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PubMed1985

Plasma catecholamines during endotoxin infusion in conscious unrestrained rats: effects of adrenal demedullation and/or guanethidine treatment.

We have examined the effect of E coli endotoxin infusion (41 micrograms kg-1 min-1 iv for 4 h) on plasma concentrations of epinephrine (E), norepinephrine (NE), and dopamine (DA) in the conscious unrestrained rat. Saline infusion did not change catecholamine concentrations from the preinfusion values of 230.8 +/- 32.9 pg ml-1 (E), 456.8 +/- 104.9 pg ml-1 (NE), and 49.0 +/- 19.9 pg ml-1 (DA). Endotoxin produced marked elevations in all three catecholamines. At 1 h, the plasma concentrations were 3,279 +/- 494.6 pg ml-1 (E), 1,670 +/- 137.0 pg ml-1 (NE), and 191.5 +/- 13.7 pg ml-1 (DA). Thereafter, concentrations of E decreased whereas concentrations of NE and DA increased. These increases were prevented by a combination of adrenal demedullation (28 days previously) and treatment with guanethidine (25 mg kg-1 iv, -24 h) ("sympathectomy"). Guanethidine alone markedly reduced the peak NE concentrations without affecting the E concentrations or the 1-h NE concentrations. Demedullation alone prevented the increase in E and reduced the 1-h NE concentrations. Survival in such "sympathectomized" animals was markedly reduced (survival at 4 h in rats receiving endotoxin alone, 100%: in "sympathectomized" animals receiving endotoxin, 12.5%). The tachycardia produced by endotoxin was attenuated in "sympathectomized" rats and mean arterial blood pressure fell rapidly. Endotoxin-induced hyperglycemia was prevented by "sympathectomy" and hypoglycemia was evident as early as 1 h after commencing the infusion. Endotoxin produced hypoinsulinemia in normal rats but did not change plasma insulin values in "sympathectomized" animals, although these animals showed a pre-endotoxin fasting hyperinsulinemia. An important protective role for catecholamines is suggested, especially in the early stages of shock.

Adrenal Medulla↗
PubMed1985

Effect of Escherichia coli endotoxin and thyrotropin-releasing hormone on prolactin in lactating sows.

Primiparous gilts were given subcutaneous injections of saline solution or 8 mg of Escherichia coli endotoxin (055:B5 strain) in saline solution on postpartum days (PPD) 2 and/or 6 and saline solution at the same site on PPD 1, 3, 5, and 7 at 1000 hours. On PPD 1 to 3 and on PPD 5 to 7, pigs were given 100 micrograms of thyrotropin-releasing hormone (TRH) IV at 1300 hours to evaluate TRH-induced prolactin (PRL) release. Blood samples were analyzed for PRL, cortisol, triiodothyronine (T3), and tetraiodothyronine (T4) concentrations. Rectal temperatures were monitored at hourly intervals between 0800 and 1500 hours on PPD 2 and 6. The PRL declined after endotoxin administration on PPD 2, but a similar decline was not seen after saline solution administration on PPD 1, 2, or 3. The PRL concentrations remained unchanged on PPD 5, 6, and 7 in gilts exposed to endotoxin for the 1st or 2nd time on PPD 6 and to saline solution on PPD 5 and 7. The TRH injection caused increases in PRL in all animals, but the PRL increase after TRH injection was significantly lower (P less than 0.05) in gilts treated with endotoxin on PPD 2. Cortisol concentrations increased after endotoxin exposure on PPD 2 and 6. Rectal temperatures increased after endotoxin exposure on PPD 2 and 6 with peak temperatures of 41.8 C and 41.6 C seen 4 and 3 hours, respectively, after endotoxin injection. The T3 and T4 response, used as an indicator of TRH perfusion of the adenohypophysis, was unchanged after endotoxin or saline solution administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Acute endotoxin shock in the dog and an attempt at its therapy.

The present study aimed at monitoring of hemodynamic changes proceeding in a standard model of acute endotoxin shock in the dog, and mainly at an attempt at the therapy of its early phases. Acute endotoxin shock represents a grave state with rapidly advancing changes in blood circulation, therefore we studied the effects of selected drugs, intended to regulate the circulation conditions in the course of shock. In a standard model in the dog, in which endotoxin shock had been induced by intravenous injection of Escherichia coli endotoxin dosed 1.75 mg.kg-1, the effects of dopamine and hydrocortisone were investigated. The course of the hemodynamic changes can be divided into three phases, as follows. In the first phase, during endotoxin infusion, the blood pressure sank steeply, and the myocardial contractility, left ventricular pressure, and renal arterial blood flow decreased. The central venous pressure rose. After the conclusion of endotoxin infusion the second phase of shock began. It was characterized by a transitory partial correction of hemodynamics. In the third phase all hemodynamic indicators gradually worsened. An especially grave phenomenon was the reduction of renal arterial blood flow. The fatal effects of the administered endotoxin dose were preventable by infusion of dopamine, or hydrocortisone, or their combination. Dopamine plus hydrocortisone raised the survival quota of animals in endotoxin shock, enhanced the renal arterial blood flow, maintained the diuresis, enhanced myocardial contractility, and elevated left ventricular blood pressure.

Animals↗
PubMed1985

Parallel line assays of endotoxins with the LAL chromogenic substrate method.

All endotoxins from the gram negative microorganisms studied sofar contain lipid A, which is considered to be responsible for the biological activity. Endotoxins may therefore react in a similar way in quantitative assays. The varying non-lipid A part of different endotoxins may potentiate or reduce the activity of the identical lipid A part without changing the slope of the log-dose vs. response curve of these endotoxins. To test whether 13 endotoxins from different microorganisms react similarly with amoebocyte lysate (LAL) log-dose response curves were made using a chromogenic substrate method. A balanced incomplete block design with 13 blocks and four replications of each endotoxin was applied. A group of eight endotoxins with a common slope was defined with the Student-Newman-Keuls procedure. Two independent potency estimates of these endotoxins were in good agreement.

Analysis of Variance↗
PubMed1983

Relation of endotoxin structure to hypoglycemic and insulinlike actions.

Various endotoxin preparations were used to determine which portion of endotoxin, lipid A, polysaccharide, or lipid-associated protein (LAP), mediates the hypoglycemic and insulinlike action in rats. Salmonella enteriditis Boivin (SEB), complete endotoxin, and S enteriditis Westphal (SEW), lacking LAP, were equally lethal to endotoxin-sensitized rats; however, S minnesota (SM) glycolipid (lipid A plus 16% polysaccharide) was comparatively more toxic. Toxic effects were prevented by alteration of lipid A through alkaline hydrolysis or polymixin B treatment. SM-lipid A (0.02% polysaccharide) was less toxic than SM-glycolipid. Similar hypoglycemic effects were produced by SEB and SEW; however, SM-glycolipid produced a significantly greater hypoglycemia. Although SEB, SEW, and SM-glycolipid all produced significant increases in adipose tissue glucose oxidation a decreasing trend in effectiveness was observed, while the SM-lipid A was without effect. However, adding detoxified hydrolysates of endotoxin to SM-lipid A produced a significant increase in glucose oxidation. In conclusion, lipid A is the primary endotoxin moiety mediating both the lethal effects of endotoxin and its hypoglycemic action. However, maximal expression of insulinlike action requires the presence of all three portions of endotoxin.

Adrenalectomy↗
PubMed1984

Protective effects and role of endotoxin in experimental septicemia.

An experimental model was used in mice in which septicemia develops following invasion of the animals' own intestinal flora after cecal ligation and puncture. Pretreatment with 1 microgram of endotoxin administered 24 hours before surgery significantly reduced the rate of lethality. Bacteria were counted and differentiated in cardiac blood at various times throughout a 48-hour period after induction of septicemia in mice, with and without pretreatment. Endotoxin levels and plasma-related interference of the Limulus-amebocyte-lysate (LAL)-endotoxin reaction also were determined as were hematologic and metabolic parameters. A shift from mixed gram-positive and gram-negative to predominantly gram-negative bacteria occurred in both groups. In pretreated mice, a reduction in aerobic bacterial counts and reduced hyperglycemia were seen in the initial phase; and a decrease in anaerobic and aerobic bacteria and in endotoxin levels were observed at the end of the experiment. This appears to be related to endotoxin-induced increased resistance against the consequences of intraabdominal sepsis. These studies also indicate that the measured amount of circulating endotoxin does not necessarily correlate to the severeness of infection. Individual differences in plasma-related interference with the LAL-endotoxin reaction also emphasize the requirement for sample-internal standardization in order to reliably quantify endotoxin in plasma.

Animals↗
PubMed1984

Gram-negative bacterial endotoxins in airborne dusts from washed and unwashed cottons.

Gram-negative bacteria possess lipopolysaccharide-protein complexes termed endotoxins as an integral portion of their cell walls. These biologically active substances elicit profound effects both in vitro and in vivo. Organic dusts from many occupational environments contain measureable amounts of gram-negative bacteria and their endotoxins. In particular, cottons and cotton dusts contain these materials, and research is directed to elucidate the association between endotoxins and the acute and chronic respiratory effects of inhaling cotton dusts. It is the purpose of this paper to describe an experimental process which removes endotoxins from cotton by washing prior to processing the baled cottons. The studies show that water washing is a reliable method for removing endotoxins, and pulmonary function studies correlate well with endotoxin levels in the air. Quantification of airborne endotoxins provides a good indicator of cleanliness and toxocity of the cotton dusts. However, the differential toxicities of different endotoxins must be considered and evaluated further.

Dust↗
PubMed1981

Insulin-like action of E. coli endotoxin in promoting skeletal muscle glucose uptake in the dog.

The effect of locally infused endotoxin on gracilis muscle glucose uptake was determined in anesthetized mongrel dogs. The effects of infusion of small amounts of E. coli endotoxin into the artery of isolated, innervated, constant-flow-perfused gracilis muscles on glucose uptake and other metabolic variables were determined. Locally infused endotoxin consistently caused a significant and substantial increase in skeletal muscle glucose uptake with no alterations in muscle arterio-venous difference of insulin, oxygen, carbon dioxide, or pH, or in venous blood hematocrit or temperature. These data demonstrate that endotoxin can act locally to increase glucose uptake by skeletal muscle, independent of the action of insulin or other metabolic factors. On the other hand, when endotoxin was given systemically to induce shock, gracilis muscle glucose uptake was maintained for the duration of the 6-hr experiment. These differences we feel reflect the reduction in plasma endotoxin concentration mediated by the reticuloendothelial system (RES). On the other hand, live E. coli septic shock was associated with an increase in glucose uptake in the constant-flow-perfused gracilis muscle after 4.5 hr of shock. We believe this increase in muscle glucose uptake resulted from the direct effects of endotoxin, whose plasma concentration presumably increases substantially as the RES is overwhelmed and becomes less effective. The contribution of this phenomenon to the progressive hypoglycemia characteristic of gram-negative endotoxin or septic shock cannot be evaluated from this study, although it is probably substantial.

Animals↗
PubMed1982

Effects of cyclooxygenase inhibitors on pulmonary vascular responses to endotoxin in unanesthetized sheep.

Pulmonary release of thromboxanes and prostaglandins occurs during the first hour after endotoxin infusion in sheep concomitant with transient, severe pulmonary hypertension (phase I) and followed by a prolonged period of increased lung vascular permeability (phase II) characterized by moderately elevated pulmonary artery pressure and high flow of protein-rich lung lymph. Indomethacin and meclofenamate both inhibited phase I pulmonary hypertension but did not prevent later increases in pulmonary artery pressure and lung lymph flow to levels seen with endotoxin alone in the same sheep. Indomethacin significantly exaggerated phase II lung lymph flow (endotoxin = 19 +/- ml/hr; indomethacin + endotoxin = 24 +/- 4 ml/hr, p less than 0.05), and meclofenamate enhanced phase II lymph protein clearance (endotoxin = 12.9 +/- 1.5 ml/hr; meclofenamate + endotoxin = 17.1 +/- 2.5 ml/hr, p less than 0.05). Hypoxemia seen with endotoxin alone was inhibited by meclofenamate. These data indicate that during endotoxemia cyclooxygenase products mediate phase I pulmonary hypertension. Inhibitors of cyclooxygenase prevent ventilation perfusion imbalance that results in endotoxin induced hypoxemia. Exaggeration of phase II lymph responses by cyclooxygenase inhibitors suggests that prostaglandin synthesis moderates phase II or that lipoxygenation products contribute to the phase II increased permeability response.

Animals↗
PubMed1981

The effect of prostacyclin infusion on endotoxin-induced lung injury.

Lung injury produced by endotoxin is characterized by both pulmonary hypertension and increased pulmonary vascular permeability. Prostacyclin (PGI2) has been found to be a vasodilator and a membrane stabilizer. The purpose of this study was to determine the effectiveness of PGI2 in preventing endotoxin injury. Eight sheep with chronic lung lymph fistula were given both Escherichia coli endotoxin (2 microgram/kg) alone and endotoxin plus an immediate infusion of PGI2 (0.1 to 0.2 microgram/kg/min) for a 5-hour period; the studies were performed 4 days apart. The endotoxin injury was characterized by early severe pulmonary hypertension, with pulmonary artery pressure increasing from 18 +/- 0.6 to 40 +/- 3.1 mm Hg and lung lymph flow (QL) increasing threefold. This was followed in about 3 hours by an increase in permeability characterized by an increasing lymph to plasma protein ratio (0.63 to 0.74) and a threefold increase in QL. In seven of eight animals infused with PGI2 the pulmonary hypertension and alteration in QL in the early and later phases were significantly decreased. In four paired studies, prostaglandins PGE, PGF2 alpha, and PGI2 as 6-keto PGF1 alpha were measured in lymph and plasma. PGF2 alpha and PGI2 were significantly increased in lung lymph during the early hypertensive phase immediately after endotoxin injection, but returned to baseline during the later phase. In the PGI2 infusion studies, PGF2 alpha showed the same pattern of response, but PGI2 was increased to much higher levels in lymph and plasma, as compared to values of endotoxin alone. The higher plasma values corresponded with less severe lung injury. The one animal not protected by PGI2 had the lowest plasma PGI2 level. We therefore found PGI2 to protect the lung against injury from endotoxin.

Animals↗
PubMed1980

Effects of endotoxin-tolerance on in vivo drug metabolism in mice.

Acute doses of endotoxin and the induction of endotoxin-tolerance lowered the apparent in vivo rates of hexobarbital and zoxazolamine metabolism in mice. Acute doses of endotoxin increased the duration of narcosis induced by these two compounds to a greater extent than did induction of the endotoxin-tolerant state. In endotoxin-tolerant mice, however, acute endotoxin treatment did not extend hexobarbital sleeping or zoxazolamine paralysis times beyond those noted in endotoxin-tolerant mice given no acute endotoxin.

Animals↗
PubMed1995

Direct action of endotoxin on cardiac muscle.

While the cardiovascular effects of endotoxin include myocardial depression, presumably due to circulating myocardial depressant substances, endotoxin itself is supposed to have no direct effect on the heart. In these experiments, we compared the direct effects of endotoxin on the contractile response of feline papillary muscle to calcium with that seen after administration to the intact animal. The contractile state of the muscle was assessed from developed tension as extracellular calcium concentrations were varied from .5 to 8.0 mM. When endotoxin was administered to the intact animal as well as given to the muscle directly in the bathing solution, endotoxin- exposed muscles showed smaller increases in contractile tension with increasing calcium concentrations than control muscles after 70-85 min. NaOH-inactivated endotoxin produced results similar to the control experiments. Previous experimenters have reported myocardial depression only after endotoxin had circulated in the intact animal for 1-2h; these experiments show a direct depressant effect of endotoxin on cardiac muscle without the release of a substance elsewhere in the body.

Animals↗
PubMed1995

Neonatal endotoxin exposure alters the development of the hypothalamic-pituitary-adrenal axis: early illness and later responsivity to stress.

The long-term consequences of neonatal endotoxin exposure on hypothalamic-pituitary-adrenal axis (HPA) function were assessed in adult female and male Long-Evans rats. At 3 and 5 d of age, pups were administered endotoxin (Salmonella enteritidis, 0.05 mg/kg, i.p.) at a dose that provokes a rapid and sustained physiological response, but with no mortality. As adults, neonatally endotoxin-treated animals exhibited significantly greater adrenocorticotrophic hormone (ACTH) and corticosterone responses to restraint stress than controls. In addition, dexamethasone pretreatment was less effective in suppressing ACTH responses to restraint stress in endotoxin-treated animals than in controls, suggesting decreased negative-feedback sensitivity to glucocorticoids. Neonatal endotoxin treatment elevated resting-state median eminence levels of corticotropin-releasing hormone (CRH) and arginine vasopressin in adult male animals, and arginine vasopressin in both adult males and females. Neonatal exposure to endotoxin also increased CRH mRNA expression in the paraventricular nucleus of the hypothalamus of adult males, with no difference in females. Finally, glucocorticoid receptor density was reduced across a wide range of brain regions in the neonatal endotoxin-treated, adult animals. These data illustrate the interactive nature of immune and endocrine systems during development. It appears that endotoxin exposure during critical stages of development decreases glucocorticoid negative-feedback inhibition of ACTH secretagogue synthesis, thus increasing HPA responsiveness to stress. The implication of these findings is that exposure to gram-negative LPS in early life can alter the development of neural systems which govern endocrine responses to stress and may thereby predispose individuals to stress-related pathology.

Adrenocorticotropic Hormone↗
PubMed1976

The effects of aspirin and indomethacin on the ocular response to circulating bacterial endotoxin in the rabbit.

A transient iridocyclitis is produced in rabbits by the intravenous injection of bacterial endotoxin. A major feature of this response is an altered vascular permeability which can be measured by the ocular accumulation of circulating 125I-labeled albumin. The present study was made to determine the effects of inhibitors of prostaglandin synthesis of the ocular response to an E. coli 055:B5 endotoxin. Aspirin pretreatment prevented the ocular response following the intravenous injection of 10 mug per kilogram of endotoxin, but had no effect following 100 mug per kilogram. Indomethacin pretreatment prevented an alteration in ocular vascular permeability 1 1/2 hours after the injection of 100 mug per kilogram of endotoxin and significantly reduced the alteration 4 hours after endotoxin. Thus inhibitors of prostaglandin synthesis can prevent the ocular response to circulating endotoxin depending on their relative potency and the amount of injected endotoxin. These results suggest that prostaglandins are important in the ocular response to circulating endotoxin in the rabbit.

Animals↗
PubMed1994

Respiratory health status in swine producers relates to endotoxin exposure in the presence of low dust levels.

We conducted an assessment of respiratory health status including questionnaire and spirographic measurements in 54 male swine producers age 36.3 +/- 11.1 years (mean +/- SD) who worked an average of 10.7 +/- 6.3 years in the industry and spent 4.7 +/- 2.1 hours per day in the swine barns, and we also measured atmospheric contaminants including carbon dioxide, ammonia, total dust, respirable dust, and airborne endotoxin. Mean atmospheric dust contaminant levels were as follows: carbon dioxide, 2632 +/- 807 ppm; ammonia, 11.3 +/- 4.2 ppm; total dust, 2.93 +/- 0.92 mg/m3; respirable dust, 0.13 +/- 0.05 mg/m3; and endotoxin, 11,332 +/- 13,492 endotoxin units/m3. Of these, endotoxin related to forced vital capacity (P < .05) and endotoxin x hours per day was related to forced vital capacity (P < .05) and to forced expiratory volume in 1 second (P = .06). Respiratory symptoms and lung function studies did not relate to categories of low, medium, and high exposure to respirable dust. However, categories of endotoxin (available on 46 workers) related to respiratory symptoms (cough, P = .02; chronic bronchitis, P = .06; and to forced vital capacity, P < .01). These data suggest that respiratory health status relates to endotoxin levels but not to dust level exposures in the presence of low dust levels and indicates that control measures should include endotoxin as well as dust control.

Adult↗
PubMed1994

Clinical and clinicopathologic changes in cows with endotoxin-induced mastitis treated with small volumes of isotonic or hypertonic sodium chloride administered intravenously.

We characterized the clinicopathologic manifestations of experimentally induced endotoxin-induced mastitis. Responses to hypertonic fluid therapy also were assessed. Eight cows received 1 mg of endotoxin by intramammary infusion in the left forequarter. Four hours after endotoxin administration, cows received 0.9% NaCl, 5 ml/kg of body weight (n = 4) or 7.5% NaCl, 5 ml/kg (n = 4) IV. Endotoxin-infused cows had expanded plasma volume, hyponatremia, transient hyperchloremia and hypophosphatemia, increased serum glucose concentration, and decreased serum activities of liver- and muscle-specific enzymes. Calculated plasma volume increased at 6 hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent observations of decreased serum protein concentration, erythrocyte count, and hematocrit supported observations of increased plasma volume. Relative plasma volume was greater in cows receiving hypertonic NaCl (124.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased voluntary water intake after IV fluid administration. Increased water consumption was not accompanied by increased body weight, indicating probable occurrence of offsetting body water loss. Serum sodium concentration in cows receiving hypertonic NaCl was increased 2 hours after fluid administration, but the magnitude of the change was minimal (< 4 mmol/L) and transient, indicating rapid equilibration with either interstitial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotoxin administration, compared with concentration prior to endotoxin administration, indicating selective loss of sodium.

Analysis of Variance↗
PubMed1993

[Effects of various doses of endotoxin on physiological and hematological parameters in conscious guinea pigs].

We investigated the effects of various doses (0.2 to 2000 micrograms/kg) of endotoxin on physiological and hematological parameters in our guinea pig model. Bronchoalveolar lavage (BAL) and lung tissue sampling were performed 6 hours after endotoxin injection. Lung damage was assessed by measuring wet to dry lung weight ratio (W/D), lung tissue to plasma accumulation of 125I-albumin (AL: albumin leakage) and BAL fluid to plasma accumulation of 125I-albumin (BALL: bronchoalveolar lavage leakage). Changes in peripheral cell counts were estimated at times 0, 1, 2, 4 and 6 hours after endotoxin injection. Pulmonary cell accumulation was determined by counting the number of cells in BAL fluid and tissue samples fixed for light microscopic examination. Increased W/D and AL were observed only in the high dose endotoxin treatment groups (200 and 2000 micrograms/kg), while BALL increased even in the low dose endotoxin treatment groups (2 micrograms/kg). Decreases in peripheral neutrophil counts at one hour were observed in all endotoxin treated groups. Increase in BAL fluid neutrophils was seen in the 20, 200, and 2000 micrograms/kg groups, while neutrophil accumulation assessed by light microscope was observed in all endotoxin treated groups. We conclude that different amounts of endotoxin are required to affect different parameters of lung injury.

Albumins↗
PubMed1993

Pentoxifylline does not prevent endotoxin induced lung and liver lipid peroxidation in the adult sheep.

Our purpose was to determine the effect of pentoxifylline pretreatment on endotoxin-induced (5 microgram/kg) lung and systemic oxidant activity, measured as lipid peroxidation. We used the awake adult sheep with lung and soft tissue lymph fistulae to monitor microvascular changes as well as to monitor oxygen delivery and consumption. Oxidant activity was monitored using the level of plasma conjugated dienes, a measure of circulating lipid peroxides, and lung and liver malondialdehyde content, a measure of tissue lipid peroxidation. Sixteen sheep were given endotoxin, eight of which were pretreated with pentoxifylline (20 mg/kg bolus) followed by a 6 mg/kg/hr infusion. We found that the degree of early endotoxin-induced pulmonary hypertension and hypoxia and later increased pulmonary microvascular permeability was not attenuated with pentoxifylline. In addition, a comparable increase in circulating conjugated dienes, lung neutrophil sequestration, and a three-fold increase in lung malondialdehyde was seen in both groups. Soft tissue QL also increased to the same degree in both groups. Liver MDA increased from a control of 110 +/- 20 nM/g tissue to 165 +/- 32 nM/g with endotoxin alone and to 260 +/- 55 nM/g with pentoxifylline pretreatment, a significant increase over both control and endotoxin alone groups. Pentoxifylline, however, did improve hemodynamic stability, required significantly less fluid, and prevented the hyperdynamic state seen at 4-5 hr post endotoxin. We conclude that pentoxifylline attenuates the initial endotoxin-induced hemodynamic instability, and later hyperdynamic state. However, pentoxifylline pretreatment does not appear to prevent endotoxin-induced oxygen radical release in the unanesthetized sheep.

Animals↗