Endogenous endotoxemia in patients with liver cirrhosis--a quantitative analysis of endotoxin in portal and peripheral blood

In order to investigate the mechanism of endogenous endotoxemia (that is, endotoxemia observed in the absence of infection) in patients with liver cirrhosis, the concentration of endotoxin in the portal (PO-Et) and peripheral blood (PE-Et) from fifty three patients undergoing abdominal surgery was simultaneously measured by a quantitative endotoxin assay. The PE-Et of the patients with liver cirrhosis (19.8 +/- 20.2 pg/ml, n = 23) was significantly elevated, when compared with that of the patients without liver cirrhosis (9.2 +/- 5.1 pg/ml, n = 30), and was close to the normal range of PE-Et obtained from thirty healthy volunteers (7.2 +/- 4.1 pg/ml, n = 30). The PO-Et was also higher in the patients with liver cirrhosis than in the patients without liver cirrhosis. Moreover, PO-Et was significantly higher than PE-Et in all the patients (p less than 0.05). The per cent difference in the endotoxin concentration between the portal and peripheral blood (percentage of delta Et) was significantly decreased in the cirrhotic patients, especially in those with esophageal varices, which was well correlated with the phagocytic activity of the reticuloendothelial system (RES) determined by the clearance of iron colloid. The endogenous endotoxemia is thus likely to be due to the impaired clearance of endogenous endotoxin in portal blood, resulting from both the decreased phagocytic activity of RES in the liver and the coexisting porta-systemic bypass.     

Perioperative change of plasma endotoxin levels in early infants

As a preliminary study to elucidate the relationship of endotoxemia to postoperative morbidity, the plasma endotoxin levels in 64 surgical neonates were quantitated by the chromogenic limulus test (Toxicolor test; Seikagaku Kogyo, Tokyo, Japan). The preoperative levels of plasma endotoxin were 64 +/- 59 pg/mL in the group of infants with perforated peritonitis (n = 9), 63 +/- 51 pg/mL in the group of infants with gastroschisis (n = 7), and 15 +/- 16 pg/mL in the group of infants with ileus (n = 28), while the mean level was 6 +/- 5 pg/mL in the remaining 20 surgical neonates who had no signs of ileus or peritonitis. In the serial determination of plasma endotoxin in 28 neonates, the levels on the first postoperative day increased significantly compared with the preoperative levels (16 +/- 18 pg/mL to 46 +/- 25 pg/mL, P less than .01). They decreased gradually to 8 +/- 5 pg/mL within a week in 15 neonates who had no postoperative complications. However, in 13 neonates who had postoperative complications such as wound infection or postoperative ileus, the postoperative levels of plasma endotoxin increased to a much higher level and remained there. In this article the relationship of clinical endotoxemia to postoperative thrombocytopenia and hyperbilirubinemia is analyzed, and the usefulness of evaluating endotoxemia in surgical neonates is discussed.     

Development and reversal of endotoxemia and endotoxin-related death in obstructive jaundice

Gut-derived endotoxemia has been implicated in postoperative complications in patients with jaundice. It is thought that absence of bile in the gut predisposes to portal absorption of endotoxin and endotoxemia is reversed by oral bile salt replacement or internal biliary drainage and return of bile to the gut, but not by external drainage. We believe that the importance of gastrointestinal bile flow has been overestimated and biliary obstruction and the integrity of hepatocyte and Kupffer cell function are more important in the development and reversal of endotoxemia. In experiment 1, serum endotoxin concentrations were measured in control rats (n = 10) after choledochovesical fistula (n = 15) and bile duct ligation (n = 15) and after relief of biliary obstruction by internal drainage (choledochoduodenostomy; n = 8) and sterile external drainage (choledochovesical fistula; n = 8), with a quantitative limulus assay. In experiment 2, mortality rates were measured in similar groups 48 hours after administration of oral endotoxin (5 mg/100 gm) and intravenous lead acetate (5 mg/100 gm). Bilirubin levels were elevated in bile duct ligation (192 +/- 13 mumols/L) compared with control animals and those with choledochovesical fistula, internal drainage, and external drainage (10.6 +/- 1.5 mumols/L). In experiment 1, significant portal endotoxemia and systemic endotoxemia occurred in bile duct ligation (portal, 130.4 +/- 12.9 pg/ml; systemic, 91.8 +/- 11.0 pg/ml) but not in choledochovesical fistula (portal, 49.3 +/- 17.1 pg/ml; systemic, 27.2 +/- 11.5 pg/ml). Relief of obstruction by both internal and external drainage reversed endotoxemia. In experiment 2, significant death occurred in bile duct ligation (13 of 15) but not in choledochovesical fistula (3 of 15), and relief of obstruction by both internal and external drainage prevented death. These results confirm that biliary obstruction is a more important factor than is gastrointestinal bile flow in the development and reversal of endotoxemia.     

Endogenous endotoxemia in patients with liver cirrhosis —A quantitative analysis of endotoxin in portal and peripheral blood

In order to investigate the mechanism of endogenous endotoxemia (that is, endotoxemia observed in the absence of infection) in patients with liver cirrhosis, the concentration of endotoxin in the portal (PO-Et) and peripheral blood (PE-Et) from fifty three patients undergoing abdominal surgery was simultaneously measured by a quantitative endotoxin assay. The PE-Et of the patients with liver cirrhosis (19.8±20.2 pg/ml, n=23) was significantly elevated, when compared with that of the patients without liver cirrhosis (9.2±5.1 pg/ml, n=30), and was close to the normal range of PE-Et obtained from thirty healthy volunteers (7.2±4.1 pg/ml, n=30). The PO-Et was also higher in the patients with liver cirrhosis than in the patients without liver cirrhosis. Moreover, PO-Et was significantly higher than PE-Et in all the patients (p<0.05). The per cent difference in the endotoxin concentration between the portal and peripheral blood (percentage of ΔEt) was significantly decreased in the cirrhotic patients, especially in those with esophageal varices, which was well correlated with the phagocytic activity of the reticuloendothelial system (RES) determined by the clearance of iron colloid. The endogenous endotoxemia is thus likely to be due to the impaired clearance of endogenous endotoxin in portal blood, resulting from both the decreased phagocytic activity of RES in the liver and the coexisting porta-systemic bypass.     

Treatment of gut-derived endotoxemia with lactulose. An experimental study

Endotoxemia plays an important role in the origination and development of many dangerous clinical diseases, for which there has been little medication so far. To determine whether lactulose has an effect on endotoxemia, we treated experimental, gut-derived endotoxemia using lactulose in vitro and in vivo. The results showed that 55 mg lactulose inactivated the activity of 0.01 mg endotoxin on limulus lysate in vitro, suggesting that lactulose may have a direct anti-endotoxin effect. In vivo study in rats showed that blood endotoxin level was significantly decreased from 78.61 +/- 6.54 pg/ml to 20.26 +/- 2.38 pg/ml (P less than 0.01), and liver damage significantly reduced after lactulose treatment. It is suggested that lactulose can prevent absorbtion of endotoxin from gut and may have an effect on gut-derived endotoxemia. The mechanism of lactulose for treating endotoxemia is discussed.     

Gut endotoxin restriction prevents catabolic changes in glutamine metabolism after surgery in the bile duct-ligated rat.

OBJECTIVE: The objective of this study was to investigate the role of gut-derived endotoxemia in postoperative glutamine (GLN) metabolism of bile duct-ligated rats. SUMMARY BACKGROUND DATA: Postoperative complications in patients with obstructive jaundice are associated with gut-derived endotoxemia. In experimental endotoxemia, catabolic changes in GLN metabolism have been reported. Glutamine balance is considered important in preventing postsurgical complications. METHODS: Male Wistar rats were treated orally with the endotoxin binder cholestyramine (n = 24, 150 mg/day) or saline (n = 24). On day 7, groups received a SHAM operation or a bile duct ligation (BDL). On day 21, all rats were subjected to a laparotomy followed 24 hours later by blood flow measurements and blood sampling. Glutamine organ handling was determined for the gut, liver, and one hindlimb. Intracellular GLN muscle concentrations were determined. RESULTS: Compared to the SHAM groups, BDL rats showed lower gut uptake of GLN (28%, p < 0.05); a reversal of liver GLN release to an uptake (p < 0.05); higher GLN release from the hindlimb (p < 0.05); and lower intracellular muscle GLN concentration (32%, p < 0.05). Cholestyramine treatment in BDL rats maintained GLN organ handling and muscle GLN concentrations at SHAM levels. CONCLUSIONS: Disturbances in postoperative GLN metabolism in BDL rats can be prevented by gut endotoxin restriction. Gut-derived endotoxemia after surgery in obstructive jaundice dictates GLN metabolism.     

Measurement of operative plasma endotoxin levels in jaundiced and non-jaundiced patients

A study of portal plasma endotoxin levels was performed using a chromogenic limulus amoebocyte lysate (LAL) assay. The assay proved sensitive and reproducible. In only 1 of 25 healthy subjects was the systemic plasma endotoxin level above 100 pg/ml (equivalent Escherichia coli 0111B4). In 30 non-jaundiced patients undergoing surgery the mean (+SEM) portal plasma endotoxin level (60 + 9 pg/ml) was significantly higher (p less than 0.05) than the mean level in the systemic blood (46 + 6 pg/ml), supporting the concept of endotoxin absorption from the intestine into the portal blood. In 20 patients with obstructive jaundice undergoing surgery 42% of portal, 45% of inferior mesenteric and 35% of systemic venous plasma endotoxin levels were above 100 pg/ml. There were significantly higher levels in the portal (p less than 0.05) and inferior mesenteric (p less than 0.05) compared with the systemic blood. Neither the presence of malignancy nor the duration of surgery appeared to influence endotoxin absorption. The significance of raised plasma endotoxin levels in obstructive jaundice is discussed.     

Liver failure after hepatic resection

Pathophysiology of hepatic resection in 89 cases was investigated from the point of endotoxemia and phagocytic function in order to clarify the mechanism of postoperative liver failure. In the control group (n = 44) and the bile stasis group (n = 9) plasma endotoxin increased to 22 to 160pg/ml early after operation and decreased thereafter: but in the liver failure group (n = 10) it increased higher corresponding to high risk operation and the massive bleeding or anastomosis leakage. In control and bile stasis groups phagocytic K value, serum CH50, plasma fibronectin decreased to half of the preoperative level on the first postoperative day, and later improved. In liver failure group these levels decreased but never improved. Liver failure group was characterized by an irreversible platelets count decrease corresponding to the increase of serum bilirubin level. It was concluded that endotoxemia in the presence of a self defence system dysfunction is thought to be a trigger for organ failure.     

Determination of blood endotoxin in severely burned patients and its clinical significance

Since October 1985 to June 1987, in 12 severely burned patients with endotoxemia was observed by using a quantitative endotoxin assay of limulus amoebocyte lysate (LAL) test with a chromogenic substrate. Among the 12 patients, 4 died and 8 survived. The average age of dead group was 31.8 years (19-45 years), mean TBSA was 63% (58-80%) and mean I 18.5%. The survival group average age of survival group was 27.5 years (18-39 years), mean TBSA was 58% (18-85%) and mean I 24.4% (6-56%). The plasma endotoxin concentrations of burn patients in dead group were 105-571 pg/ml, significantly higher than that of survival group (30-240 pg/ml) and healthy human (6.44 +/- 1.96 pg/ml). It was found that the increase of endotoxemia was closely related to burn wound sepsis, positive of blood culture, systemic disseminated septicaemia. Systemic use of sensitive antibiotics may increase the level of blood endotoxin in severe gram-negative bacillus infection. Polymixin-B is an exception.     

Kupffer cell blockade, tumour necrosis factor secretion and survival following endotoxin challenge in experimental biliary obstruction

BACKGROUND: Gram-negative sepsis and its sequelae frequently complicate invasive procedures in patients with obstructive jaundice. In response to endotoxin, Kupffer cells secrete tumour necrosis factor (TNF), a pivotal early mediator of sepsis. An investigation was carried out into the specific role of Kupffer cell TNF secretion following endotoxin challenge in obstructive jaundice. METHODS: Survival following intraperitoneal administration of endotoxin (2.0, 0.02 and 0.0002 mg per 100 g) was determined in rats following bile duct ligation (BDL) or sham operation. Plasma TNF concentration was quantified following endotoxin administration (0.0002 mg per 100 g) at 1, 2 and 6 h. Subsequently, the effect of Kupffer cell blockade by gadolinium chloride on survival and plasma TNF concentration was assessed. RESULTS: Jaundiced animals showed a significantly increased mortality rate following intraperitoneal injection of endotoxin 2.0 mg per 100 g (BDL 100 per cent versus sham 0 per cent) and 0.02 mg per 100 g (BDL 70 per cent versus sham 0 per cent; P = 0. 002, Fisher's exact test). Median plasma TNF concentration was significantly greater in jaundiced animals 1 h after endotoxin administration (BDL 943 (interquartile range (i.q.r.) 211-3900) pg/ml versus sham 64 (i.q.r. 47-127) pg/ml; P = 0.002, Mann-Whitney U test). Kupffer cell blockade with gadolinium chloride increased the survival rate following endotoxin administration in BDL animals (BDL-GdCl3 100 per cent versus BDL-saline 40 per cent; P = 0.0003, Fisher's exact test) and decreased median plasma levels of TNF (BDL-GdCl3 88 (i.q.r. 0-1065) pg/ml versus BDL-saline 16 550 (1255-29 360) pg/ml; P = 0.002, Mann-Whitney U test). CONCLUSION: Kupffer cell blockade improved survival and suppressed systemic TNF activity after endotoxin challenge. In obstructive jaundice, hypersecretion of TNF by Kupffer cells may supplement systemic cytokine production and be responsible for significant complications.     

肝硬变患者门腔静脉分流术前后胰高血糖素水平的动态观察

目的 研究肝硬变门静脉高压症患者行门腔静脉分流术后血浆胰高血糖素水平的变化。方法 应用放射免疫分析法测定了１６例肝硬变门静脉高压闰行门腔静脉分流术和１６例对照组患者血浆Ｇｌｃ水平。     

Endotoxemia,disturbance of coagulation,and obstructive jaundice

A prospective study of coagulation disturbances and endotoxemia in 42 patients having major pancreatic or biliary surgery was performed. Endotoxin, soluble fibrin, and fibrin degradation products were measured before and after operation in 28 patients with obstructive jaundice and in 14 nonjaundiced controls. In the control group there was one death and no unexplained fever or postoperative hemorrhage. The jaundiced group had more complications: seven deaths, nine episodes of fever, and six episodes of hemorrhage. Soluble fibrin was detected only in patients with obstructive jaundice, in whom it occurred in 38 percent before operation. Positive endotoxin assay was as common in control patients as in the jaundiced group, but in the latter endotoxin was associated (p < 0.05) with increased FDP and soluble fibrin. Patients with endotoxin or increased FDP levels before operation for jaundice carry a poor prognosis (7 of 11 died). Preoperative bowel preparation in 16 of the jaundiced patients did not affect the outcome.     

Elevation of serum interleukin-18 levels and activation of Kupffer cells in biliary atresia

BACKGROUND/PURPOSE: Interleukin-18 (IL-18)/interferon-gamma-inducing factor (IGIF) is a novel proinflammatory cytokine that can induce interferon gamma (IFN-gamma). In addition, IL-18 enhances intracellular adhesion molecule-1 (ICAM-1) expression as well as Fas ligand (FasL) expression, and induces apoptosis in hepatic injury. The aim of this study was to clarify the potential role of IL-18 in the pathogenesis of the progressive inflammation and fibrosis in biliary atresia (BA). METHODS: Six children with BA before hepatic portoenterostomy (HPE), 13 with BA including 7 without jaundice and 6 with persistent jaundice after HPE, and 16 healthy controls were examined. Blood samples were obtained preoperatively from 6 patients, after HPE from 13, and after liver transplantation from 4. The IL-18 level was determined by an enzyme-linked immunosorbent assay (ELISA). Immunohistochemically, liver specimens from BA patients were studied using a monoclonal antibody to macrophage-associated antigen (CD68). RESULTS: IL-18 levels were elevated in the patients before HPE compared with those of the controls (349+/-54 pg/mL v. 138+/-13 pg/mL, P<.0001). After HPE, extremely high concentrations of IL-18 were observed in patients with persistent jaundice (532+/-95 pg/mL, P<.0001), and the IL-18 levels were significantly high even in the patients without jaundice (249+/-29 pg/mL, P<0.005). The high IL-18 level lasted for a long time even in the patients without jaundice after HPE. In contrast, the IL-18 levels immediately decreased after liver transplantation. Immunohistochemically, the number of CD68-positive Kupffer cells was significantly higher, and the size was larger in the livers of the patients than in the controls. The proliferation of CD68-positive cells was much more conspicuous in the liver specimens obtained during liver transplantation than in those at the time of HPE. CONCLUSIONS: Our findings showed elevation of serum IL-18 levels and activation of Kupffer cells in BA. IL-18 released from activated Kupffer cells might play an important role in the pathophysiology of the progressive inflammation and fibrosis in BA. Furthermore, IL-18 level may be related to the prognosis in patients with BA.     

Study on mechanism of onset of endogenous endotoxemia during obstructive jaundice--with special reference to involvement of biliary infection

To clarify how biliary infections affect onset of endogenous endotoxemia during obstructive jaundice, I tried to review the clinical result of 104 cases of obstructive jaundice, and conducted a Limulus test of portal and peripheral blood in 20 cases of obstructive jaundice and an animal study using 38 rabbits. In cases of obstructive jaundice complicated by biliary infections, clinical improvement of jaundice became significantly unfavorable, and the outcome of surgical operation was significantly inferior to the cases without biliary infections. The endotoxin positive rate in the portal blood of obstructive jaundice was 65% (13 of 20 cases), among which 10 cases (79.6%) was also positive in the peripheral blood. Of these 10 cases, 7 cases manifested endogenous endotoxemia with no infectious focus, and prognosis of these cases was poor. The endotoxin positive rate in portal blood of obstructive jaundice group was also significantly higher than that of non-jaundice group in animal study, and when the reticuloendothelial system was blocked, the endotoxin positive rate in the peripheral blood showed an increasing tendency. In the animal group with experimental cholangitis, all the endotoxin positive animals in the portal blood were also positive in the peripheral blood. This result suggests that biliary infections accelerate a decrease in the reticuloendothelial function during obstructive jaundice. From these results, endogenous endotoxemia seems to affect the onset of various complications during obstructive jaundice and unfavorable prognosis.     

Enteral administration of high-fat nutrition before and directly after hemorrhagic shock reduces endotoxemia and bacterial translocation

OBJECTIVE: To determine whether potential enhancement of endotoxin neutralization via high-fat enteral nutrition affects endotoxemia and bacterial translocation after hemorrhage. SUMMARY BACKGROUND DATA: Endotoxin and bacterial translocation due to gut barrier failure are important initiating events in the pathogenesis of sepsis after hemorrhage. Systemic inhibition of endotoxin activity attenuates bacterial translocation and distant organ damage. Triacylglycerol-rich lipoproteins constitute a physiological means of binding and neutralizing endotoxin effectively. We hypothesized that enhancement of triacylglycerol-rich lipoproteins via high-fat enteral nutrition would reduce endotoxemia and prevent bacterial translocation. METHODS: A rat model of nonlethal hemorrhagic shock was used. Hemorrhagic shock (HS) rats were divided into 3 groups: rats starved overnight (HS-S); rats fed with a low-fat enteral diet (HS-LF), and rats receiving a high-fat enteral diet (HS-HF). RESULTS: Circulating triacylglycerol and apolipoprotein B, reflecting the amount of triacylglycerol-rich lipoproteins, were elevated in HS-HF rats compared with both HS-S rats (P 相似文献   

Effect of Oral Glutamine Administration on Bacterial Tanslocation, Endotoxemia, Liver and Ileal Morphology, and Apoptosis in Rats with Obstructive Jaundice

Postoperative complications in patients with obstructive jaundice remain increased when associated with endotoxemia and the inflammatory response due to gut barrier failure. Administration of glutamine has been proposed to maintain the integrity of the gut mucosa and thus reduce bacterial translocation (BT), but the effects of this pretreatment on apoptosis and histologic morphology of various organs affected by BT in obstructive jaundice have not been studied. We therefore studied the effects of oral glutamine supplementation on endotoxemia, BT, liver and terminal ileal morphology, and apoptosis in an experimental model of obstructive jaundice. A total of 60 male Wistar rats were randomly divided into four groups of 15 each: I, controls; II, sham-operated; III, bile duct ligation (BDL); IV, BDL + glutamine (4.5 g/kg/day in drinking water). Ileal samples for histology, DNA and protein content, liver biopsies, mesenteric lymph nodes (MLNs) for culture, and portal and systemic blood samples for endotoxin measurements were obtained 10 days later. Compared to the controls, a significant increase in contaminated MLN and liver samples and increased endotoxemia were noted in group III (p < 0.01) but were significantly reduced in group IV (p < 0.05). Group IV also had a significantly higher number of mitoses per crypt (M/c) (p < 0.05), less apoptotic body counts (ABCs) (p < 0.05), and a higher DNA content than did group III (p < 0.05). Liver biopsies from group III displayed typical changes of large duct obstruction that significantly improved after glutamine treatment, with decreased ductular proliferation. We concluded that supplementation of oral glutamine in the presence of obstructive jaundice ameliorates BT, endotoxemia, and apoptosis and improves the ileal and liver histology.     

Endotoxemia and acute-phase proteins in major abdominal surgery

BACKGROUND: Translocation of endotoxin is a controversial issue. The ability of plasma to inactivate endotoxin is an indirect measure of endotoxemia. Endotoxin is a potent stimulator of the inflammatory response and affects the innate immune system. OBJECTIVE: To elucidate the kinetics of endotoxemia and the ability of plasma to inactivate endotoxin in patients with major abdominal operations. To demonstrate the early time course of the acute-phase proteins C-reactive protein (CRP), serum amyloid A (SAA), alpha(1)-antitrypsin, alpha(2)-macroglobulin, transferrin, and interleukin 6 (IL-6), and to correlate them with the amount of endotoxemia. METHODS: Twenty patients with elective major abdominal operation and 10 healthy controls were investigated. Blood was collected preoperatively, during the operation and regularly up to 12 days after surgery. Endotoxin was measured by Limulus amebocyte lysate test (LAL), the ability of plasma to inactivate endotoxin by modified LAL, the acute-phase proteins nephelometrically, and IL-6 by enzyme-linked immunosorbent assay (ELISA). RESULTS: Preoperative endotoxin plasma level (0.026 +/- 0.004 EU/mL) did not differ from healthy volunteers but increased during operation (0.09 +/- 0.02 EU/mL, P = 0.02). Endotoxemia peaked 1 hour after the surgical procedure (0.16 +/- 0.03 EU/mL; P <0.0001 versus preoperative) and decreased to almost normal values after 48 hours. The capability of plasma to inactivate endotoxin was significantly reduced during (recovery, 0.16 +/- 0.03 EU/mL), 1 hour (0.25 +/- 0.04 EU/mL) and 24 hours (0.16 +/- 0.02 EU/mL) after the operation compared with preoperative (0.068 +/- 0.01 EU/mL) values. Plasma IL-6 was significantly increased for 48 hours with a peak 1 hour after surgery (470 +/- 108 pg/mL). CRP peaked at 210 +/- 19 mg/L (P <0.0001 versus preoperative) 48 hours after operation and was significantly elevated for the rest of the observation period. SAA was significantly increased 24 hours after surgery (249 +/- 45 mg/L) and peaked additional 48 hours later (456 +/- 86 mg/L). alpha(1)-Antitrypsin, although a positive acute-phase protein, decreased initially to 1.38 +/- 0.1 g/L (preoperative, 2.33 +/- 0.18 g/L; P <0.0001) and increased thereafter until day 12 (3.05 +/- 0.35 g/L, P = 0.11 versus preoperative). The same was true for alpha(2)-macroglobulin (preoperative, 2.2 +/- 0.16 g/L; intraoperative, 1.36 +/- 0.13 g/L; day 5, 2.8 +/- 0.4 g/L). Transferrin decreased already during surgery (1.6 +/- 0.1 g/L versus preoperative 2.8 +/- 0.17 g/L, P <0.0001) and remained on this level for 5 days. Correlation analysis revealed a relationship between endotoxemia and the ability of plasma to inactivate endotoxin (r = 0.67, P <0.0001) and also a relation between intraoperative endotoxemia on one hand and alpha(2)-macroglobulin (-0.53 > r > -0.6, P <0.05) as well as alpha(1)-antitrypsin (0.64 > r >0.55, P <0.05) on the other. CONCLUSION: Major abdominal surgery is associated with transient endotoxemia and a transient reduced endotoxin inactivation capacity of the plasma. Endotoxemia correlates with the endotoxin inactivation capacity. The surgical procedure causes substantial changes in plasma concentrations of acute-phase proteins. alpha(2)-Macroglobulin and alpha(1)-antitrypsin correlate moderately with endotoxemia.     

Therapeutic Apheresis for Septic Patients with Organ Dysfunction: Hemoperfusion using a Polymyxin B Immobilized Column

A prospective clinical study was performed to evaluate a new method of treatment of endotoxin shock, a column containing polystyrene fibers with covalently bound immobile polymyxin B. Direct hemoperfusion using the column removes circulating endotoxin by adsorption. All of the patients studied, 37 in the treatment group and 33 in the control group, had endotoxemia and failure of 1 or more organs. The perfusion was performed 1–7 times per patient, 2 h/session. The survival rate was significantly higher in the treatment group (54%) than in the controls (36.4%). The mean plasma endotoxin concentration was significantly lowered by the treatment from 83.7 pg/ml before perfusion to 56.4 pg/ml immediately after and 28.5 pg/ml the day after the treatment, and the posttreatment level was much lower in those who survived (mean, 18.8 pg/ml) compared to those who died (mean, 88 pg/ml). Various parameters of cardiac function also improved after the treatment.     

肝细胞癌合并肝硬化患者肝脾联合切除术后免疫功能变化的研究

目的　探讨肝细胞癌合并肝硬化患者肝癌切除时联合脾切除术后免疫功能的变化。方法　将 16例肝癌合并肝硬化患者分成 2组 ,即肝癌切除联合脾切除组 ( 7例 )和单纯肝癌切除组 ( 9例 ) ,于术前、术后 2个月取外周血 7ml,采用流式细胞仪检测CD4、CD8、CD4 /CD8,ELISA法检测IL 2、IFN γ、IL 10。　结果　 2组患者术前CD4、CD8、CD4 /CD8、IL 2、IFN γ、IL 10水平差异无显著性 ;术后 2个月 ,切脾组CD4 ( 3 8 2 %± 3 7% )、CD4 /CD8( 1 7%± 0 3 % )高于保脾组CD4 ( 3 2 5 %± 4 0 % )、CD4 /CD8( 1 1%± 0 1% ) ,而CD8( 2 3 7%± 3 7% )低于保脾组CD8( 2 9 4 %± 4 0 % ) (P <0 0 5 ) ;切脾组IFN γ[( 10 4 4± 14 9)pg/ml]、IL 2 [( 98 6± 18 6)pg/ml]高于保脾组 [IFN γ( 70 5± 12 6)pg/ml、IL 2 ( 80 9± 13 5 )pg/ml],而IL 10 [( 5 5 5± 11 2 )pg/ml]低于保脾组 [IL 10 ( 89 4± 10 )pg/ml](P <0 0 5 )。　结论肝癌切除时联合脾切除不但没有降低机体T细胞亚群和Th细胞的平衡 ,反而促进其恢复平衡 ,并改善机体抗肿瘤免疫功能     

Effect of plaunotol on bacterial translocation in the rat small intestine

BACKGROUND AND AIMS: Bacterial translocation is precipitated by an increase in bacteria or endotoxin, depression of the membrane barrier, and an increase in mucosal permeability. Plaunotol is a mucosal protective agent, and observed to have a strong suppressive effect on superoxide production. In this study, the effect of plaunotol on bacterial translocation was examined using the model of ischemia and reperfusion. METHOD: Male Sprague Dawley rats were used to create the following model for evaluation of bacterial translocation: (i) the control group; (ii) the preventive dose group (plaunotol 30 mg/kg/day one week before surgery); (iii) the therapeutic dose group (plaunotol 30 mg/kg/day one week after surgery); and (iv) the full dose group (plaunotol 30 mg/kg/day one week before surgery and one week after surgery). Bacterial translocation was assessed as the blood concentration of the endotoxin. RESULTS: In the control group, the endotoxin increased significantly 3 days postsurgery (13.7+/-5.6 pg/ml) compared with before surgery (1.1+/-0.1 pg/ml). In the preventive and full-dose groups, the erndotoxin decreased significantly 3 days postsurgery (4.4+/-2.8 pg/ml, 5.7+/-2.7 pg/ml, respectively) compared with that of the control group. CONCLUSION: Plaunotol in the preventive and full-dose groups decreased the endotoxin. This suggests that plaunotol is one of the protectors for bacterial translocation.