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PubMed1998

Leucine metabolism in rat liver after a bolus injection of endotoxin.

To evaluate the contribution of hepatic tissue to alterations in the metabolism of proteins and the branched-chain amino acids (BCAA) leucine, isoleucine, and valine in systemic inflammatory response syndrome, we studied the changes of leucine metabolism in isolated perfused liver (IPL) of endotoxin-treated rats. Male albino rats were injected with the endotoxin of Salmonella enteritidis (5 mg x kg(-1)) or saline (control). Four hours later, leucine and ketoisocaproate (KIC) oxidation and incorporation into liver proteins were determined in IPL using the single-pass liver perfusion technique. L-[1-(14)C]leucine and alpha-keto[1-(14)C]isocaproic acid were used as a tracer in two separate experiments. Endotoxin treatment resulted in a decrease of plasma BCAA levels, an increase of leucine oxidation, and a decrease of KIC oxidation by IPL. Leucine incorporation into liver proteins was lower in endotoxin-treated rats, and we did not find measurable incorporation of the labeled carbon of KIC in liver proteins in either group of animals. The sum of individual amino acid concentrations in the effluent perfusate was higher in endotoxin-treated animals, although only leucine and phenylalanine increased significantly. The decrease in KIC oxidation indicates a decreased capacity of hepatic tissue to oxidize branched-chain ketoacids (BCKA). The increase in leucine oxidation by IPL of endotoxin-treated rats indicates an increase in BCAA aminotransferase activity. These changes demonstrate an important response of the body that enables the resynthesis of essential BCAA from their ketoanalogs delivered to the liver from peripheral tissues, particularly muscle.

Amino Acids, Branched-Chain↗
PubMed1997

Obstructive jaundice in rats results in exaggerated hepatic production of tumor necrosis factor-alpha and systemic and tissue tumor necrosis factor-alpha levels after endotoxin.

BACKGROUND: Obstructive jaundice (OJ) predisposes patients to postoperative sepsis. We determined whether OJ led to an increased endotoxin stimulated tumor necrosis factor-alpha (TNF-alpha) production by macrophage-rich organs and whether a lack of intraluminal gut bile contributed to this increased sensitivity. METHODS: Rats underwent laparotomy and common bile duct ligation and division (CBDL) or sham operation after they were given low-dose endotoxin or saline solution (NS). TNF-alpha levels in plasma, perfusate from the isolated perfused rat liver, and tissue from lung, spleen, and liver were measured 90 minutes later. An additional group underwent creation of a choledochal-vesical fistula and endotoxin administration. RESULTS: The plasma TNF-alpha, liver perfusate TNF-alpha, and the tissue TNF-alpha levels in liver, lung, and spleen were significantly elevated in the CBDL + endotoxin (CBDL + ETX) group compared with the SHAM + ETX and CBDL + NS groups (p < 0.05). The choledochal-vesical fistula group after endotoxin had plasma TNF-alpha levels only 27% that of the CBDL + ETX group (p < 0.05). CONCLUSIONS: OJ sensitizes macrophage-rich organs to produce larger amounts of TNF-alpha in response to endotoxin. This sensitization is not solely due to decreased intraluminal gut bile.

Animals↗
PubMed1978

Accelerated ovum transport in rabbits induced by endotoxin II. Changes in oviductal smooth muscle activity.

Oviductal mortility, measured with open-ended perfused catheters in anesthetized animals injected with human Chorionic Gonadotropin (hCG), is depressed 2 h following endotoxin injection and returns to control levels by 3 h after endotoxin injection. This decrease in motility is prevented by indomethacin. Endotoxin did not affect spontaneous or phenylephrine (PE)-induced contractions of oviduct when it was added to the bathing medium of in vitro tissues. Oviductal segments removed 2 h after endotoxin (26 h after hCG) showed electrical activity confined to the ampullary-isthmic-junction (AIJ), where ova were located; the dose-response curve for PE was shifted to the right and the maximum contraction was depressed. Activity of tissues removed 4 h after endotoxin more closely resembled control tissues except that the maximum contraction to PE was depressed, ova had passed out of the oviduct and a proovarian bias in the isthmus was not present. The response of the oviduct to prostaglandins (PGs) in vivo is critically dependent on the previous exposure to PGs. In endotoxin-treated animals PGE then PGF levels increase and the decrease in motility coincides with increased PGE levels, but accelerated ovum transport with the return of motility and activation of the isthmus.

Animals↗
PubMed1995

Ability of bacterial endotoxin to diffuse through human dentin.

An in vitro system was developed to determine whether bacterial endotoxin is capable of diffusing through dentin without the use of filtration pressure. Cavities were prepared in five third molar teeth in order to produce a split chamber device consisting of occlusal and pulpal chambers with 0.5 mm of intervening dentin. Endotoxin was introduced into the occlusal chamber and the effluent in the pulpal chamber was sampled every 30 min for 5 h and at 24 h using the limulus lysate assay. In four specimens the initial appearance of endotoxin in the effluent ranged from 15 min to 4 1/2 h. In two specimens the concentration of endotoxin in the effluent leveled off in 4 1/2 and 5 h, respectively, whereas in another two the concentration continued to increase throughout the experiment. In one specimen no endotoxin was detected. The results indicate that endotoxin is capable of passing through 0.5 mm of dentin.

Aggregatibacter actinomycetemcomitans↗
PubMed1992

Endotoxin and gram-negative bacteria in the rat periapical lesions.

The purpose of this study was to measure the amount of endotoxin as well as to identify Gram-negative bacteria in experimental periapical lesions in rats. Molar pulps were exposed and infected and the amount of endotoxin in the periapical tissue of the right mandibular first molar was measured by Endospecy, while the colony number of Gram-negative bacteria was determined in the same region of the left mandibular first molar. In the control animals, the amount of endotoxin in the periapical tissues did not change at all during the experimental period, and no Gram-negative bacteria were isolated. In the experimental animals, the amount of endotoxin in the periapical tissues increased gradually from 1 to 70 days, and its level was significantly greater than that of control animals after 7 days. Gram-negative bacteria were isolated from the periapical tissues and their number gradually increased from 1 to 14 days (26 to 82%), but decreased at 21 days. It was approximately 60% from 28 to 70 days. The results of this study showed that the amount of endotoxin in the periapical tissues gradually increased with increasing time and that Gram-negative bacteria were isolated from the same region but did not increase in number concurrently with the increase in the amount of endotoxin.

Animals↗
PubMed2002

Increase in milk metalloproteinase activity and vascular permeability in bovine endotoxin-induced and naturally occurring Escherichia coli mastitis.

An endotoxin-induced mastitis model was used to study permeability changes associated with increased milk matrix metalloproteinase (MMP) activity in early inflammation. One quarter of two cows was inoculated with endotoxin (Escherichia coli 055:B5). Blood, milk, and whey were collected before and repeatedly after inoculation for 48 h. The profile and amounts of gelatinolytic MMPs were determined by zymography; gelatinase A (72 kD MMP-2) and gelatinase B (92 kD MMP-9) were identified by Western immunoblotting. Bovine serum albumin (BSA) and trypsin inhibitor capacity (TIC) were used as markers of capillary permeability with parallel examination of neutrophil penetration from blood to milk. Five clinical E. coli mastitis milk samples and five milk samples from cows with healthy udders were analyzed to detect whether increased levels of gelatinolytic MMP-2 and MMP-9 have a role in naturally occurring mastitis with endotoxin involvement. Milk MMP levels increased 2h after the endotoxin challenge. Both MMP-2 and MMP-9 were involved in this early proteolytic event. These increased MMP levels are associated with increased capillary permeability, evidenced first by the penetration of small molecular weight proteins, such as BSA and TIC. Later, 6-12h post endotoxin inoculation, neutrophilic leucocytes also entered the site, as they require larger tissue damage in basal membrane and interstitial tissue structures than BSA and TIC to extravasate. In naturally occurring disease, increased MMP-2 and MMP-9 levels were detected in milk. Thus, gelatinases, especially MMP-2, are involved in the early degradation of the blood-milk barrier, which precedes the penetration of blood-derived cellular components into milk in endotoxin-induced mastitis. In the future, measuring MMP in milk/whey might be a useful tool for diagnosing early mastitis.

Animals↗
PubMed1997

Modulation of endotoxin-induced inflammation in the bovine teat using antagonists/inhibitors to leukotrienes, platelet activating factor and interleukin 1 beta.

A leukotriene biosynthesis inhibitor (MK886), a platelet-activating factor (PAF)-receptor antagonist (WEB 2086), a recombinant human interleukin-1 receptor antagonist (IL-1ra) and a polyclonal antibody to recombinant bovine IL-1 beta (anti-rBoIL-1 beta) was used to investigate the involvement of leukotrienes, PAF and IL-1 beta during endotoxin-induced inflammation in the bovine teat cistern. Endotoxin alone was infused into one teat cistern and endotoxin in combination with an inhibitor/antagonist was infused into another teat cistern of the same animal. Teat cistern samples were taken before infusion and at 3.5 and 7 h after infusion, and the numbers of neutrophils were counted. Saline infusion was used as control. The inhibitors/antagonists were also tested in combination with leukotriene B4 (LTB4), PAF and rBoIL-1 beta, respectively. MK886 or WEB 2086 significantly reduced the accumulation of neutrophils mainly between 3.5 and 7 h after infusion, indicating roles for leukotrienes, probably LTB4, and PAF in neutrophil accumulation during endotoxin-induced inflammation. As WEB 2086 also reduced cell accumulation between 0 and 3.5 h, PAF was implicated also in the early influx of neutrophils. WEB 2086 almost completely inhibited PAF-induced cell accumulation between 0 and 3.5 h. LTB4 did not induce significant cell accumulation in the teat cistern. IL-1ra did not affect endotoxin-induced neutrophil accumulation whereas anti-rBoIL-1 beta reduced total cell accumulation and, to some degree, accumulation between 0 and 3.5 h after infusion. Infusion of IL-1ra significantly inhibited cell accumulation induced by rBoIL-1 beta. Anti-rBoIL-1 beta also significantly reduced neutrophil accumulation induced by rBoIL-1 beta, but to a lesser degree. The results suggest roles for leukotrienes, most likely LTB4, and PAF, and to a lesser extent IL-1 beta, during endotoxin-induced neutrophil migration into the bovine teat cistern. The potential of the inhibitors/antagonists as therapeutic agents for bovine mastitis should be investigated.

Adjuvants, Immunologic↗
PubMed2001

Removal of tightly bound endotoxin from biological products.

The method for endotoxin removal described in this paper is useful for separation of tightly bound endotoxin from biological products, particularly those produced in Escherichia coli in the form of inclusion bodies for which a denaturation step is required to solubilise the product. We employed guanidine hydrochloride and ammonium sulphate in combination with hydrophobic interaction chromatography (HIC). These conditions enable binding of the endotoxin to the matrix, giving unbound product in the column flow-through. This makes the method generally applicable to biological products. An endotoxin reduction of about 3.7 logs was achieved; from as much as 1,100,000 EU mg(-1) in the solubilised material to about 200 EU mg(-1) in the product purified by this method. The method was developed for a cervical dysplasia vaccine, a fusion protein comprising L2, E7 and E6 from Human Papilloma Virus type 16, because both conventional and commercially available methods of endotoxin removal were ineffective in removing the tightly bound endotoxin from this product.

Chromatography↗
PubMed1996

Bacterial endotoxin-induced gene expression in the choroid plexus and paraventricular and supraoptic hypothalamic nuclei of the sheep.

The febrile and neuroendocrine responses to circulating endotoxin are effected, at least in part, by a central action of prostaglandins with interleukins serving as intermediaries. Data from rodents suggest that prostaglandin and interleukin (IL-1 beta) synthesis in response to endotoxin challenge may occur within the circumventricular organs of the brain, especially the choroid plexus; the present study investigated this possibility using the sheep as an experimental model. A pyretic dose of bacterial endotoxin (40 micrograms lipopolysaccharide) was given intravenously to sheep (n = 5) and the effect on gene expression in the choroid plexus after a 40 min interval was compared with that observed in vehicle-treated animals (n = 5) using in situ hybridisation histochemistry. Evidence of activational and synthetic events following endotoxin administration was provided by significant increases in c-fos (P < 0.05) and IL-1 beta (P < 0.01) mRNA expression. Constitutive cyclooxygenase (cox-1 mRNA) and inducible cyclooxygenase (cox-2 mRNA) synthesis were unchanged. The investigation also sought to provide evidence for endotoxin effects on neuroendocrine activity in this species by examining changes in hypothalamic gene expression. The results showed that c-fos mRNA increased in the paraventricular (P < 0.01) and supraoptic (P < 0.05) nuclei and that CRH mRNA was upregulated in the paraventricular nucleus (P < 0.001). However, in agreement with previous work, there was no change in vasopressin gene expression although oxytocin mRNA was enhanced throughout the paraventricular nucleus (P < 0.05). These findings suggest the following: (1) possible involvement of the choroid plexus in the response of sheep to immunological challenge: (2) endotoxin-induced changes in gene expression in the ovine hypothalamus similar in those caused by other stressors: and (3) possible changes in oxytocin synthesis concomitant with fever in the sheep.

Animals↗
PubMed2003

Escherichia coli endotoxin enhances acute renal failure in rats after thermal injury.

This study was designed to evaluate the burned rat model to determine whether there are any differences in endotoxin-sensitive kidney functions between an infant rat (10-day-old pup) and an adult rat (10-week-old rat). Renal failure was observed in the infant burned rat and histological changes showed the adhesion of inflammatory cells in the glomerular capillaries and vacuolar changes in the renal proximal tubular cell. A horseradish peroxidase (HRP) tracer experiment suggested that the intestinal barrier damage of the infant burned rat was more severe than that of the adult burned rat. Therefore, more bacterial translocation of the intestinal flora, rich in endotoxin, might be expected in the infant versus the adult rats. Renal failure was not observed in the adult burned rat, so we investigated to determine the effects of endotoxin on the kidney function of the adult burned rat with low lethal lipopolysaccharide (LPS) or carrageenan (CAR). CAR is known to increase sensitivity to the lethal effects of endotoxin in rodents. Our present data demonstrated that renal failure was observed in the LPS- or CAR-treated adult burned rat and LPS- and CAR-treated adult rat (non-burned). These results show the possibility that endotoxin enhances renal failure in a burned rat model and provide additional support for the hypothesis that postburn renal failure is mediated, in part, by endotoxin associated with bacterial translocation.

Acute Kidney Injury↗
PubMed2003

Effect of endotoxin treatment on the expression of cyclooxygenase-2 and prostaglandin synthases in spinal cord, dorsal root ganglia, and skin of rats.

Peripheral inflammation causes upregulation of cyclooxygenase in the spinal cord and subsequent increase in prostaglandin biosynthesis. However, prostaglandin synthases, which are downstream of cyclooxygenase control the type of prostaglandin that is formed predominantly. Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats. Endotoxin (2 mg/kg i.p.) induced the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in spinal cord, dorsal root ganglia, and skin as determined by reverse transcription polymerase chain reaction. In contrast, basal expression of lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia was not significantly altered by endotoxin. Dexamethasone (1 mg/kg s.c. at -18 h and -1 h) attenuated the effect endotoxin on the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in all tissues investigated, but did not significantly influence expression of lipocalin prostaglandin D synthase mRNA in spinal cord and dorsal root ganglia. In situ hybridisation histochemistry showed endotoxin-induced expression of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA throughout gray and white matter of spinal cord sections. In dorsal root ganglia, expression of membrane bound prostaglandin E synthase seemed primarily located to non-neuronal cells, while cyclooxygenase-2 messenger RNA was not detectable. The results show that the immune response elicited by endotoxin induced cyclooxygenase-2 and membrane bound prostaglandin E synthase, but not lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia of rats. The distribution of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA expressing cells suggests major involvement of non-neuronal cells in spinal prostaglandin biosynthesis. Determination of the regulation of enzymes downstream of cyclooxygenase at the messenger RNA level may represent a valuable tool to investigate effects of analgesic/anti-inflammatory drugs on the regulation of spinal prostaglandin biosynthesis.

Animals↗
PubMed2003

Thymulin reverses inflammatory hyperalgesia and modulates the increased concentration of proinflammatory cytokines induced by i.c.v. endotoxin injection.

The immunomodulatory thymic hormone thymulin has been shown previously to possess anti-inflammatory actions in the periphery. In this study, we have examined the effect of i.c.v. injections of either endotoxin (ET) or thymulin, in separate groups of conscious rats, on pain-related behavior and cytokine levels in different areas of the brain. Furthermore, we investigated the effect of pretreatment with either i.c.v. or i.p. injections of thymulin on endotoxin-induced hyperalgesia and the effect of pretreatment with i.c.v. thymulin on endotoxin-induced up-regulation of cytokine levels. Our results demonstrate that i.c.v. injection of endotoxin (1 microg in 5 microl saline) resulted in a significant decrease in the nociceptive thresholds as assessed by different pain tests, with peak hyperalgesia at 3 h. However, thymulin at different doses, when injected (i.c.v.), had no significant effect on pain related behavior. Pretreatment (i.c.v.) with thymulin (0.1, 0.5 and 1 microg in 5 microl saline) 20 min before endotoxin (i.c.v.) injection (1 microg in 5 microl saline) reduced, in a dose dependent manner, the endotoxin-induced hyperalgesia and exerted differential effects on the up-regulated levels of cytokines in different areas of the brain. The results provide behavioral and immunochemical characterization of a rat model for intracerebral inflammation and indicates a neuroprotective role for thymulin in the CNS.

Animals↗
PubMed2002

Potentiation of tumor metastasis in adulthood by neonatal endotoxin exposure: sex differences.

Previous research in rodents has demonstrated that neonatal exposure to bacterial endotoxin alters the hypothalamic-pituitary-adrenal (HPA) axis resulting in hypersecretion of corticosterone in response to stress in adulthood. Given the known interactions between glucocorticoids and the immune system we tested the hypothesis that such alterations may impact on immune outcomes. Male and female Fischer 344 neonate rats were treated with endotoxin (0.05 mg/kg lipopolysaccaride from Salmonella enteritidis) or vehicle on days 1, 3, 5 and 7 postpartum. In adulthood, animals were subjected to chronic stress and the effect on resistance to tumor colonization (Exp. 1), natural killer (NK) cell activity (Exp. 2), and HPA reactivity (Exp. 3) was assessed. Neonatal endotoxin treatment was found to significantly impair NK cell activity and decrease resistance to tumor colonization in male but not female rats (P<0.05). Neonatal endotoxin exposure did not affect corticosterone responses to chronic stress in male or female rats, but the corticosterone response to acute stress was potentiated by endotoxin exposure, most notably in females. In conclusion, neonatal endotoxin exposure was found to be associated with a sexually differentiated impairment in tumor colonization and NK activity and long-term alterations in corticosterone responses to stress. The effect on tumor colonization and NK activity was not, however, critically mediated by corticosterone levels. These findings suggest that neonatal bacterial infections may have long-term health implications, specifically in terms of resistance to cancer spread in adulthood.

Animals↗
PubMed2001

Method for reducing endotoxin in Moraxella catarrhalis UspA2 protein preparations.

The UspA2 protein from the bacterium Moraxella catarrhalis is a potential vaccine candidate for preventing human diseases caused by this organism. Before a vaccine can be administered parentally, the level of endotoxin must be reduced as much as possible. However, in this case the endotoxin was very tightly complexed with the UspA2 protein and could not be dissociated with Triton X-100. It was found that it dissociated from the protein with the zwitterionic detergents Zwittergent 3-12 and Zwittergent 3-14. The endotoxin could then be separated from the protein by either ion-exchange or gel filtration chromatography. Using the limulus amoebocyte lysate assay for quantitation, the endotoxin was reduced approximately 20,000-fold. The removal of residual endotoxin from UspA2 preparations had no detrimental effect on the immunological properties of the protein. Mouse antisera raised against UspA2 prior to, and following endotoxin reduction exhibited comparable antibody and bactericidal titers against the tested strains. Further, mice immunized with both preparations, followed by pulmonary challenge with either a homologous or a heterologous isolate, exhibited comparable levels of clearance.

Animals↗
PubMed1997

Membrane adsorbers for selective removal of bacterial endotoxin.

Surface-modified flat-sheet microfiltration membranes were functionalised with poly-L-lysine, polymyxin B, poly(ethyleneimine), L-histidine, histamine, alpha-amylase and DEAE as well as deoxycholate. Their suitability to remove endotoxin from both buffers and protein solutions was examined using bovine serum albumin, murine IgG1 and lysozyme as model proteins. In protein-free solutions reduction from 6000 EU/ml to <0.1 EU/ml was achieved with all applied ligands; only alpha-amylase as well as L-histidine and histamine, when immobilized via the non-ionic spacer bisoxirane, exhibited low clearance factors at neutral pH. The adsorption of endotoxin is mainly ruled by electrostatic interaction forces. Thus in multi-component systems, such as endotoxin-contaminated protein solutions, competing interactions take place: acidic proteins compete with endotoxin for binding sites at the membrane adsorbers, basic proteins compete with the ligands for endotoxin and act as endotoxin carriers. With properly chosen conditions the membrane adsorbers presented here show exceptional effectiveness also in the presence of proteins. They are generally superior to functionalised Sepharose chromatographic sorbents and allow fast processing. They may contribute to reduce the risks in the application of parenterals and diagnostics.

Adsorption↗
PubMed2003

Endotoxin inhibition of luteinizing hormone in sheep.

Administration of endotoxin suppresses circulating concentration of luteinizing hormone (LH) in a number of species, including rats, sheep, cattle, and non-human primates. Specifically, endotoxin administration decreases circulating concentration of LH and LH pulses frequency in castrated male sheep. Endotoxin could alter circulating concentrations of LH via actions at the hypothalamus through altered GnRH production and/or release, or endotoxin could alter circulating concentrations of LH at the level of the pituitary via inhibition of LH production and release or inhibition of LH in response to GnRH. The site of endotoxin suppression of circulating concentrations of LH as well as possible mediators of endotoxin suppression of circulating concentrations of LH, including cortiocotropin-releasing hormone, arginine vasopressin, glucocorticoids, inflammatory cytokines, prostaglandins, and opioids, are discussed.

Animals↗
PubMed2003

Pavlovian conditioning of endotoxin-tolerance in rats.

The most fascinating example of the bi-directional interaction between the central nervous system (CNS) and immune system is the behavioral conditioning of immune functions. We therefore investigated the behavioral conditioning of lipopolysaccharide (LPS)-induced endotoxin tolerance using the taste aversion paradigm. The conditioned stimulus (CS) saccharin was paired with the unconditioned stimulus (UCS) LPS over a five (CONDl) or four (COND2) days learning trial. Controls received drinking water with (SHAM) or without (UNT) LPS. Endotoxin tolerance was tested by determination of LPS-induced tumor necrosis factor (TNF)-alpha release. After the avoidance of the induced endotoxin-tolerance the CS saccharin was re-presented in all experimental groups. A the end of the re-exposure period a complete endotoxin tolerance was noticed in the CONDl- and COND2-group. In contrast, no effect of saccharin administration was observed in the SHAM- or UNT-group. Our data demonstrate for the first time the behavioral conditioning of endotoxin tolerance. Furthermore, these results contribute new aspects to the mechanisms underlying the development and modulation of endotoxin tolerance.

Animals↗
PubMedDate not supplied

Effects of total parenteral nutrition on endotoxin translocation and extent of the stress response in burned rats.

Postburn endotoxin translocation has been well documented. However, the relationship between the secretion of catabolic hormones, degree of endotoxin translocation, and intestinal atrophy has not been previously demonstrated. In this experiment, modulation of the secretion of catabolic hormones according to the route of nutrient administration was examined in burned animals. A total of 55 rats, with and without a burn injury, were orally or parenterally fed. Urinary excretion of epinephrine and norepinephrine (U-EN) of each rat was measured for 48 h after burn injury as an indicator of the stress response. Evaluations of intestinal atrophy and endotoxin contents in the liver and spleen were also done 48 h after burn injury. U-EN after burn injury in rats administered total parenteral nutrition (TPN) was higher than in those fed orally. Endotoxin translocation and intestinal atrophy after thermal injury were also augmented by TPN. A significant positive correlation between U-EN and endotoxin content of the liver, and a negative correlation between U-EN and weight of the intestine, were observed. TPN enhances the stress response after burn injury. An increase in endotoxin translocation and intestinal atrophy by TPN are closely related to enhancement of the stress response.

Animals↗