深入开展烧伤后早期脏器损害的研究

严重烧伤后早期，由于微血管通透性增加，体液外渗，有效循环血量降低，导致微循环灌注不足，组织发生缺血、缺氧、能量代谢障碍，诱导细胞因子、炎症介质和蛋白酶的过度产生和激活，启动全身炎症反应，引起早期脏器损害。     

烧伤后“休克心”的研究

目的 探讨烧伤后休克心及其发生机制。方法 动物实验与临床研究相结合。采用心功能、心肌细胞损伤、细胞膜及骨架结构损伤、心肌生物力学、心肌病理等指标观测心肌损伤程度;通过心肌营养性血流量、心肌细胞氧利用、能量代谢及其释放的细胞因子等指标探讨其机制。靖暴严重烧伤后心功能、心肌力学指标、心肌营养性血流量、心肌细胞氧利用及能量代谢、心肌细胞黏弹性等均显降低,细胞膜及骨架结构受损,心肌纤维灶性溶解、断裂,血浆肌球蛋白轻链1、肌钙蛋白T及心肌组织细胞因子显增高。结论 严重烧伤休克期心肌即发生明显器质性损害,心肌缺血再灌流损伤、心肌细胞氧利用及能量代谢障碍、心肌组织水肿、失控性炎症反应等是发生休克心的主要机制。     

重视缺血缺氧与细胞因子在"休克心"发生机制中的作用

严重烧伤早期，各种原因引起的心肌损害并导致心功能减退、诱发或使烧伤休克加重的现象称为“休克心”。一方面，由于大量体液自血管内渗出或吸入性损伤引起呼吸功能障碍，直接造成心肌的缺血缺氧损害；另一方面，由于应激反应、再灌注损伤、失控性炎症反应等，致血管内皮细胞和中性粒细胞结构和功能改变，进一步引起微循环障碍，并使心肌细胞合成和释放细胞因子增多，由此加重心肌的缺血缺氧和心肌损害。     

细胞因子在重症急性胰腺炎发病机制中的作用

重症急性胰腺炎是胰酶异常激活引起的全身炎症反应,受损的胰腺组织可作为抗原或炎性刺激物,使免疫系统和炎症反应中活化的细胞产生炎症介质、细胞因子、促发细胞冈子的级联反应,从而使局部病变发展为全身性的病损过程.促炎因子介导并加重组织损伤,而抗炎因子则平衡前者的损伤作用.抗炎促炎因子的相互作用,导致抗炎反应和促炎反应失衡,全身炎症反应综合征的出现,甚至发展成为多器官功能障碍综合征.     

心肌损伤标志物与心脏手术预后的关系

心肌损伤标志物是心肌细胞受损后释放入循环的特异性蛋白,心脏手术术后患者心肌损伤标志物水平的异常改变与手术后患者的长期发病率和死亡率相关。心脏手术后监测心肌损伤标志物的改变有利于了解术后心肌损伤情况,对心脏术后患者危险程度分级和评价预后具有积极的价值。该文介绍围手术期心肌损伤标志物水平变化与心脏手术后患者预后之间的关系。     

烧伤大鼠心肌组织三磷酸腺苷酶活性和钙离子含量的变化

烧伤后心脏功能明显抑制可能与心肌细胞器质性损害有关。作者利用大鼠３０％ＩＩＩ度烧伤模型，研究了烧伤对心肌组织三磷酸腺苷酶活性和钙离子含量的影响。提示烧伤后心肌存在着能量代谢异常和离子泵功能障碍，造成心肌细胞反常性钙超载，进而导致心肌器质性损伤。     

心室辅助循环后心肌间质变化的研究进展

心室辅助使心室处于无负荷状态,改善缺血心脏血流动力学及能量代谢状况,不仅使心力衰竭引起的多器官功能衰竭得到改善,还使心脏功能及心肌细胞的损伤得到恢复。近年来通过对心肌间质的研究发现,心室辅助循环对心肌间质中的主要结构蛋白-型、型胶原及其代谢调节系统产生影响,使心肌间质胶原含量及分布发生变化,从而逆转不利的心肌间质重构,改善心功能。现就这一主题的相关研究进行综述。     

腹腔复苏治疗失血性休克的研究进展

失血性休克是指机体有效循环血容量下降导致脏器组织灌注缺乏,致使细胞代谢紊乱、功能下降,常见于大血管破裂、门静脉高压导致侧支循环出血、脏器破裂出血等,如不及时止血及补充血容量将危及生命.腹腔复苏（intraperitoneal染resuscitation,IR）又称为腹膜复苏,由美国路易斯维尔大学Zakaria及Garrison等[1-3]于2003年提出,是通过腹腔内注射液体使腹腔脏器血液循环得以恢复 来治疗休克,避免脏器衰竭的发生.腹腔复苏法为临床抢救失血性休克患者提供了新思路.     

极化型心脏停搏液研究进展

现代心脏手术中常规应用高钾溶液使心脏停搏.高钾停搏液的代表是St.Thomas液.其中的高钾成分使心肌细胞膜去极化,跨膜电位降低,不能形成和传播动作电位,心脏处于舒张期停搏.但细胞膜的去极化会导致持续性Na+/Ca2+窗口电流离子交换,引起持续性能量消耗和Ca2+超载,致使线粒体损伤、细胞死亡,引发术后心功能不良和缺血再灌注损伤[1].理想的心脏停搏液应使心肌细胞的跨膜电位处于极化状态,从而关闭离子通道,达到避免离子失衡和继发损伤的目的.细胞膜去极化程度越小,心肌保护的效果就越好,再灌注损伤的的程度就越轻[2].     

炎性介质与SIRS、CARS、MODS和CBP治疗

近年来研究证明机体的炎症细胞被各种损伤过度激活后产生大量的炎性介质,导致机体炎症反应失控是发生全身性炎症反应综合征(SIRS)、代偿性抗炎反应综合征(CARS)和多器官功能障碍综合征(MODS)的重要环节,而早期控制炎症反应,阻断其发展或有效清除循环中的炎性介质可能是防治SIRS和MODS的关键。因此,近年来研究连续性血液净化(CBP)对机体炎性介质的清除也成为一个热点。     

Intradialytic hypotension and splanchnic shifting: Integrating an overlooked mechanism with the detection of ischemia‐related signals during hemodialysis

In the most simple analysis, a patient's hematocrit during hemodialysis will rise when the rate of ultrafiltration exceeds the rate at which the fluid is mobilized from extravascular spaces; the greater the rise in hematocrit, the lower blood volume is and the more likely intradialytic hypotension (IDH) is to occur. A secondary mechanism of IDH may be due to sudden shift of blood volume away from the heart under conditions of borderline cardiac filling. A substantial portion of blood volume resides in the splanchnic venous system. During the early part of dialysis, a centripetal shift of red cells from this anatomical region to the central circulation has been documented to occur. The magnitude of this shift is unpredictable, and it may depend on the level of splanchnic vasoconstriction predialysis. The amount of splanchnic shift may also be reduced in patients with autonomic dysfunction. Once this central shift in blood volume has occurred, it can be reversed during further ultrafiltration due to ischemia‐induced release of vasodilatory molecules that cause dilation of upstream splanchnic arterioles; this causes increased transmission of arterial pressure to the splanchnic veins, acutely increasing their capacity. The increased splanchnic venous capacity may cause a sudden shift of blood away from the central circulation to fill these veins under conditions where cardiac filling has already been reduced. The result can be severe IDH due to insufficient cardiac filling and cardiac output. One fruitful preventive approach might be to continuously monitor the blood or dialysate for the sudden appearance of such ischemia‐related molecules or other signals which may herald not only dialysis hypotension but tissue stunning, warning that the fluid removal rate should be immediately reduced.     

液体治疗在急性肠梗阻治疗中价值及评价

肠梗阻是外科常见的急腹症之一，其救治的首要任务是通过液体治疗纠正因消化液丢失、炎症渗出增加导致的有效循环血容量不足，并稳定病人的血流动力学状态。因此，根据肠梗阻病人体液丢失的病理生理学特点，正确选择液体治疗的时机、液体量和成分以及科学合理地根据心脏前负荷、组织灌注和氧代谢评估液体治疗效果是优化肠梗阻液体治疗的关键。     

Importance of microcirculatory disturbances in the pathogenesis of pancreatitis.

Pancreatic microvascular control is a complex physiological process which is incompletely understood. Blood flow in the pancreas is altered by a large number of endogenous and exogenous factors in the context of acute and chronic pancreatitis. The frequency of progression from acute pancreatitis to a chronic form is a controversial question. In acute pancreatitis reductions in blood flow and alterations of microvascular integrity resulting in impaired tissue oxygenation play an important part in the progression and possibly the initiation of the disease. Endothelin and nitric oxide are believed to be two of the most effective vasoactive mediators. The beneficial effect of therapeutic strategies affecting vasoactive mediators is confirmed in experimental studies. Chronic disease is associated with decreased pancreatic blood flow and histological changes in the vasculature in both patients and animal models. Further studies are needed to clarify whether ischemia in chronic pancreatitis is more important in perpetuating the disease or as primary cause of the inflammatory processes.     

Pathophysiology of the burn wound

The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid oedema formation, due to increased microvascular permeability, vasodilation and increased extravascular osmotic activity. These reactions are due to the direct heat effect on the microvasculature and to chemical mediators of inflammation. The earliest stage of vasodilatation and increased venous permeability is commonly due to histamine release. Damage to the cell membranes partly caused by oxygen-free radicals released from polymorphonuclear leucocytes would activate the enzymes catalyzing the hydrolysis of prostaglandin precursor (arachidonic acid) with rapid formation of prostaglandin as the result. Prostaglandins inhibit the release of norepinephrine and may thus be of importance in modulating the adrenergic nervous system which is activated in response to thermal injury. The morphological interpretations of the changes in the functional ultrastructure of the bloodlymph barrier following thermal injury seem to be an increase in the numbers of vacuoles and many open endothelial intercellular junctions. Furthermore changes of the interstitial tissue after burn trauma are of great importance. The continuous loss of fluid from the blood circulation within the thermally damaged tissue causes increased haematocrit levels and a rapid fall in plasma volume, with decreased cardiac output and hypoperfusion on the cellular level. If the fluids are not adequately restored burn shock develops. Furthermore, the burn wound provides a vast area of entry of surface infection with a high risk of septic shock. Four main principles are of utmost importance in the current management of patients with severe thermal injury, namely early wound closure, prevention of septic complications, adequate nutrition and control of the external environment.     

Therapy for microcirculatory disorders in severe acute pancreatitis: Effectiveness of platelet-activating factor receptor blockade vs. endothelin receptor blockade

Many of the complications of severe acute pancreatitis are the result of the amplifying effects of microcirculatory disruption. The factors causing microcirculatory disorders in acute pancreatitis involve vasoactive mediators such as platelet-activating factor (PAF) and endothelin-1 (ET) activated during the inflammatory response to pancreatic injury. To further evaluate the potential therapeutic role of specific receptor antagonists (RA) to these mediators, the present study compares the effect of PAF and ET receptor blockade on microcirculation and organ function in a well-established rodent model of severe acute pancreatitis. Six hours after acute pancreatitis induction, rats were randomized to therapy with ET-RA (50 mg/kg LU-135252), PAF-RA (82 μg/kg WEB-2170), or NaCl 0.9% (volume equivalent). After 18 hours of fluid resuscitation, animals were relaparototnized for intravital microscopic determination of capillary blood flow, leukocyte rolling, and capillary permeability in the pancreas and colon. Other measurements included cardiorespiratory parameters, hematocrit, pleural effusions, ascites, urine production, and survival. Compared to saline treatment both ET-RA and PAF-RA significantly improved capillary blood flow in the pancreas and colon, reduced leukocyte rolling, and stabilized capillary permeability. The beneficial effects of receptor antagonist treatment on microcirculation were associated with decreased fluid loss into the third space, improved renal and respiratory function, and survival. Although both receptor antagonists likewise improved capillary blood flow, ET-RA was significantly more effective in counteracting leukocyte rolling and capillary leakage, thereby further reducing fluid sequestration. The present study confirms the beneficial effects of PAF and ET receptor blockade on microcirculation inside and outside the pancreas, organ function, and survival when given at the early stage of severe pancreatitis. Because ET-RA was more effective in stabilizing capillary permeability and avoiding subsequent fluid loss into the third space, we propose that ET-RA should be tested in a clinical trial (either in comparison or in addition to PAF-RA). Presented at the Thirty-Ninth Annual Meeting of The Society for Surgery of the Alimentary Tract, New Orleans, La., May 17–20, 1998.     

Volumenstatus und zentraler Venendruck

Values of intramural or even transmural central venous pressure (CVP) as well as values of pulmonary artery occluded pressure do not correlate with the values of measured circulating blood volume or with responsiveness to fluid challenge. The veins contain approximately 70% of the total blood volume and are 30 times more compliant than arteries, therefore, changes in blood volume within the veins are associated with relatively small changes in venous pressure. The main reason for a lack of correlation between CVP values and blood volume is that the body does everything possible to maintain homeostasis and adequate transmural CVP is a must for cardiovascular function. The most accurate measurement of volume status would be the mean circulatory filling pressure (MCFP), which cannot be measured in a clinical setting. Stressed volume determines MCFP and directly affects venous return and cardiac output whereas unstressed volume is a reserve of blood that can be mobilized into circulation when needed. Both stressed and unstressed volume cannot be adequately measured. Therefore, considering the complexity of the physiologic feedback and clinical picture, robust reflexes and homeostatic mechanisms, CVP is insufficient as a surrogate parameter for assessing the volume status.     

Perioperative fluid management: comparison of high, medium and low fluid volume on tissue oxygen pressure in the small bowel and colon

BACKGROUND AND OBJECTIVE: Insufficient blood flow and oxygenation in the intestinal tract is associated with increased incidence of postoperative complications after bowel surgery. High fluid volume administration may prevent occult regional hypoperfusion and intestinal tissue hypoxia. We tested the hypothesis that high intraoperative fluid volume administration increases intestinal wall tissue oxygen pressure during laparotomy. METHODS: In all, 27 pigs were anaesthetized, ventilated and randomly assigned to one of the three treatment groups (n = 9 in each) receiving low (3 mL kg-1 h-1), medium (7 mL kg-1 h-1) or high (20 mL kg-1 h-1) fluid volume treatment with lactated Ringer's solution. All animals received 30% and 100% inspired oxygen in random order. Cardiac index was measured with thermodilution and tissue oxygen pressure with a micro-oximetry system in the jejunum and colon wall and subcutaneous tissue. RESULTS: Groups receiving low and medium fluid volume treatment had similar systemic haemodynamics. The high fluid volume group had significantly higher mean arterial pressure, cardiac index and subcutaneous tissue oxygenation. Tissue oxygen pressures in the jejunum and colon were comparable in all three groups. CONCLUSIONS: The three different fluid volume regimens tested did not affect tissue oxygen pressure in the jejunum and colon, suggesting efficient autoregulation of intestinal blood flow in healthy subjects undergoing uncomplicated abdominal surgery.     

Comparison of Lipase Activity in Peritoneal Fluid of Dogs with Different Pathologies – A Complementary Diagnostic Tool in Acute Pancreatitis?

A clinical diagnosis of acute pancreatitis is often difficult to obtain. Histopathology remains the gold standard, whereas clinical signs, diagnostic imaging and laboratory testing, even in combination, may be insufficient. In a prospective study, lipase activity in ascitic fluid of various aetiologies was determined in 44 dogs in order to investigate its performance in cases of acute pancreatitis. Data of simultaneously determined blood lipase activities were available in 27 dogs. Lipase activity was measured by a colorimetric assay. A complete peritoneal fluid analysis was performed. Dogs were divided into four groups, according to their final diagnosis: acute pancreatitis (A), abdominal trauma (B), abdominal neoplasia (C) and others (hepatic or cardiac diseases) (D). Dogs with acute pancreatitis had a significantly higher peritoneal lipase activity than those in other groups (P ≤ 0.024), while no significant difference was found between the other groups (P ≥ 0.734). Blood lipase activity as well as protein content and total cell count of the ascitic fluid did not show any significant difference between groups. Data show that determination of lipase activity in dogs that develop ascites may be useful in complementing the diagnosis of acute pancreatitis.     

Splanchnic circulation following coeliac plexus block

Both the capacitance vessels and the resistance vessels of the splanchnic area are innervated by the sympathetic nerve fibers. We investigated the effect of abdominal visceral sympathectomy on splanchnic circulation, and the effect of altered splanchnic circulation on systemic circulation in ten mongrel dogs. Abdominal visceral sympathectomy was induced by coeliac plexus block with 1 ml/kg (body weight) of 1 % lidocaine infiltrated around the coeliac artery. Comparison was made with infiltration of physiologic saline of the same volume. The saline infiltration caused no significant changes in the hemodynamic parameters of systemic and splanchnic circulation. Mean arterial pressure decreased significantly from 18.2 ±2.0 to 14.4±1.9 kPa following the coeliac plexus block, with a concomitant decrease in the cardiac index from 2.63 ± 0.46 to 2.30 ± 0.54 1 × min^-1 × m^-2, while systemic vascular resistance was unchanged. Portal vein blood flow, hepatic artery blood flow and, therefore, splanchnic blood flow decreased by 8 to 17%. Portal vascular and hepatic artery resistances were not affected by abdominal sympathectomy. It was concluded that the capacitance vessels in splanchnic circulation are dilated during abdominal sympathetic denervation, causing a blood shift from systemic to splanchnic circulation. On the other hand, the resistance vessels in splanchnic circulation are affected little by abdominal visceral sympathectomy.     

通里攻下法治疗急性胰腺炎的机理研究

目的 探讨中医通里攻下法治疗急性胰腺炎的疗效原理。方法 回顾文献并加以综述。结果 通里攻下法治疗急性胰腺炎作用机理广泛,主要包括增强胃肠道运动功能;改善腹腔脏器血供和毛细血管通透性,促进炎症吸收;减少内毒素吸收,防治细菌移位;抑制全身炎症反应,保护组织器官;以及菌毒并治作用等。结论 通里攻下法在多个环节阻断或抑制了急性胰腺炎的病理生理过程,为其治疗急性胰腺炎提供了理论依据。