pituitrin and Escherichia-coli-Infections

Topics: Adrenal Insufficiency; Adult; Amputation, Surgical; Anti-Bacterial Agents; Disseminated Intravascular Coagulation; Epoprostenol; Escherichia coli; Escherichia coli Infections; Female; Gangrene; Humans; Hydrocortisone; Hypotension; Kidney Calculi; Leg; Metatarsus; Pain; Platelet Aggregation Inhibitors; Purpura Fulminans; Shock, Septic; Vasopressins

The effects of vasopressin, norepinephrine, and L-arginine alone or combined on intestinal microcirculation were evaluated in the septic mouse by intravital microscopy, with which we measured the erythrocyte flux and velocity in villus tip arterioles and the density of perfused villi.. Controlled animal study.. University research laboratory.. Female BALB/c mice weighing between 18 and 21 g.. Anesthetized and ventilated mice received at t0 an intravenous injection of Escherichia coli endotoxin (2 mg/kg bolus intravenously), inducing after 1 hr (t60) a decrease in mean arterial blood pressure to 40-50 mm Hg associated with a significant decrease in erythrocyte flux and velocity in villus tip arterioles and in the density of perfused villi. The mice then received a randomly different treatment for endotoxin-induced shock. Treatments consisted in continuous intravenous infusion for 1 hr with either saline (control group), norepinephrine, vasopressin, L-arginine, vasopressin+L-arginine, or norepinephrine+L-arginine. The doses of vasopressors (used alone or combined with L-arginine) were titrated to restore mean arterial pressure to the baseline level.. At the end of the treatment (t120), we observed in the control group further decreases in arteriolar flux and velocity and in the density of perfused villi. In the groups treated by a vasopressor alone, mean arterial pressure returned to baseline and there were no additional decreases in arteriolar flux and velocity or in the density of perfused villi. However, these latter three variables did not return to their preshock baseline values. Even though L-arginine did not restore mean arterial pressure, the infusion of L-arginine alone prevented the decrease in flux or erythrocyte velocity occurring between t60 and t120 and conserved to some extent the density of perfused villi compared with that in the control groups. In addition, we found that simultaneous administration of norepinephrine or vasopressin with L-arginine improved all microcirculation variables more efficiently than either vasopressor alone.. From these data, we conclude that a) restoring mean arterial pressure after 1 hr of endotoxemia was not sufficient to restore ad integrum intestinal mucosa microvascular perfusion; b) L-arginine could have a beneficial effect at the microcirculatory level, which was independent of mean arterial pressure; and c) administration of L-arginine combined with the maintenance of perfusion pressure by vasopressive drugs allowed a better preservation of intestinal microcirculation at an early stage of endotoxemia.

Topics: Animals; Arginine; Blood Pressure; Disease Models, Animal; Drug Therapy, Combination; Endotoxemia; Escherichia coli Infections; Female; Ileum; Mice; Mice, Inbred BALB C; Microcirculation; Norepinephrine; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Arginine; Blood Pressure; Drug Synergism; Drug Therapy, Combination; Endotoxemia; Escherichia coli Infections; Humans; Ileum; Microcirculation; Norepinephrine; Vasoconstrictor Agents; Vasopressins

The effect of low-dose vasopressin (AVP) on vital regional circulations may be clinically relevant but has not been fully described. We sought to determine the effect of low-dose AVP on systemic haemodynamics, coronary, mesenteric and renal circulations in the conscious normal and septic mammal. We studied seven Merino sheep using a prospective randomized cross-over double-blind placebo-controlled animal design. We inserted flow probes around aorta, coronary, mesenteric and renal arteries and, three weeks later, we infused low-dose AVP (0.02 IU/min) or placebo in the normal and septic state induced by intravenous E. coli. In normal sheep, AVP (0.02 IU/min) induced a 17% decrease in mesenteric blood flow (393.0+/-134.9 vs 472.1+/-163.8 ml/min, P<0.05) and a 14% decrease in mesenteric conductance (P<0.05). In septic sheep, AVP decreased heart rate and cardiac output by 28% and 22%, respectively (P<0.05). It also decreased mesenteric blood flow and mesenteric conductance by 23% (flow: 468.5+/-159.7 vs 611.3+/-136.3 ml/min, P<0.05; conductance: 6.3+/-2.7 vs 8.2+/-2.7 ml/min/mmHg; P<0.05). Renal blood flow was unchanged but urine output and creatinine clearance increased (P<0.05). We conclude that low-dose AVP infusion has similar effects in the normal and septic mammalian circulation: bradycardia, decreased cardiac output, decreased mesenteric blood flow and conductance and increased urine output and creatinine clearance. This information is important to clinicians considering its administration in humans.

Topics: Animals; Catheterization, Peripheral; Creatinine; Escherichia coli Infections; Hemodynamics; Infusions, Intravenous; Ovariectomy; Regional Blood Flow; Renal Circulation; Sepsis; Sheep; Splanchnic Circulation; Urodynamics; Vasoconstrictor Agents; Vasopressins

During sepsis, limited data on the survival effects of vasopressors are available to guide therapy. Therefore, we compared the effects of three vasopressors on survival in a canine septic shock model. Seventy-eight awake dogs infected with differing doses of intraperitoneal Escherichia coli to produce increasing mortality were randomized to receive epinephrine (0.2, 0.8, or 2.0 microg.kg(-1).min(-1)), norepinephrine (0.2, 1.0, or 2.0 microg.kg(-1).min(-1)), vasopressin (0.01 or 0.04 U/min), or placebo in addition to antibiotics and fluids. Serial hemodynamic and biochemical variables were measured. Increasing doses of bacteria caused progressively greater decreases in survival (P <0.06), mean arterial pressure (MAP) (P <0.05), cardiac index (CI) (P <0.02), and ejection fraction (EF) (P=0.02). The effects of epinephrine on survival were significantly different from those of norepinephrine and vasopressin (P=0.03). Epinephrine had a harmful effect on survival that was significantly related to drug dose (P=0.02) but not bacterial dose. Norepinephrine and vasopressin had beneficial effects on survival that were similar at all drug and bacteria doses. Compared with concurrent infected controls, epinephrine caused greater decreases in CI, EF, and pH, and greater increases in systemic vascular resistance and serum creatinine than norepinephrine and vasopressin. These epinephrine-induced changes were significantly related to the dose of epinephrine administered. In this study, the effects of vasopressors were independent of severity of infection but dependent on the type and dose of vasopressor used. Epinephrine adversely affected organ function, systemic perfusion, and survival compared with norepinephrine and vasopressin. In the ranges studied, norepinephrine and vasopressin have more favorable risk-benefit profiles than epinephrine during sepsis.

Topics: Animals; Anti-Bacterial Agents; Blood Pressure; Cardiac Output; Disease Models, Animal; Dogs; Epinephrine; Escherichia coli Infections; Infusions, Intravenous; Norepinephrine; Shock, Septic; Vasoconstrictor Agents; Vasopressins

We sought to determine the role of oxidative stress in the development of vascular dysfunction in inflammation.. Hyporeactivity to catecholamines and other vasoconstrictors is present in acute inflammation. Because oxidative stress plays a significant role in inflammation, impaired responsiveness may be overcome by anti-oxidants.. In randomized, double-blind, cross-over studies, forearm blood flow (FBF) responses to norepinephrine (NE), angiotensin II (ANG II), and vasopressin (VP) were assessed before and 4 h after induction of systemic inflammation by low doses of Escherichia coli endotoxin (lipopolysaccharide [LPS], 20 IU/kg intravenously) or after placebo in healthy volunteers. Furthermore, the effect of intra-arterial vitamin C (24 mg/min) or placebo on NE-induced or ANG II-induced vasoconstriction was studied after LPS.. Administration of LPS caused systemic and forearm vasodilation, increased white blood cell count, elevated body temperature, and reduced vitamin C plasma concentrations. Lipopolysaccharide decreased the responses of FBF to NE by 59%, to ANG II by 25%, and to VP by 51% (n = 9, p < 0.05, all effects). Co-administration of vitamin C completely restored the response to NE and to ANG II, which was comparable to that observed under baseline conditions (n = 8).. E. coli-endotoxemia reduces FBF responsiveness to vasoconstrictors. The hyporeactivity can be corrected by high doses of vitamin C, suggesting that oxidative stress may represent an important target for inflammation-induced impaired vascular function.

Topics: Adult; Angiotensin II; Antioxidants; Ascorbic Acid; Endotoxemia; Escherichia coli Infections; Humans; Inflammation; Male; Oxidative Stress; Regional Blood Flow; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Although disorders of ADH secretion associated with meningitis are usually consistent with the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), central diabetes insipidus (DI) is an exceptional complication of meningitis. Transient DI as a complication of Escherichia coli (E. coli) meningitis due to ventriculoperitoneal shunt in an 18-month-old boy is presented. Blood and spinal fluid cultures yielded E. coli, sensitive to cefotaxime. The DI arose on the day 3 after admission and continued to the day 20. Treatment comprised cefotaxime, dexamethasone, fluid adjustment and vasopressin. The course of our case supports that in cases of bacterial meningitis, initial fluid restriction may occasionally result in dangerous conditions. Therefore, all children with bacterial meningitis should be followed closely not only in terms of SIADH but also DI. To our knowledge this is the first transient DI associated with E. coli-caused meningitis case reported.

Topics: Dandy-Walker Syndrome; Deamino Arginine Vasopressin; Diabetes Insipidus; Escherichia coli Infections; Humans; Infant; Male; Meningitis, Bacterial; Polyuria; Radioimmunoassay; Renal Agents; Tomography, X-Ray Computed; Vasopressins; Ventriculoperitoneal Shunt

In hypermetabolic sepsis, gluconeogenesis is markedly elevated during fasting, and is manifested as an increased rate of glucose appearance (Ra). The likely causes of such a change are alterations in 1) concentration of systemic hormones, 2) concentration of glucose precursors, especially lactate, 3) activity of the key enzymes of the pathway, and 4) hormone receptors and/or transmembrane signalling mechanisms, involved in the hormonal regulation of the pathway. In this study, we investigated the importance of the latter two factors in the increase of gluconeogenesis during hypermetabolic sepsis. Rats were rendered septic by repeated subcutaneous administration of live Escherichia coli. The livers were perfused in vitro in a nonrecirculating mode to measure the rate of gluconeogenesis from saturating concentrations of lactate (5 mM) or lactate (5 mM) + pyruvate (0.5 mM), and the response of gluconeogenesis to vasopressin (VP, 0.1 and 1.0 nM), glucagon (Glc, 0.1 and 1.0 nM), and prostaglandin (PG) F2 alpha (5 microM). The rate of gluconeogenesis without precursor supply was approximately 20-30 mumoles/100 g b w/hr during the first 4-6 min of perfusion, followed by a continuous decline to very low levels. Infusion of lactate (5 mM) or lactate (5 mM) + pyruvate (0.5 mM) increased glucose output, and maintained it at approximately 100-110 and approximately 130-140 mumoles/100 g b w/hr, respectively. VP, Glc, and PGF2 alpha stimulated the rate of gluconeogenesis in a dose-dependent manner (VP and Glc). No differences were observed between control and septic rats using these stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Dinoprost; Disease Models, Animal; Escherichia coli Infections; Glucagon; Gluconeogenesis; Hormones; In Vitro Techniques; Injections, Subcutaneous; Kinetics; Liver; Male; Perfusion; Rats; Rats, Sprague-Dawley; Vasopressins

Previous investigations on the antipyretic properties of arginine vasopressin have used bacterial endotoxins or pyrogens to induce fever. Because these experimental models of fever fail to mimic all aspects of the responses to infection, we felt it was important to examine the role of endogenously released vasopressin as a neuromodulator in febrile thermoregulation during infection. Therefore the present study examines the effects of chronic infusion of a V1-receptor antagonist or saline (via osmotic minipumps into the ventral septal area of the brain) on a fever induced by injection of live bacteria. Telemetry was used for continuous measurement of body temperature in the awake unhandled rat. Animals infused with the V1-antagonist exhibited fevers that were greater in duration compared with those of saline-infused animals. These results support the hypothesis that vasopressin functions as an antipyretic agent or fever-reducing agent in brain. Importantly, they suggest that endogenously released vasopressin may play a role as a neuromodulator in natural fever.

Topics: Animals; Arginine Vasopressin; Body Temperature Regulation; Brain; Drinking; Eating; Escherichia coli Infections; Fever; Infusion Pumps; Male; Rats; Rats, Sprague-Dawley; Vasopressins

Plasma vasopressin concentrations, measured by radioimmunoassay, were remarkably elevated during endotoxin and E. coli shock. The concentrations were often above 500 pg/ml in dogs and above 300 pg/ml in baboons; they reached 1200 pg/ml in two dogs and 1800 pg/ml in another. Plasma concentration in a quiet, hydrated subject is 4 pg/ml; osmoregulation is maximally effective at 20 pg/ml. Elevation of plasma vasopressin occurred by 15 minutes after beginning infusion of endotoxin or E. coli and reached concentrations of 200-350 pg/ml with a decrease in cardiac output but before hypotension, which suggests decreased thoracic blood volume and decompression of left atrial stretch receptors. Even higher vasopressin levels were associated with a reduction of arterial blood pressure. The typical pattern was an early peak elevation followed by a sustained plateau of plasma vasopressin concentration in dogs and baboons with endotoxin and/or E. coli-induced circulatory shock.

Topics: Animals; Blood Pressure; Cardiac Output; Dogs; Endotoxins; Escherichia coli; Escherichia coli Infections; Lethal Dose 50; Papio; Shock, Septic; Vasopressins; Water-Electrolyte Balance

Plasma vasopressin concentration was measured by radioimmunoassay in lightly anesthetized baboons and dogs before and during experimental Escherichia coli septic shock. Since vasopressin is a potent vasoconstrictor, and activator of clotting factors and a myocardial depressant, we postulated that, if found in substantial amounts in the plasma, vasopressin may contribute to the physiopathology of the septic shock syndrome. Quite high plasma vasopressin concentrations were found in both baboons and dogs. In the baboons, increased plasma vasopressin concentrations occurred, while mean arterial blood pressure was still within normal limits and remained elevated for as long as 12 hours during septic shock. Plasma vasopressin concentrations of this magnitude have been previously reported only with direct hypothalamic stimulation or after hypotensive shock secondary to hemorrhage.

Topics: Animals; Dogs; Escherichia coli Infections; Papio; Radioimmunoassay; Sepsis; Shock, Septic; Vasopressins

The effect of early bilateral pyelonephritis on urinary concentrating ability was studied in rats injected intravenously with enterococci or Staphylococcus aureus and in rats inoculated with Escherichia coli into the medullae of both kidneys. The mean maximum urinary osmolality of normal rats was 2352 mOsm/kg of water. Inoculation of E. coli caused reversible pyelonephritis with sterilization of the kidneys within 12 wk. By 1 day after injection the mean maximum urinary osmolality had decreased to about 1100 mOsm. remained at this level for 3 wk, and then rose to normal by 12 wk. After injection of enterococci and staphylococci, the mean maximum urine osmolality decreased over 3-4 days to about 1000 and 800 mOsm respectively. In the enterococcal infection (which is chronic) the maximum urine osmolality remained about 1200 mOsm for at least 12 wk whereas in the staphylococcal infection (which is reversible) the osmolality gradually rose. Antimicrobial therapy of E. coli renal infection with colistimethate sodium and S. aureus infection with ampicillin rapidly reduced bacterial titers in the kidneys with an associated rise in maximum urinary osmolality. Therapy of enterococcal renal infection with ampicillin produced less impressive decreases in bacterial titers in the kidneys and little or no improvement in urinary concentrating ability. With antimicrobial therapy or with the self-limited infections, the rate of increase in concentrating ability was directly correlated with the rate of decrease of bacterial titers. However, there was poor correlation between histological findings in the kidneys and urinary concentrating ability. These studies demonstrate that early experimental pyelonephritis is associated with a concentrating defect that can be rapidly reversed and therefore is not related to permanent renal damage.

Topics: Ampicillin; Animals; Anti-Bacterial Agents; Colistin; Creatinine; Escherichia coli Infections; Kidney; Kidney Concentrating Ability; Male; Osmolar Concentration; Pyelonephritis; Rats; Staphylococcal Infections; Streptococcal Infections; Vasopressins

Topics: Aged; Aging; Alcaligenes; Aminohippuric Acids; Bacteriuria; Escherichia coli Infections; Female; Glomerular Filtration Rate; Humans; Infusions, Parenteral; Inulin; Kidney; Kidney Concentrating Ability; Kidney Function Tests; Klebsiella Infections; Male; Methods; Pseudomonas Infections; Staphylococcal Infections; Urinary Catheterization; Urinary Tract Infections; Vasopressins

Topics: Animals; Biomedical Research; Blood Circulation; Blood Pressure; Carotid Arteries; Dogs; Endotoxins; Escherichia coli Infections; Felypressin; Femoral Artery; Hemodynamics; Inulin; Kidney; Kidney Function Tests; Lipopolysaccharides; Pharmacology; Research; Shock, Hemorrhagic; Shock, Septic; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Arginine Vasopressin; Bacteremia; Corticosterone; Escherichia coli Infections; Hypophysectomy; Hypothalamo-Hypophyseal System; In Vitro Techniques; Negotiating; Physiology; Pituitary Gland; Rats; Research; Sepsis; Vasopressins