失血性休克对猪一氧化氮与内皮素的影响

目的 探讨内源性一氧化氮（NO）与内皮素（ET）在失血性休克中的变化及其意义。方法 14头体重为14～17kg的健康雄性家猪,随机均分为失血性休克组（H组）和对照组（C组）。H组按照Wigger’s改良法制作失血性休克模型,经股动脉快速放血使MAP降至40mmHg,维持90min,然后回输血液及等量的复方氯化钠。C组处理同H组,但未放血。各组分别在休克前、休克末、复苏末、复苏后30、60、120、240min记录MAP、HR、CVP、肺动脉压（PAP）、肺动脉楔压（PCWP）的变化,同时测定血浆NO与ET水平以及动脉血乳酸盐浓度（Lac）的变化。结果 H组休克末MAP、PAP和CVP降低而HR升高,PCWP无显著变化。血浆NO水平在休克后逐渐升高,复苏后60min显著高于休克前和C组水平（P〈0．05）,此后一直维持较高水平,240min时达到高峰;休克后ET水平显著增加,并显著高于C组及休克前（P〈0．05）,复苏后逐渐下降。结论 失血性休克后血浆NO、ET水平增加,在失血性休克的病理生理过程可有一定意义。     

RheA对失血性休克大鼠血管反应性的调节作用

目的 观察Rhea在失血性休克大鼠血管反应性调节中的作用.方法 采用sD大鼠复制休克模型,取离体血管环和原代血管平滑肌细胞(VSMC),观察在休克不同时期血管反应性的变化以及RheA活性调节剂对失血性休克后大鼠离体血管环和VSMC收缩反应性的影响.结果 在休克早期和短暂缺氧后,离体血管环和VSMC对NE收缩反应性均有所升高,其Emax和60 min累计渗透率分别为(1.684±0.101)S/mg组织和68.99±6.83,RhoA的激动剂U-46619可进一步升高休克早期或短暂缺氧后血管反应性,RhoA特异性抑制剂C3enzyme可明显降低休克早期和短暂缺氧所引起的血管收缩反应性的升高,其Emax和60 min累计渗透率分别为(0.736±0.112)g/mg组织和53.91±5.53.而在休克晚期或长时间缺氧后,离体血管环和VSMC对NE收缩反应性明显降低,其Emax和60 min累计渗透率分别为(0.608±0.045)g/mg组织和38.53±4.87,RhoA激动剂U-46619可明显升高休克晚期或长时间缺氧所致血管反应性的降低,Emax和60 min累计渗透率分别为(0.934±0.110)g/mg组织和57.99±6.83,U-46619的这一作用可被RheA抑制剂C3enzyme所拮抗.结论 休克后血管反应性呈双相变化,休克早期升高,休克晚期降低,Rhea参与了休克血管反应性的调节.     

Glucocorticoid effects on gluconeogenesis during hemorrhagic shock

This study was undertaken to determine if there was evidence of impaired gluconeogenesis during shock and to test the effectiveness of steroids on gluconeogenesis during such conditions. Hemorrhagic shock in previously adrenalectomized rats was produced by bleeding the animals to a mean arterial pressure of 40 mm Hg, which was maintained for 2 hr. Liver and kidney slices from control animals and from animals in shock were prepared and incubated under aerobic conditions for 3 hr at 37°C in Krebs-Henseliet bicarbonate buffer containing 10 mM alanine or glutamine in the presence or absence of steroids. Following incubation, glucose and urea production in the medium was measured. Hydrocortisone addition at 10^?7M increased the quality of glucose and urea appearing in the medium by 16% in the presence of control slices as well as in the presence of slices from animals in shock. The addition of 10^?4M hydrocortisone inhibited gluconeogenesis by 30%, whereas with 10^?2M hydrocortisone there was complete inhibition of gluconeogenesis with both groups of slices. Similar results were obtained using dexamethasone or hydrocortisone 21-sodium succinate. Thus, basal gluconeogenic capability was unaltered during shock in an adrenalectomized animal and steroids were as effective in stimulating or inhibiting gluconeogenesis during hemorrhagic shock as they were under control conditions.     

重组血红蛋白对大鼠失血性休克的治疗效果

目的 探讨两种重组血红蛋白及清蛋白对失血性休克的治疗效果。方法24只大鼠随机等分为3组,由股动脉抽血建立失血性休克模型,保持平均动脉压(MAP)40 mm Hg45 min。休克后对照组输入人体清蛋白(HSA),其他两组分别输入重组血红蛋白rHb 1.1和rHb 2.0。测定休克前后不同时间点MAP、肠系膜上动脉血流、股动脉血气和肠系膜上静脉血气值。结果 rHb 1.1输入后30rainMAP显著高于休克前(P<0.01)和其他两组(P<0.05);在休克后各时间点上,肠系膜上动脉血流量接近休克前水平,但显著低于rHb2.0和HSA组(P<0.01)。重组血红蛋白可恢复并维持MAP休克前水平60-90min,清蛋白只能维持30min。动脉及肠系膜上静脉血气分析显示两种重组血红蛋白治疗效果相似,显著高于HSA组(P<0.05)。结论 重组血红蛋白治疗失血性休克效果优于清蛋白,rHb 2.0是较理想的血液替代品。     

The residual effects of hemorrhagic shock on pain reaction and c-fos expression in rats

To investigate the residual effects of hemorrhagic shock on pain reaction and c-fos expression, we performed formalin tests after hemorrhage and reinfusion in rats. Twenty adult male Sprague-Dawley rats were divided into Control (n = 10) and Postshock (n = 10) groups. The mean blood pressure of the Control group was 100-120 mm Hg, and that of the Postshock group was kept at 50-60 mm Hg for 30 min by draining blood. After 15 min of returning mean blood pressure to normal levels in the Postshock group, 10% formalin (3.7% formaldehyde solution, 100 microL) was injected into the left rear paw of both groups. Nociceptive behaviors were observed for 1 h after the formalin injection. The rats were killed at 2 h after the formalin injection, and the lumbar spinal cord was then stained for c-fos immunohistochemistry by using the avidin-biotin-peroxidase method. Animals in the Postshock group showed considerably less nociceptive behavior than those in the Control group. C-fos expression in the deep layer (IV-VI) of the spinal cord was significantly less in the Postshock group. In conclusion, decreases of nociceptive behaviors and c-fos expression were observed under normotensive conditions after hemorrhagic shock. The mechanisms governing these reactions remain unclear. IMPLICATIONS: Formalin tests were performed after hemorrhage and reinfusion in rats. A stress-induced analgesia was observed under normotensive conditions after hemorrhagic shock. The mechanisms remain unclear.     

The pathophysiology of irreversible hemorrhagic shock in monkeys

Irreversible shock was produced in pig-tail monkeys by hemorrhaging them to a mean arterial pressure of 40 mm Hg and maintaining that pressure until (15%) “uptake” of blood signaled decompensation. Reinfusion of the remainder of the blood, plus additional lactated Ringer's solution restored hemodynamic function and urine flow temporarily, but in spite of continuing and increasing crystalloid infusions, refractory circulatory failure ensued, characterized by decreasing mean arterial pressure, widening pulse pressure, decreased systemic vascular resistance, progressive hemodilution, diminished systemic oxygen transport, and narrowed arteriovenous oxygen differences. Cardiac outputs were normal or supranormal, central venous, right atrial, and pulmonary artery pressures were well sustained and left atrial and left ventricular end diastolic pressures were normal or low indicating that neither inadequate venous return nor cardiac failure were to blame. Significant anatomic systemic arteriovenous shunting did not occur but either abnormal oxygen transport or inability of cells to utilize oxygen seemed likely. Regional blood flows, with the exception of renal, splenic, and bronchial flows were restored to normal in the postresuscitative period and myocardial adrenal, hepatic, and intestinal flows became supranormal. The pattern observed is unlike that after endotoxin administration and may provide a clue to the identity of the factor(s) responsible for this vasomotor collapse.     

Beneficial effects of fructose 1,6 diphosphate on hemorrhagic shock in rats

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The homeostasis assessment by hemorrhagic shock

The comparative analysis of different protocols of infusion therapy of the hemorrhagic shock stage III was performed. The infusion of the colloid solution of hydroxiethylstarch 200/0.5 and non-balanced crystalloid 0.9% solution of natrium chloride leads to the development of negative changes in homeostasis. Whereas infusion of the 4% solution of the modified gelatin and balanced crystalloid solition (sterofundin) allows to avoid the registered changes in electrolyte and alkaline balance.     

Vasopressin in hemorrhagic shock

We describe the treatment of two patients with hemorrhagic shock unresponsive to volume replacement and catecholamines. Both patients responded to a small-dose infusion of vasopressin, which allowed tapering off of the catecholamines. The possible role of small-dose infusions of vasopressin in fluid- and catecholamine-resistant hemorrhagic shock is discussed.     

The cardiocirculatory and metabolic effects of endotoxin challenge after canine resuscitated hemorrhagic shock

Although adequate volume resuscitation has decreased mortality from hemorrhagic shock, recovery in many patients is complicated by sepsis. To determine whether a subject debilitated by hemorrhagic shock would exhibit greater cardiocirculatory dysfunction when challenged with sepsis, ten dogs (Group I) were hemorrhaged to a mean arterial blood pressure of 30 mm Hg. After 2 hours of hypotension, shed blood and lactated Ringer's solution (50 ml/kg) were given, and the dogs were observed for 3 to 6 days. Ten dogs were sham hemorrhage and served as controls (Group II). On the experimental day, all cardiovascular and hemodynamic parameters were measured in both groups of animals before endotoxin challenge. There was no significant difference in cardiac output, stroke volume, stroke work, +dP/dt max, myocardial blood flow, myocardial oxygen metabolism, or acid-base balance in the two groups. Compared to sham-hemorrhaged dogs, resuscitated shock dogs had a significantly lower mean arterial blood pressure (127 +/- 7 vs. 110 +/- 6 mm Hg; p less than 0.05), and heart rate was significantly higher (86 +/- 6 vs. 109 +/- 7 beats/minute; p less than 0.05). Furthermore, maximal rate of left ventricular pressure fall (-dP/dT max) was significantly lower in the animals previously hemorrhaged, suggesting a persistent defect in left ventricular relaxation. Blood glucose and insulin levels were significantly elevated in the resuscitated shocked dogs, likely due to increased circulating catecholamine concentrations and enhanced glycogenolysis. Endotoxin shock caused significant hypotension, acidosis, and impaired regional perfusion in all dogs. In addition, cardiac output, stroke volume, dP/dT, and left ventricular end-diastolic pressure fell and hyperglycemia and hyperinsulinemia occurred in all dogs after endotoxin injection.(ABSTRACT TRUNCATED AT 250 WORDS)     

氨基胍在重度失血性休克中的应用研究

目的：研究氨基胍（AG）在重度失血性休克中的治疗效果。方法：采用兔失血性休克－复苏模型,分为休克组,AG组（复苏时应用AG）,观察休克前后血浆内毒素（ET）,肿瘤坏死因子（TNF）－α,白细胞介素（IL）－6,IL－8,一氧化氮（NO）的变化,观察动物24,48h存活率。结果：兔失血性休克后,血浆内毒素,TNF－α,IL－6,IL－8,NO水平明显升高;复苏后,AG组动物血浆中上述物质水平明显低于休克组,该组动物的存活率明显高于休克组。结论：内毒素血症,TNF－α,IL-6,IL-8,NO在失血性休克的发展过程中起着重要作用,AG作为诱导型一氧化氮合酶（iNOS)抑制剂,有助于改善重度失血性休克的预后。