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Träfflista för sökning "WFRF:(Lundberg C) srt2:(1985-1989)"

Search: WFRF:(Lundberg C) > (1985-1989)

  • Result 1-10 of 11
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  • Gerdin, Bengt, 1947-, et al. (author)
  • Permeability-increasing ability of PAF-acether in rat skin.
  • 1985
  • In: Inflammation. - 0360-3997 .- 1573-2576. ; 9:1, s. 107-12
  • Journal article (peer-reviewed)abstract
    • Platelet-activating factor (PAF-acether), a phospholipid compound with effects on several cells, e.g., platelets and polymorphonuclear leukocytes (PMNs), was examined for its effect on microvascular permeability in rat skin. It was found to increase microvascular permeability, measured as exudation of [125I]human serum albumin, in amounts exceeding 1 pmol, and was more than 1000 times as potent as histamine. The effect was independent of cell infiltration, as no accumulation of PMNs, measured as the amount of myeloperoxidase in the skin, occurred and as the response was unaltered in animals rendered neutropenic due to treatment with an antiserum against PMNs.
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  • Gerdin, Bengt, 1947-, et al. (author)
  • Selective tissue accumulation of manganese and its effect on regional blood flow and haemodynamics after intravenous infusion of its chloride salt in the rat.
  • 1985
  • In: International journal on tissue reactions. - 0250-0868. ; 7:5, s. 373-80
  • Journal article (peer-reviewed)abstract
    • Manganese chloride (MnCl2), with or without the addition of trace amounts of 54Mn2+, was administered as a 7-min i.v. infusion in rats. Tissue accumulation of 54Mn2+ was determined 0-15 min after the infusion, and cardiac output, regional blood flows and vascular resistances were measured 5 and 60 min after the infusion by the microsphere technique. The plasma half-life of 54Mn2+ was found to be 4.7 min. Mn2+ accumulated in several organs, the highest relative concentrations being seen in the liver, duodenum, jejunum, kidney and heart, and intermediate concentrations in the ileum, colon, stomach and spleen. There was no uptake in the lung, skeletal muscle or brain. During the infusion of 180 mumol/kg b.w. of Mn2+, the arterial blood pressure fell from a mean of 123 +/- 5 mm Hg to a minimum of 85 +/- 7 mm Hg, and thereafter returned to normal. Five minutes after termination of the infusion, there was a decrease in cardiac output and minute work but not in total peripheral resistance, a finding interpreted as a negative inotropic effect of Mn2+. At this time blood flow was decreased in the stomach, ileum, colon, spleen and skin, and increased in duodenum, jejunum and liver. The blood flows were normalized 60 min after termination of the infusion in all organs except the liver and heart. The effects are probably due to the calcium-antagonistic properties of Mn2+ and the tissue accumulation is most probably a result of intracellular accumulation through calcium channels. The relation between tissue accumulation and tissue selectivity of blood-flow alterations is unexplained.
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  • Laato, M, et al. (author)
  • Inflammatory reaction and blood flow in experimental wounds inoculated with Staphylococcus aureus.
  • 1988
  • In: European Surgical Research. - 0014-312X .- 1421-9921. ; 20:1, s. 33-8
  • Journal article (peer-reviewed)abstract
    • Wound healing and granulation tissue formation can be accelerated by inoculation with live pathogenic microorganisms. For further elucidation of this phenomenon the present work was undertaken to study the effects of Staphylococcus aureus microorganisms on the inflammatory reaction and blood flow in developing granulation tissue in rats. Cylindrical hollow sponge implants were used as an inductive matrix for the growth of granulation tissue. In control animals 1 ml of wound fluid was withdrawn from the central dead space of the implant immediately after implantation and replaced with 1 ml of physiological saline. In experimental animals the implants were injected with live staphylococci, 10(2) or 10(5) microorganisms/ml. Wound fluid was analyzed 3, 7, 10 and 14 days after implantation, whereas measurements of local blood flow and albumin extravasation in the granulation tissue were made after 7 days. Implants inoculated with 10(5) organisms developed infection with pus formation while implants contaminated with 10(2) organisms showed no infection. In wound fluid specimens collected from the infected implants correlation between the number of polymorphonuclear leukocytes and prostaglandin E2 concentration was statistically significant. The most prominent finding in contaminated but uninfected implants was an enhanced local blood flow. This may explain some of the mechanisms leading to S. aureus-induced acceleration of wound healing.
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  • McCann, E, et al. (author)
  • Selective actions of calcium antagonistic drugs on the haemodynamics and regional organ blood flow in rats.
  • 1986
  • In: International journal on tissue reactions. - 0250-0868. ; 8:3, s. 205-12
  • Journal article (peer-reviewed)abstract
    • Six substances, all of which influence calcium utilization by smooth muscle, namely nimodipine (50 micrograms/kg), flunarizine (1 mg/kg), verapamil (0.2 mg/kg), lidoflazine (1 mg/kg), magnesium (600 mumol Mg++/kg), and manganese (180 mumol Mn++/kg), were given intravenously to rats and their effects on regional blood flows and on cardiac output were determined by the radioactive microsphere technique. All compounds caused a temporary fall in mean arterial blood pressure. Cardiac output was decreased by manganese, and minute work by nimodipine, manganese and lidoflazine. Nimodipine increased blood flow in the liver, skeletal muscle and heart and decreased that in the stomach, ileum, colon, kidney, spleen and skin; manganese increased flow in the duodenum, jejunum, liver and myocardium and decreased that in the stomach, ileum, colon, spleen and skin; flunarizine increased flow in the liver, heart and brain; and magnesium increased flow in the liver, spleen and brain. Lidoflazine and verapamil, although leading to haemodynamic alterations, had no selective effect on organ blood flow. Selective actions by calcium effector drugs can provide information on mechanisms of calcium flux in various types of vascular smooth muscle, and show that it is possible to tailor combinations of anti-calcium agents with optimal effects on a given organ.
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  • Sandler, H, et al. (author)
  • Antiserum-induced neutropenia in the rat : characterization of a rabbit anti-rat neutrophil serum.
  • 1987
  • In: British journal of experimental pathology. - 0007-1021. ; 68:1, s. 71-80
  • Journal article (peer-reviewed)abstract
    • A heterologous rabbit anti-rat neutrophil serum (ANS) based on peptone-stimulated peritoneal exudate neutrophils (PMNLs) from Sprague Dawley rats was prepared. Leucoagglutination and indirect immunofluorescence assays revealed high titres of antibodies to rat PMNLs (1/2560), lower titre of antibodies to rat lymphocytes (1/160) and a very low titre against rat platelets (1/20). ANS given intravenously (i.v.) to rats in doses of up to 42 mg of protein/kg b.w. caused transient neutropenia, lasting about 10 min after administration, and thrombocytopenia, lasting about 5 min. Two minutes after an i.v. injection of 21 mg of ANS/kg b.w. there was profound uptake of 51Cr-labelled PMNLs in the lung, increased release of 51Cr to plasma, an increased amount of 51Cr in the spleen and consumption of greater than 98% of total complement (CH50). Two hours later there was high activity of 51Cr in the plasma, spleen and liver, while lung radioactivity had decreased to below baseline and CH50 had recovered to 55% of baseline. An intraperitoneal (i.p.) injection of ANS was followed by prolonged neutropenia with a maximum after 12 h. Simultaneously peripheral mononuclear cells slightly decreased. There was no change in the number of peripheral platelets in the blood or in the plasma concentration of fibrinogen, alpha 2-antiplasmin, plasminogen or plasminogen activators. Intraperitoneal administration of ANS did not affect CH50. It was concluded that the raised ANS had good specificity against rat PMNLs and was able to induce prolonged neutropenia after i.p. injection without affecting the complement of fibrinolytic system.
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