mechanisms of α₁-acid glycoprotein into consideration, the partially protective effects of the preparation are explained by enhancing the capillary barrier function and thereby maintaining perfusion of vital organs.     

内毒素休克发生机制的实验研究(内脏微血管中微聚物的电镜观察)

本实验用狗静脉注射灭活大肠杆菌,取其肺、肝、肾、心肌组织,采用超薄切片法和冷冻断裂法作TEM和SEM观察。结果发现,内毒素休克早期肺、肝、肾的微血管内均有以血小板为主的微聚物出现。内毒素休克晚期,微聚物逐渐演变,导致DIC。后者对休克的恶化及多发性器官功能衰竭的形成起着重要作用。     

Plasminogen concentrations and functional activities and concentrations of plasmin inhibitors in plasma samples from normal subjects and patients with septic shock

Plasma levels of plasminogen (Pg), α₂-antiplasmin (α₂AP), α₂-macroglobulin (α₂M) and α₁-antitrypsin (α₁AT) together with “immediate” (IAP) and “total” (TAP) antiplasmin activities and fibrin-(ogen)-degradation products (FDP's) were determined in samples from ten healthy volunteers and eight patients with septic $\text{shock}$. Samples were also examined for α₂AP-plasmin complexes. Five patients who died had significantly reduced Pg and α₂AP levels and IAP and TAP activities. Samples from two patients contained α₂AP-plasmin complexes. Three patients who recovered had lower Pg concentrations than normal, but significantly higher Pg concentrations than the patients who died. These patients also had normal antiplasmin activities and significantly higher α₂AP levels than the fatal group. Plasma samples from one recovery patient contained α₂AP-plasmin complexes. α₂M levels were significantly lower and α₁AT levels significantly higher than normal in both groups of patients. Samples from all patients taken during septic shock contained FDP's. These results confirm that the fibrinolytic system is activated during septic shock and in sepsis of fatal outcome a pronounced consumption of Pg and α₂AP occurs. In our limited number of recovery patients the fibrinolytic system appeared to have been less activated.