THE EFFECTS OF PROSTAGLANDIN E<sub>1</sub>, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

Grennan, D M; Mitchel, Weston; Miller, William L.; Zeitlin, I. J.

doi:10.1111/j.1476-5381.1977.tb07747.x

Cited by 22 publications

(2 citation statements)

References 11 publications

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“…There is much evidence to suggest that kinin release may be implicated in producing inflammatory symptoms in various arthritides. In dog synovium, bradykinin increases blood flow (Dick, Grennan & Zeitlin, 1976) and permeability (Grennan et al, 1977) in nanogramme concentrations and has a powerful pain-producing action which is potentiated by prostaglandins (Fereira, Moncada & Vane, 1974). Injection of bradykinin into the dog knee-joint produces an acute inflammatory reaction with warmth and swelling @elman et al., 1967).…”

Section: Discussionmentioning

confidence: 99%

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

Sharma

Zeitlin

Brooks

et al. 1980

Clin Exp Pharma Physio

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1. When six female seropositive rheumatoid patients were given placebo therapy for 48 h, their plasma kininogen level, 9.2 +/- 0.7 microgram bradykinin equivalents (bk eq) per ml, was found to be 59% greater than that of a group of eight healthy female volunteers (5.8 +/- 0.5 microgram/ml). 2. When the rheumatoid patients received aspirin therapy for 1 week, their mean plasma kininogen concentration fell by 31% to 6.3 +/- 0.8 microgram Bk eq/ml. This was accompanied by a 20.4% fall in mean plasma alpha 2-globulin level. Haematocrit and total plasma protein were not significantly altered (P > 0.05). 3. The fall in kininogen was very rapid, the main reduction occurring within the first hour. 4. Aspirin therapy greatly reduced the pain assessments but had no effect on plasma concentrations of IgG, IgA, IgM, complement component C3, nor on ESR, haemoglobin, leucocyte count, nor ring size. Left hand grip strength was increased while right hand grip strength was unchanged. 5. The action of aspirin on plasma kininogen and alpha 2-globulin was similar to that of indomethacin. Plasma kininogen has been considered to be an acute phase reactant. The possible diagnostic value of plasma kininogen estimation is discussed.

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Section: Discussionmentioning

confidence: 99%

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

Sharma

Zeitlin

Brooks

et al. 1980

Clin Exp Pharma Physio

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“…Chronic inflammation has been associated with elevated levels of PGE2 at the site of injury. PGE2 is a vasodilator (10), enhances vascular permeability (11), and plays a role in the regulation of the immune response by modulating T lymphocyte proliferation, macrophage cytotoxicity, and lymphokine production (12).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Whiteley¹,

Needleman²

1984

J. Clin. Invest.

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Abstract. Chronic inflammation is associated with an infiltration of mononuclear cells, fibroblast proliferation, and elevated levels of prostaglandin (PG) E2. Mononuclear cell conditioned factor (MNCF) medium (5%) stimulated a 100-fold increase in basal human dermal fibroblast PGE2 release over 48 h as compared with fibroblasts that were incubated with control medium (conditioned medium prepared without cells). The MNCF-induced PGE2 production was suppressed by protein synthesis inhibitors. Fibroblasts pretreated with control medium released PGE2 only modestly in response to 1 nM bradykinin for 1 h (basal, 50±7 pg PGE2/,g protein; stimulated, 104±12 pg PGE2flsg protein), whereas cells that had been pretreated with MNCF showed a greatly facilitated bradykinin-induced release of PGE2. (basal, 297±59 pg PGE2/,g protein; stimulated, 866±85 pg PGE2/Ag protein). The exaggerated agonist response is not specific for bradykinin because plateletderived growth factor elicits a similar response. Exogenous arachidonic acid conversion to PGE2 was also facilitated (two-to threefold) by MNCF pretreatment as compared with control. Both the enhanced agoniststimulated and exogenous arachidonic acid-induced PGE2 release from the MNCF pretreated cells were inhibited by actinomyin D or cycloheximide. A kinetic study of microsomal cyclooxygenase prepared from fibroblasts pretreated with MNCF showed a threefold increase in the maximum velocity (Vmax) but the same Michaelis constant (Kin) as control-treated cells. This augmented arachidonic acid metabolism and subsequent enhanced PGE2 production may play an important role

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Even low‐grade synovitis significantly accelerates the clearance of protein from the canine knee: implications for measurement of synovial fluid “markers” of osteoarthritis

Myers

Brandt²,

Eilam

1995

Arthritis & Rheumatism

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Objective. In recent studies, the synovial fluid concentration of molecules derived from the extracellular matrix of articular cartilage has been used to deduce the magnitude of cartilage destruction or repair in osteoarthritic (OA) joints. Because low-grade synovitis is often present in such joints, we assessed the effect of synovial inflammation on the clearance of a prototypical protein, albumin, from synovial fluid.Methods. '311-labeled albumin (RISA) was injected into 1 (control) knee of each of 14 dogs. The concentration of RISA in synovial fluid aspirated 7 hours after the injection and serial measurements of surface radioactivity were used to calculate the volume of distribution ( v d ) and clearance of RISA. One week later, synovitis was induced in the contralateral knee by intraarticular injection of various quantities of calcium pyrophosphate dihydrate (CPPD) crystals, after which RISA was injected into that joint and these measurements were repeated.Results. Intraarticular injection of 500 pg of CPPD crystals produced intense synovitis, with a mean synovial fluid white blood cell (WBC) count of 43,200 cells/mm3, and values for RISA v d and RISA clearance (36.5 ml and 33.7 pVminute) were much higher than those for saline-injected control knees (2.7 ml and 1.5 pl/minute, respectively). Injection of 0.5 pg of CPPD

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THE EFFECTS OF PROSTAGLANDIN E₁, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

Cited by 22 publications

References 11 publications

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Even low‐grade synovitis significantly accelerates the clearance of protein from the canine knee: implications for measurement of synovial fluid “markers” of osteoarthritis

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THE EFFECTS OF PROSTAGLANDIN E1, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

Cited by 22 publications

References 11 publications

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

The Action of Aspirin on Plasma Kininogen and Other Plasma Proteins in Rheumatoid Patients: Relationship to Disease Activity

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Even low‐grade synovitis significantly accelerates the clearance of protein from the canine knee: implications for measurement of synovial fluid “markers” of osteoarthritis

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THE EFFECTS OF PROSTAGLANDIN E₁, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY