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PubMed1975

Endotoxic lipopolysaccharides stimulate steroidogenesis and adenylate cyclase in adrenal tumor cells.

Lipopolysaccharides (endotoxins) from Escherichia coli, Serratia marcesens and Salmonella typhosa stimulated steroid production in Y-1 adrenal tumor cells in culture with a latent period of 3-4 h. Lipid A, derived from Escherichia coli lipopolysaccharide, also stimulated steroidogenesis. Lipopolysaccharides and lipid A also stimulate adenylate cyclase activity and cause rounding of the cells. In contrast, lipopolysaccharides do not stimulate steroidogenesis in receptor-deficient adrenal tumor cells (OS-3) or Leydig tumor cells (I-10). This tends to rule out contamination by enterotoxin to which these lines respond. Although both hormone and lipopolysaccharide responses are lost in these lines, there was no interaction between these sites as judged by the failure of lipopolysaccharides to block, during their latency, the response to corticotropin in Y-1 cells. The possibility that the lipopolysaccharide effect is one on membrane conformation is discussed.

Adenylyl Cyclases↗

PubMed1995

Reduction of gastrointestinal injury in acute endotoxic shock by flurbiprofen nitroxybutylester.

Nitric oxide has been reported to have paradoxical effects in experimental endotoxic shock, contributing to the hemodynamic consequences of endotoxin administration, but apparently protecting the gastrointestinal mucosa. A novel class of nitric oxide-releasing nonsteroidal anti-inflammatory drug (NSAID) derivatives has recently been described which exert anti-inflammatory activities but produce significantly less gastrointestinal injury than the parent nonsteroidal anti-inflammatory drugs from which they are derived. Thus, the present study was performed to determine the effects of one of these derivatives, flurbiprofen 4-nitroxybutylester, compared to the native nonsteroidal anti-inflammatory drug, flurbiprofen, in an experimental model of endotoxic shock. Intravenous administration of endotoxin from Salmonella typhosa to rats pretreated with flurbiprofen produced a profound decrease in systemic arterial blood pressure, an increase in hematocrit and extensive gastric and small intestinal damage. In rats pretreated with flurbiprofen 4-nitroxybutylester, endotoxin produced comparable changes in blood pressure and hematocrit to those seen in rats treated with flurbiprofen; however, the severity of gastrointestinal damage was significantly reduced. Gastric blood flow was profoundly decreased following endotoxin administration, but was significantly higher in rats pretreated with flurbiprofen 4-nitroxybutylester than in rats pretreated with flurbiprofen. These results demonstrate that despite not affecting the acute systemic effects of endotoxin administration, flurbiprofen 4-nitroxybutylester is capable of protecting the gastrointestinal mucosa from injury, possibly through preservation of mucosal blood flow.

Animals↗

PubMed1997

Haemodynamic effects of dopexamine and nitric oxide synthase inhibition in healthy and endotoxaemic sheep.

Chronically instrumented awake healthy sheep (n = 6) received the synthetic catecholamine, dopexamine, during or without a background infusion of the nitric oxide synthase inhibitor. L-nitro-arginine-methylester (L-NAME). Three days later, hypotensive-hyperdynamic circulation was induced and maintained by continuous infusion of Salmonella typhosa endotoxin (10 ng/kg per min). After 24 h of continuous endotoxin infusion, the dopexamine L-NAME protocol was repeated. In healthy and endotoxaemic animals with and without nitric oxide synthase inhibition dopexamine caused the same haemodynamic changes: heart rate and cardiac output increased, mean arterial pressure and systemic vascular resistance decreased. L-NAME infusion induced normalisation of the hypotonic-hyperdynamic circulation in endotoxaemic animals. Dopexamine reduced some adverse effects of L-NAME treatment, like increased pulmonary vascular resistance and decreased oxygen delivery. In conclusion the haemodynamic effects of dopexamine are independent of the amount of nitric oxide production. Dopexamine may attenuate some of the adverse effects of nitric oxide synthase inhibition.

Adrenergic beta-Agonists↗

PubMed1981

Immunization against bacteria- and endotoxin-induced hypotension.

The characteristics of hypotension induced in rabbits by intravenous injection of viable Salmonella typhosa 0901 organisms were studied and found to be a function of the number and age of the bacterial cells. Effective neutralization of the blood pressure lowering was achieved by immunization with homologous organisms as well as heterologous endotoxins and a detoxified derivative. In addition, native endotoxins derived from a number of different genera of gram-negative bacilli, as well as lipopolysaccharides deficient in either the polysaccharide or lipid components, were tested for their ability to induce hypotension in rabbits and tolerance to the lowering of blood pressure. Hypotension was elicited by intravenous injection of all native endotoxins as well as polysaccharide-deficient endotoxins, but was absent in preparations from which the lipid was removed. On the other hand, protection against the hypotension effect could be induced after injection of either the lipid- or polysaccharide-deficient derivatives.

Animals↗

PubMed2004

Cloricromene in endotoxemia: role of NF-kappaB.

In this study we investigated, for the first time in vivo, the effect of cloricromene, a cumarine derivative, on NF-kappaB activation in endotoxin-treated rats. Endotoxemia was induced in male rats by the intravenous injection of Salmonella typhosa lipopolysaccharide (LPS; 2 mg/kg/i.v.). In vivo treatment with cloricromene (2 mg/kg/i.v.) 30 min before lipopolysaccharide administration reversed the LPS-induced loss in tone of the aortic rings, improved their reactivity to phenylephrine, decreased both nitric oxide (NO) and TNF-alpha serum levels by inhibiting LPS-induced inducible NO synthase and TNF-alpha mRNA expression, and interestingly inhibited LPS-induced NF-kappaB activation. Our data suggest that cloricromene protects rats from LPS by blocking LPS-induced NF-kappaB activation, leading to inhibition of NO and TNF-alpha overproduction and thereby reversing the LPS-induced vascular hyporeactivity.

Animals↗

PubMed1996

Abnormal activation of K+ channels underlies relaxation to bacterial lipopolysaccharide in rat aorta.

We have examined the role of K+ channels in mediating vasorelaxation produced by bacterial lipopolysaccharide (LPS) in endothelial-denuded strips of rat aorta precontracted with phenylephrine (1 microM). Salmonella typhosa LPS (0.1 microgram/ml) caused significant relaxation of tension which peaked at approximately 4hr. The K+ channel blocker, tetraethylammonium chloride (TEA; 10 mM), fully reversed these relaxations whether applied before or after long term exposure to LPS. L-arginine, the substrate for nitric oxide synthase, caused large relaxations in tissues incubated with LPS that were markedly inhibited by TEA. In contrast, TEA or L-arginine had little effect on phenylephrine contractions in control tissues. Furthermore, the inducible nitric oxide synthase inhibitor, aminoguanidine (0.4 mM), reversed the effects of LPS and blocked responses to TEA. These results suggest that activation of K+ channels, possibly Ca-activated K+ channels, through induction of the nitric oxide synthase pathway, may well be responsible for endotoxin-mediated hyporeactivity to vasoconstrictor agents in vascular smooth muscle.

Acetylcholine↗

PubMed2000

Nitric oxide production by murine spleen cells stimulated with Porphyromonas gingivalis-derived lipopolysaccharide.

The aim of the present study was to determine whether Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) may stimulate nitric oxide (NO) production by murine spleen cells. Spleen cells derived from Balb/c mice were cultured in the presence of Pg-LPS or LPS from Salmonella Typhosa. The cell were also cultured in the presence of Pg-LPS with or without L-arginine, L-arginine plus NG-monomethyl-L-arginine (NMMA), or IFN-gamma. Furthermore, the plastic non-adherent spleen cells were stimulated with Pg-LPS and L-arginine. The results showed that Pg-LPS failed to stimulate splenic NO production by themselves. Exogenous L-arginine or IFN-gamma up-regulated the NO production of Pg-LPS-stimulated spleen cells, but the stimulatory effects of L-arginine were completely blocked by NMMA. It was also demonstrated that in the presence of Pg-LPS and L-arginine, splenic macrophages were the cellular source of NO. These results suggest, therefore, that P. gingivalis-LPS may induce murine splenic macrophages to produce NO in a L-arginine and an IFN-gamma-dependent mechanism.

Animals↗

PubMedDate not supplied

Rheumatoid factor induction in the mouse: sex differences and the effect of the sex steroids.

Female CBA mice produced a significantly higher plasma rheumatoid factor (RF) response to Salmonella typhosa lipopolysaccharide than did male mice. The peak level in females was observed on day 5-6 after injection and in males on day 7-8. Elevated RF levels continued to be detected more than 30 days later. A second injection of LPS, 38 days after the first, to assess the secondary response, had no more than an additive effect on plasma RF concentration, although the day of peak response was earlier by two days in both sexes. Administration of oestradiol-17 beta by Silastic implant brought forward the day of peak response by two days in both sexes although it reduced its amplitude considerably. Testosterone had little effect on the peak concentrations achieved in both sexes, but did produce a slower decay in plasma RF level. This investigation indicates that the sex hormones can influence the response to LPS, a polyclonal B cell activator. This may have implications for the sex differences seen in autoimmune diseases.

Animals↗

PubMed1982

Secretion of serum amyloid protein and assembly of serum amyloid protein-rich high density lipoprotein in primary mouse hepatocyte culture.

The serum amyloid protein (apo-SAA) is a unique high density lipoprotein apoprotein exhibiting dramatic increases in plasma concentration following host injury. The events involved in the secretion of apo-SAA and assembly of apo-SAA-rich lipoprotein particles were studied in primary, serum-free culture of adult BALB/c mouse hepatocytes harvested 3 h following administration of the potent apo-SAA inducer, bacterial endotoxin (50 micrograms of intraperitoneally administered Salmonella typhosa lipopolysaccharide). An approximately 3.5-fold increase in the initial rate of apo-SAA secretion was observed over that of hepatocytes isolated from control mice, whereas the rate of apo-A-I secretion was unchanged by endotoxin administration. Sodium dodecyl sulfate-gel electrophoresis and autoradiography of [35S]methionine-labeled cell products indicated the synthesis of both major mouse apo-SAA isotypes by hepatocytes. Essentially all of the secreted apo-SAA chromatographed in Sephadex G-150 with an elution volume corresponding to a molecular weight of approximately 12,000. Approximately 90% of the secreted apo-SAA was recovered in fractions (d greater than 1.21 g/ml) following ultracentrifugal fractionation. In media supplemented with human lipoproteins (100 micrograms/ml), approximately 50% of the secreted apo-SAA was recovered in the high density lipoprotein fraction. These results suggest that mouse apo-SAA is secreted in monomeric form and becomes associated with lipoproteins in the intravascular compartment.

Amyloid↗

PubMed1996

Regulation of ram scrotal temperature during heat exposure, cold exposure, fever and exercise.

1. We measured body core and scrotal temperatures (Tbody and Tscrotum, respectively) of rams during 5 h of hot (40 degrees C) and cold (6 degrees C) exposure, for 6 h following intravenous injections of saline (0.9% NaCl) or 0.4 micrograms kg-1 of the purified lipopolysaccharide endotoxin of Salmonella typhosa (LPS), during 40 min of treadmill exercise, and for several days in their pens. 2. At 20-23 degrees C ambient temperature there were significant, but out of phase, circadian variations in Tbody and Tscrotum. Tscrotum was 3.30 +/- 0.03 degrees C lower than Tbody on average. 3. During cold exposure the tunica dartos muscles contracted, nevertheless Tscrotum fell and Tbody-Tscrotum increased. During heat exposure the tunica dartos muscle relaxed and scrotal sweat glands were activated, nevertheless Tscrotum rose and Tbody-Tscrotum decreased. There was no change in Tscrotum after LPS injection or during exercise, but Tbody increased in both cases. 4. We suggested that Tscrotum is regulated independently of Tbody via a feedback circuit involving scrotal thermoreceptors and effectors in the form of tunica dartos muscle activity and scrotal sweat gland activity. This local circuit is not affected by adjustments to the general thermo-regulatory control system during fever. The effector mechanisms were insufficient to maintain Tscrotum during the extremes of heat and cold exposure.

Animals↗

PubMed1994

Elevation of plasma ACTH concentration in rabbits made febrile by systemic injection of bacterial endotoxin.

This study was carried out to investigate the adrenocorticotropic hormone (ACTH) response in rabbits made febrile by systemic injection of lipopolysaccharide (LPS, Salmonella typhosa endotoxin). Intravenous (i.v.) injection of LPS (0.1 microgram/kg and 1.0 microgram/kg) increased rectal temperature (biphasic fever) and the plasma concentration of ACTH (ACTH response) in a dose-related manner. These responses were suppressed by pretreatment with indomethacin (20 mg/kg, subcutaneously). Intracerebroventricular (i.c.v.) administration of indomethacin (400 micrograms) had no effect on the ACTH response to LPS, although it significantly suppressed febrile response. Small increases in plasma concentration of ACTH and significant fevers followed i.c.v. administration of prostaglandin E2 (2 micrograms) or F2 alpha (2 micrograms). I.v. administration of corticotropin releasing factor (CRF) antagonist [alpha-helical CRF (9-41) (200 micrograms/kg)] partly suppressed the ACTH increase induced in plasma by i.v. LPS. These results suggest that prostaglandins synthesized outside the blood-brain barrier play an important role in the ACTH response and that the mechanism for induction of the ACTH response is not exactly the same as that for the febrile response, although prostaglandins are involved in both responses.

Adrenocorticotropic Hormone↗

PubMed1991

Response of body temperature and serum iron concentration to repeated pyrogen injection in rabbits.

We measured body temperature and serum iron concentration after five daily consecutive injections of febrile doses of Salmonella typhosa lipopolysaccharide (0.1 micrograms/kg) and two doses of Staphylococcus aureus cell walls (1 x 10(7) and 5 x 10(7) cells) in rabbits. Tolerance to endotoxin injection, as manifest by a significant attenuation in the body temperature elevation, developed after the first injection of endotoxin. The endotoxin-induced fall in serum iron concentration was attenuated significantly by the 5th day of endotoxin injection. In contrast, no tolerance developed in either the body temperature or serum iron response following repeated daily injections of S. aureus. Rabbits rendered tolerant to endotoxin showed normal febrile and serum iron responses to subsequent S. aureus injection. Rabbits given serial injections of S. aureus, although not tolerant to S. aureus itself, exhibited attenuated body temperature responses but not serum iron responses to endotoxin injection. We suggest that repeated injection of endotoxin diminishes the ability of endotoxin to stimulate endogenous pyrogen (EP) synthesis and/or release, a property not shared by the gram-positive pyrogen S. aureus. However, repeated injection of S. aureus weakens the central endotoxin-EP pathway.

Animals↗

PubMed2006

Effects of thoracic epidural anesthesia on hemodynamics and global oxygen transport in ovine endotoxemia.

Besides providing effective analgesia, thoracic epidural anesthesia (TEA) has been shown to decrease perioperative morbidity and mortality. Because of its vasodilatory properties in association with the sympathetic blockade, however, TEA may potentially aggravate cardiovascular dysfunctions resulting from sepsis and systemic inflammatory response syndrome. The objective of the present study was to assess the effects of TEA on hemodynamics, global oxygen transport, and renal function in ovine endotoxemia. After a baseline measurement in healthy sheep (n = 18), Salmonella typhosa endotoxin was centrally infused at incremental doses to induce and maintain a hypotensive-hypodynamic circulation using an established protocol. The animals were then randomly assigned to one of two groups. In the treatment group, continuous TEA was initiated with 0.1 mL.kg of 0.125% bupivacaine at the onset of endotoxemia and maintained with 0.1 mL.kg.h. In the control group, the same amount of isotonic sodium chloride solution was injected through the epidural catheter. In the animals surviving the entire experiment (n = 7 per group), cardiac index and mean arterial pressure decreased in a dose-dependent manner during endotoxin infusion. In the TEA group, neither systemic hemodynamics nor global oxygen transport were impaired beyond the changes caused by endotoxemia itself. Urinary output was increased in the TEA group as compared with the control group (P < 0.05). In this model of endotoxic shock, TEA improved renal perfusion without affecting cardiopulmonary hemodynamics and global oxygen transport.

Anesthesia, Epidural↗

PubMed1978

Impaired host resistance to endotoxin and malaria in polychlorinated biphenyl- and hexachlorobenzene-treated mice.

The in vivo effect of polychlorinated biphenyl (PCB) and hexachlorobenzene (HCB) on murine endotoxin sensitivity and resistance to malaria (Plasmodium berghei NYU-2) infection was studied. The dietary administration of 167 ppm (167 microgram/g) of PCB 1242 or HCB for 3 weeks resulted in an enhanced sensitivity to gram-negative endotoxin (Salmonella typhosa), which was further increased in animals maintained on the diets for 6 weeks. By 6 weeks, a 5.2- or 32-fold increase in endotoxin sensitivity was seen in mice fed PCB or HCB, respectively. A 20% decrease in mean survival time of mice fed PCB 1242 for 3 or 6 weeks and inoculated with malaria was demonstrated. Infected mice that received HCB for 3 or 6 weeks manifested a reduction in mean survival time of 24 or 31%, respectively. Histopathological examination revealed a normal thymus, spleen, mesenteric lymph nodes, and lungs. Centrilobular and pericentral hepatocyte hypertrophy, common to organochlorine exposure, was observed. Electron capture gas chromatographic analysis for PCB 1242 or HCB in the tissues examined histologically revealed a significant deposit of the xenobiotics. HCB concentration was approximately 16 to 25 times greater than that of PCB. The data indicate that environmental chemicals impair host resistance and that the alteration may be related to the presence of the chemicals in the lymphoreticular organs.

Animals↗

PubMed1974

On the mechanisms responsible for selection of hepatic veins as target for thrombosis following injection of endotoxin in hyperlipemic rats.

The feeding of a butter-rich diet, to sensitize rats for studying the phenomenon of hepatic vein thrombosis, is shown to produce severe liver steatosis leading to a sinusoidal barrage and portal hypertension. The portal pressure in these animals was 210 +/- 4 mm of saline, as compared to 113 +/- 3 mm in the normal rat. Blood circulation studies using carbon suspensions revealed production of a vascular stasis in the hepatic veins after 60 to 90 minutes, when endotoxin (Salmonella typhosa, 0.3 mg/kg) is introduced into the blood circulation to initiate hepatic vein thrombosis. Similar results were observed after 15 minutes with ellagic acid (1 mg/kg/min). The stasis was found in connection with an additional intrahepatic resistance to blood flow as evidenced by a rise in portal pressure and by a reduction in liver perfusion in relation with development of systemic hypotension. In contrast with this, endotoxin initiated only slight and transient changes in the normal rat. Thrombosis immediately followed production of stasis in the hepatic vein, whether the phenomenon was initiated by endotoxin or ellagic acid. Furthermore, inhibition of the vascular stasis of alpha-adrenergic blockade (phenoxybenzamine, 3 mg/kg) was accompanied by prevention of hepatic vein thrombosis. It is concluded that stasis in the hepatic veins resulting from a mechanical obstruction of the circulation by steatosis and by an additional reduction in blood flow initiated by endotoxin, is responsible for selection of hepatic veins as targets for thrombosis following injection of endotoxin in hyperlipemic rats.

Animals↗

PubMed1986

Ureteral blockade sensitizes to the generalized Shwartzman reaction.

Renal cortical necrosis (RCN) has been reported in the normal kidney of patients with a contralateral ureteral occlusion (UO). So far, studies have examined the mechanisms protecting the affected kidney from glomerular thrombosis and cortical necrosis; but to the authors' knowledge, none has ever investigated the potential role of UO on the occurrence of the associated disseminated intravascular coagulation (DIC) episode leading to RCN. Female rats with a ligature of the right or left ureter were given injections, at different times after surgery, of 400 micrograms Salmonella typhosa 0901 endotoxin. Other experimental groups included normal and sham-operation rats and animals with a unilateral nephrectomy or with one kidney rendered ischemic by complete ligature of the renal vessels and of the ureter. All the animals were sacrificed 4 hours after endotoxin, and kidney sections stained with PTAH were examined for the presence of fibrin thrombi. Glomerular thrombosis was never observed in any hydronephrotic kidney, but occurred with a low incidence (16%) in the contralateral organ in the group given endotoxin the second day after UO. The incidence and severity of glomerular capillary thrombosis gradually increased in the normal kidney as the delay between surgery and endotoxin was prolonged; the incidences (P less than 0.01) were 45% and 83%, respectively, after 6 and 10 days. Endotoxin failed totally to initiate the lesion 1 day after UO as well as in normal, sham-operation and unilaterally nephrectomized rats, and in animals with combined UO and ligature of the renal circulation. We conclude that the perfused hydronephrotic kidney liberates a factor(s) that sensitizes to DIC and glomerular thrombosis, typical of the generalized Shwartzman reaction.

Animals↗

PubMed1978

Endotoxin-induced alterations in canine granulopoiesis: colony-stimulating factor, colony-forming cells in culture, and growth of cells in diffusion chambers.

Salmonella typhosa endotoxin injected into dogs produced elevated plasma CSF levels, transient leukopenia followed by leukocytosis, and stimulation of marrow granulopoiesis and mobilization of granulocyte-macrophage progenitors cells into the the peripheral circulation. The number of marrow CFU-c decreased to 65% of the control number within 6 h, returned to control levels by 24 h, and increased to 370% of the control number by 48h after endotoxin. The granulopoietic response was supported by a concomitant increase in the M:E ratio, an increased fraction of marrow-derived CFU-c susceptible to 3H-TdR suicide, and increased granulo-monocytopoietic activity of marrow- and peripheral blood-derived cells grown in diffusion chamber cultures. These results are consistent with the concept that endotoxin-induced CSF is a physiologic regulator of canine granulopoiesis, and that canine marrow responds to endotoxin with a significant increase in the concentration of marrow-derived granulocytic progenitors and with mobilization of granulocyte-macrophage progenitors into the peripheral circulation.

Animals↗

PubMed1982

Changes in high density lipoprotein content following endotoxin administration in the mouse. Formation of serum amyloid protein-rich subfractions.

Bacterial endotoxin is a potent inducer of the serum amyloid protein (apo-SAA), a high density lipoprotein (HDL) apoprotein. In a study of the induction of apo-SAA and the structure of apo-SAA-rich lipoprotein particles in mice, we have observed that, following intraperitoneal administration of Salmonella typhosa lipopolysaccharide (50 micrograms), plasma apo-SAA levels rose from base-line levels of less than 1% to greater than 20% of the HDL protein content at 20 h postinjection. No changes in the relative content of other HDL apoproteins were noted; analysis of apo-SAA-rich HDL lipid content indicated a significant decrease (10%) in phospholipid content relative to that of control HDL. Two major apo-SAA isotypes, apo-SAA1 and apo-SAA2, were identified, having apparent molecular weights of 12,600 and 11,800, respectively, and isoelectric points of 6.35 and 6.20, respectively. Quantitative immunoprecipitation experiments indicated that essentially all of the apo-SAA was bound to lipoprotein particles containing apo-A-I. Apo-SAA was distributed among higher density HDL subfractions than were other HDL apoproteins following density gradient centrifugation, and subfractions having apo-SAA:apo-A-I molar ratios of greater than 2:1 were identified. These results indicate the formation of a subset of apo-SAA-rich HDL particles following apo-SAA induction by endotoxin.

Amyloid↗