低压复苏对非控制性出血性休克的作用

目前国内外的动物实验和部分临床研究结果显示，低压复苏是治疗非控制性出血性休克较为合理的方案，但还没有人从增加血容量，减少应激反应引起的血管收缩、改善组织微循环氧供方面进行研究。本研究拟观察低压及低压扩容复苏对腹腔实质脏器损伤非控制性出血性休克的治疗效果。     

高渗氯化钠右旋糖酐溶液在休克治疗中的作用

高渗氯化钠右旋糖酐溶液（ＨＳＤ）对休克期间血流动力学的改善归因于对血容量的恢复，与单独应用高渗氯化钠和右旋糖酐７０溶液相比较，ＨＳＤ对血容量扩充的程度和持续的时间都更为明显。ＨＳＤ输注后可改善内脑微循环，增加组织灌流量。ＨＳＤ适用于出血性休克或低血容量状况的早期容量复苏，此外，对感染性休克、颅脑创伤、烧伤的治疗亦极为有利。治疗剂量为４ｍｌ／ｋｇ时一般对机体无明显不良影响。     

失血性休克期间器官血流量的变化

本文研究了氯胺酮麻醉犬出血性休克期间器官血流量的变化。杂种犬７只，放血２６７±２０．５８ｍｌ，休克持续４５ｍｉｎ，用电磁血流量计测得失血性休克期间肝动脉血流量、门静脉血流量、右肾动脉血流量、颈内动脉血流量降低非常显著，心率显著增快。     

高渗氯化钠右旋糖酐溶液在休克治疗中的作用

高渗氯化钠右旋糖酐溶液(HSD)对休克期间血流动力学的改善归因于对血容量的恢复,与单独应用高渗氯化钠或右旋糖酐70溶液相比较,HSD对血容量扩充的程度和持续的时间都更为明显。HSD输注后可改善内脏微循环,增加组织灌流量。HSD适用于出血性休克或低血容量状况的早期容量复苏,此外,对感染性休克、颅脑创伤、烧伤的治疗亦极为有利。治疗剂量为4ml/kg时一般对机体无明显不良影响。     

出血性休克的扩容和茛菪类药疗法

休克是由于微循环灌流不足并以细胞代谢障碍为特征的严重病理生理综合征。出血而致休克,循环血量最少要缺失15～25％以上。我们基于失血性休克病理生理和微循环障碍的特点,提出以莨菪类药改善微循环的液体疗法。一、微循环障碍大量失血后组织灌流显著障碍,灌流的毛细血管数比失血前静息状态减少了50～70％,残存灌流的血液变化也有明显异常。在出血性休克的动物骨骼肌内,微循环改变如图1所示:     

氯胺酮在出血性休克术中的应用

出血性休克行急诊手术,麻醉有一定困难,在积极输血、输液同时,宜选用对循环无抑制或抑制轻的麻醉药。氯胺酮镇痛作用强,给药方便,对循环有兴奋作用,许多作者推荐用于出血性休克的急诊手术麻醉。现将我院1984年1月至1986年8月在出血性休克急诊手术中应用此法共49例作一小结。临床资料男性38例,女性11例。病种有多处伤19例,上消化道出血19例,女性以宫外孕致失血性休克11例。年龄最小为19岁,最大为62岁。     

类固醇类激素在出血性和创伤性休克中的作用

动物实验表明,药理剂量的类固醇类激素有助于实验性内毒素性休克和临床上感染性休克的治疗。这两种休克均可伴有DIC,而DIC的毒性效应对其病发率和死亡率均起着重要作用。药理剂量的类固醇类激素在治疗出血性休克中的有益作用尚缺乏证据。如果将狗制以创伤并引起非致死性出血性休克,产生DIC后即死亡。制以这种创伤导致大量溶血,从而可使非致死性出血性休克狗死亡。给予少量自体溶血血液将与创伤所致溶血的作用相同。这种溶血血液的作用如同凝血酶原物,它在出血性休克时可导致DIC。因此,创伤(或溶血)加     

氯胺酮在出血性休克麻醉中的应用

出血性休克存在血容量不足,在此情况下行急症手术麻醉有一定困难,诱导期因心血管受抑制血压将进一步下降,甚至循环骤停。对于这类病人,在积极输血输液的同时,宜选用对循环无抑制或抑制轻的麻醉药物。当前认为氯胺酮较为理想,它镇痛性能强、给药方便、对循环有兴奋作用,许多作者推荐适用于出血性休克病人,现综述于下。     

肠道是出血性休克后脓毒症的来源

鼠严重出血性休克期间有相当数量发生菌血症,所有存活48小时以上的动物血培养均为阳性,大部分细菌为革兰阴性,提示细菌可能来源于胃肠道。本实验应用~(14)C-油酸标记大肠杆菌观察低血压后易位肠道细菌的来源。取体重350～450g雄性S-D大鼠,出血性休克实验组(组1)15只,假休克对照组(组2)5只。实验前48小时在轻度氯胺酮麻醉下用1ml注射器及18号导管     

发生于出血性休克期及休克后的菌血症

20多年来,出血性休克与脓毒性休克被作为两个病种来加以研究。为了探讨两者的关系,作者设计了一种出血性休克模型。他们用40条体重为300～400g的雄性Sprague-Dawley鼠,在氯胺酮腹腔麻醉下作股动脉插管,导管上接一可旋转接头并固定在挽具上,让鼠清醒后能自由活动。以肝素化乳酸钠林格液加20％葡萄糖作连续滴注,给鼠以每日所需的电解质、液体和     

Role of the pancreas in stability of mitochondrial function in hemorrhagic shock

The pancreatectomized rats showed the more rapid depletion of energy stores during hemorrhagic shock than the non-pancreatectomized animals. In pancreatectomized rats the oxidative and phosphorylative activities of the mitochondria decreased markedly to about 40% of the preshocked levels at 1 hr after hemorrhagic shock, though those in control rats remained almost unchanged. The decreases in mitochondrial oxidative and phosphorylative activities and hepatic energy charge levels in pancreatectomized rats were not restored by the reinfusion of the shed blood after 1-hr hemorrhagic shock. Thus, it is suggested that the pancreas plays an important role in hepatic energy metabolism during hemorrhagic shock, possibly due to maintaining the integrity of mitochondrial membrane.     

Hyperoxic condition prevents bacterial translocation and elevation of plasma microorganism components during hemorrhagic shock.

To evaluate the influence of hyperoxic conditions on bacterial translocation (BT) and microorganism components during hemorrhagic shock, rats were divided into a group breathing 100% oxygen and a group breathing room air. The groups were then subjected to hemorrhagic shock. Systemic blood and mesenteric lymph nodes were cultured for BT, and systemic plasma concentrations of microorganism components were measured by the silkworm larvae plasma (SLP) test and the endotoxin test. Hyperoxic conditions prevented both BT and plasma SLP-reactive substance (peptidoglycan and beta-glucan) elevation during hemorrhagic shock. Our findings suggest that hyperoxic treatment might improve host conditions during hemorrhagic shock.     

The gut as source of sepsis after hemorrhagic shock

In a model of severe hemorrhagic shock in rats, blood culture findings became positive within 2 to 4 hours of shock. The organisms cultured were primarily gram-negative. To test the hypothesis that the gut was the source of the bacteria, E. coli labeled with carbon-14 oleic acid were fed to rats undergoing hemorrhagic shock. Their plasma was then assayed for carbon-14 activity. Seven of the 14 shocked animals demonstrated increased plasma carbon-14 activity during or after shock. The mortality rate was 100 percent 80 hours postshock, and all animals had E. coli on subsequent blood culture. The seven rats without increased plasma carbon-14 activity had a survival rate of 83 percent postshock. Sham-shocked animals did not exhibit plasma carbon-14 levels greater than the background levels. These data suggest that bacterial translocation occurs during hemorrhagic shock and that the gut is the source of the bacteremia seen during hemorrhagic shock.     

Effects of various catecholamines on high-energy phosphates of rat liver and brain during hemorrhagic shock measured by31p-NMR spectroscopy

The effects of dopamine, epinephrine and norepinephrine on energy metabolism as well as intracellular pH in rat liver and brain during hemorrhagic shock were examined by in vivo ³¹P-NMR spectroscopy. The hemorrhagic shock was induced by arterial bleeding to a mean arterial pressure (MAP) of 30–40mmHg. Upon the induction of hemorrhagic shock, there was a dramatic fall in adenosine triphosphate (ATP) and a rise in inorganic phosphate (Pi) in the liver. The intracellular pH indicated severe acidosis. However, no change in these parameters was observed in the brain during hemorrhagic shock. After infusion of the above catechollamines following 10min of hemorrhagic shock, MAP increased to 90–100% of its control value. Only dopamine improved hepatic energy metabolism, whereas brain evergy metabolism was not affected by any of them. This suggests that dopamine protects liver function during hemorrhagic shock without affecting brain energy metabolism.(Okuda M, Muneyuki M, Sogabe T et al.: Effects of various catecholamines on high-energy phosphates of rat liver and brain during hemorrhagic shock measured by ³¹P-NMR spectroscopy. J Anesth 3: 200–209, 1989)     

Splanchnic blood flow response to intraaortic balloon pump assist of hemorrhagic shock

Hemorrhagic shock results in marked changes in splanchnic arterial blood flow. We studied the effects of intraaortic balloon pump assist (IABP) upon splanchnic blood flow during sustained hemorrhagic shock and following volume resuscitation. Hemorrhagic shock was induced (mean blood pressure = 30 mm Hg) for 120 min in 20 dogs. Controls (n = 11) underwent resuscitation with shed blood and lactated Ringers solution only. In the study group (n = 9), IABP was begun after 60 min of hemorrhagic shock and continued throughout a 90-min period after resuscitation. Hemodynamic parameters were assessed and splanchnic blood flow was estimated (radioactive microsphere technique) at baseline, through 120 min of sustained hypotension, and during the resuscitation period. Splanchnic blood flow was significantly reduced in both the control and the IABP groups during the period of hemorrhagic shock. Interestingly, the IABP group was found to have a return to preshock splanchnic viscera perfusion without the hyperemic reperfusion phenomenon seen in control animals resuscitated with shed blood and Ringers lactate alone. IABP assist of hemorrhagic shock appears to improve vasomotor control of splanchnic blood flow in this experimental preparation of shock. This may result in less reperfusion injury to the splanchnic viscera during the resuscitation of severe hemorrhagic shock.     

Choice of anesthetic alters the circulatory shock pattern as gauged by conscious rat endotoxemia

A standardized rat endotoxin shock model was used to assess the differential effects of four commonly used anesthetics upon hemodynamics before and during endotoxin shock. Forty-nine male Sprague-Dawley rats weighing 307 +/- 4 g were divided into five groups:freely-moving conscious, enflurane (2%), isoflurane (1.4%), pentobarbital (6 mg.kg-1.h-1 i.v.), and ketamine (45 mg.kg-1.h-1 i.v.). Anesthetic doses were chosen as 1.0 MAC equivalent. Anesthetized rats were intubated and ventilated with oxygen. The right carotid artery was cannulated with a thermocouple-catheter for aortic blood pressure, heart rate, and thermodilution cardiac output measurements. The right jugular vein was cannulated for measurement of central venous pressure and for i.v. injections. Data were collected over a 30-min baseline period and for 4 h after an i.v. bolus of endotoxin (40 mg.kg-1, LD100 within 24 h). Gross small intestinal pathology was rated on a 0-4 scale. Anesthetic effects were judged in terms of significant deviations from the awake data on each parameter. Despite differing patterns, total deviations were similar for enflurane, ketamine, and pentobarbital, although the latter drug was the least preferable due to particularly high systemic vascular resistance. Significantly less hemorrhagic small intestinal pathology occurred with enflurane. Ketamine offered no advantage over the inhalation anesthetics. Among the four anesthetics tested, results were closest to the awake pattern with isoflurane anesthesia, thus making it the logical choice for hemodynamic studies in experimental shock research.     

Comparative effects of autologous blood transfusion and isovolemic colloids transfusion on hemorrhagic shock: measurement of NO production and tissue oxygen pressure

Effects of autologous blood transfusion and isovolemic colloids transfusion on hemorrhagic shock model in rats were investigated. The hemorrhagic shock model in rats was prepared by rapid exsanguination and the blood pressure was kept at 40 mmHg for 30 min. As a marker of hemodynamic change, the blood gas analysis was performed, and the tissue oxygen pressure of the liver and the spleen was also measured. Furthermore, we analyzed the changes in NO production in the liver and the spleen of the hemorrhagic shock model. By hemorrhagic shock, Ht, HCO3-, base excess, and PaO2 levels decreased, and liver NO level, but not spleen NO, increased rapidly. However, the liver PtO2 did not show any changes during hemorrhagic shock, although the spleen PtO2 tended to decrease. These changes seen at the hemorrhagic shock were equally restored after the treatment with either autologous blood transfusion or isovolemic colloids transfusion. These results indicate that either autologous blood transfusion or isovolemic colloids transfusion can be useful for the therapy of severe hemorrhagic shock, and the NO production in the liver can participate in the maintenance of homeostasis under hemorrhagic shock.     

Effect of gastric cold irrigation on stress ulceration

Gastric cold irrigation is widely used in the treatment of gastric bleeding. The purpose of this study was that of studying the effect of cooling on gastric mucosal lesions induced by hemorrhagic shock. The gastric transmucosal potential difference (GTPD) and the severity of ulceration were assessed in rats subjected to continuous gastric irrigation with 0.1 N HCl at a temperature of 37 or 5 degrees C. The effect of gastric cooling was evaluated in basal conditions and in rats subjected to hemorrhagic shock. Although gastric cooling has been able to cause ulcers in basal conditions, it showed a protective effect during hemorrhagic shock, reducing the degree of ulceration and improving the GTPD recovery. It is likely that the decrease in cellular metabolic requirements induced by cooling plays an important role in mucosal protection during hemorrhagic shock.     

Effect of WEB 2086 on leukocyte adherence in response to hemorrhagic shock in rats

BACKGROUND: The pathogenesis of generalized microvascular injury after hemorrhagic shock is known to involve the generation of platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine [PAF]). The release of PAF is manifested in several ways, including by increased vascular permeability, altered vascular reactivity, and increased leukocyte adherence to the endothelium. WEB 2086 is a PAF antagonist that has been shown experimentally to improve survival after hemorrhagic shock. The purpose of this study was to examine the efficacy of WEB 2086 in attenuating leukocyte adherence before, during, and after hemorrhagic shock. METHODS: After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mm Hg for 30 minutes in urethane-anesthetized rats. Mesenteric venules in a transilluminated segment of the small bowel were examined to quantitate leukocyte adherence using intravital microscopy. RESULTS: In sham-operated rats (control), there was minimal to no leukocyte adherence throughout the experiment. Hemorrhagic shock resulted in a significant increase in leukocyte adherence postshock during resuscitation (10.9 +/- 1.8 cells/100 microm, p < 0.01) when compared with controls. WEB 2086, when given before shock, significantly attenuated leukocyte adherence (0.1 +/- 0.08 cells/100 microm, p < 0.01) when compared with hemorrhagic shock alone. This effect of WEB 2086 on adherence could be demonstrated even when it was given during (3.5 +/- 0.9 cells/100 microm, p < 0.01) and 10 minutes into (5.8 +/- 1.1 cells/100 microm, p < 0.05) hemorrhagic shock. CONCLUSION: Our findings suggest that WEB 2086 may be of therapeutic benefit against the microvascular damage sustained after hemorrhagic shock.