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Biomedical subjects

B L Kidd

Publications and source records attributed to B L Kidd.

At least 19 recordsLinked to original sources
PubMed1992

The effects of calcitonin gene-related peptide on formation of intra-articular oedema by inflammatory mediators.

1. The temporal and quantitative effects of inflammatory mediators on plasma extravasation in the rat knee were investigated by use of a perfusion technique. 2. Intra-articular perfusion of substance P (SP), bradykinin or histamine over a 5 min test period produced rapid-onset and prolonged plasma extravasation in a dose-dependent fashion. The rank order of potency was bradykinin greater than SP greater than histamine. 3. Calcitonin gene-related peptide (CGRP) did not induce plasma extravasation but enhanced substance P-induced plasma extravasation in a dose-dependent fashion. A 5 min co-perfusion of the two agents produced short-term enhancement lasting 10 min while continuous co-perfusion produced enhancement for the duration of the perfusion. 4. A 5 min perfusion of CGRP enhanced plasma extravasation when co-perfused with bradykinin but not histamine. However, when CGRP and histamine were continuously co-perfused over a 20 min test period, an enhanced response was apparent. 5. The results indicate that intra-articular perfusion of CGRP enhances synovial plasma extravasation induced by agents that increase vascular permeability, but suggest that the response is not uniform and is critically dependent on the duration of perfusion within the joint.

Animals↗
PubMed1992

Immune complexes in ankylosing spondylitis.

Immune complexes have been reported in ankylosing spondylitis (AS) and may implicate infectious agents. Serum samples from 49 patients with AS were assayed for immune complexes by polyethylene glycol precipitation, followed by radial immunodiffusion and pepsinogen binding immunoassay. Both methods showed increases in IgA containing immune complexes, which correlated with serum IgA and with IgA rheumatoid factor concentrations, but did not show increases in other immune complex components. Increased immune complexes were associated with peripheral joint synovitis, but showed no correlation with other clinical or laboratory indices of disease activity. Immune complexes from nine AS serum samples and one AS synovial fluid were electrophoretically separated then probed with anti-Klebsiella pneumoniae, but AS specific antigens were not identified. This study did not suggest a major role for immune complexes in AS without peripheral disease, nor provide serological evidence for the involvement of klebsiella antigens.

Antigen-Antibody Complex↗
PubMed1992

Localisation and characterisation of substance P binding to human synovial tissue in rheumatoid arthritis.

The neuropeptide substance P is found in perivascular and free unmyelinated nerve fibres in human synovial tissue. Quantitative receptor autoradiography was used to show specific, high affinity (Kd = 0.75 (0.21), nmol/l (mean (standard error of the mean)), low capacity (Bmax = 27.8 (7.9) amol/mm2) binding sites for substance P Bolton Hunter-labelled with iodine-125 localised to vascular endothelial cells in human synovial tissue. The binding could be saturated, was reversible, and was dependent on the magnesium concentration. Unlabelled substance P and neurokinin A competitively inhibited specific binding with 50% inhibition at concentrations of 1.25 (0.21) and 175 (29) nmol/l respectively. Neurokinin B (mumol/l) and calcitonin gene related peptide (1 mumol/l) did not inhibit binding. These binding sites show characteristics of the neurokinin 1 tachykinin receptor subtype. This provides further evidence that substance P may play a part in the vascular control of human synovium and may influence inflammatory processes in joints.

Adult↗
PubMed1992

Localization of the enzyme neutral endopeptidase to the human synovium.

Neuropeptides, contained within sensory nerve fibers in the synovium, are present in inflammatory joint fluids. The potency of these peptides in vitro has led to the hypothesis that enzyme degradation systems are operative in vivo. To address this question we localized neutral endopeptidase (NEP; EC 3.4.24.11) in human synovium. The normal human synovium failed to show any immunoreactivity for NEP. In the disease groups there was intense staining of cells surrounding blood vessels. Our data are consistent with the hypothesis that a proportion of synovial fibroblasts are the major source of this enzyme in the arthritic joint.

Adult↗
PubMed1990

Substance P-, calcitonin gene-related peptide- and C-flanking peptide of neuropeptide Y-immunoreactive fibres are present in normal synovium but depleted in patients with rheumatoid arthritis.

By means of antisera to cytoplasmic components of nerve fibres and neuropeptides which are known to be present in sensory or sympathetic nerves we have examined the distribution of both total and different types of nerve fibres in normal and inflamed human synovial tissue. Samples of synovia were obtained at surgery from five normal and five rheumatoid patients (age range 10-77 years). In order to map the overall neural innervation of the synovium, antiserum to the general neuronal marker protein gene product 9.5 was employed. Substance P and calcitonin gene-related peptide antisera were employed to identify sensory fibres and antisera to the C-flanking peptide of neuropeptide Y to distinguish sympathetic nerves. In normal synovium protein gene product 9.5-immunoreactive fibres were numerous, in particular, the vasculature was densely innervated. Free protein gene product 9.5-immunoreactive fibres were less numerous but were present in all synovia examined, and in many cases these extended to the intimal layer. Neuropeptide immunostaining was predominantly found in perivascular networks. Fibres immunoreactive for the C-flanking peptide of neuropeptide Y were exclusively located around blood vessels whereas free fibres were immunoreactive for substance P or calcitonin gene-related peptide. As with free protein gene product 9.5-immunoreactive fibres, fibres expressing substance P or calcitonin gene-related peptide immunoreactivity were often seen in the intimal cell layer. In rheumatoid arthritis a similar innervation to that seen in normal synovium was apparent in the deep tissue but fibres immunoreactive for protein gene product 9.5, the C-flanking peptide of neuropeptide Y, substance P or calcitonin gene-related peptide were not visible in the more superficial tissues or the intimal cell layer. In addition, immunostaining of neuropeptides in the deep tissue was weaker in the diseased tissues than in normal controls. The data unequivocally demonstrate that synovial tissues are richly innervated and confirm the presence of both sensory and sympathetic nerves. The absence of nerves which innervate the superficial synovium in rheumatoid arthritis might suggest that there is increased release of substance P, calcitonin gene-related peptide and the C-flanking peptide of neuropeptide Y, reducing the stores in the nerves to levels below that detectable by immunocytochemistry. However, since protein gene product 9.5-immunoreactive nerves were not seen in the inflamed tissue it is probable that synovial growth outflanks neural growth and consequently as the disease progresses neural structures become restricted to deeper tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Specific antibody response to the mycobacterial 65 kDa stress protein in ankylosing spondylitis and rheumatoid arthritis.

Immune responses to conserved, immunogenic homologues of the mycobacterial 65 kDa stress protein (SP65) have been implicated in inflammatory arthritis. Serum anti-SP65 was measured in AS, RA and healthy controls using an indirect enzyme immunoassay with recombinant SP65. IgA anti-SP65 was elevated in 19 of 59 AS patients, but the elevation in median level was not statistically significant. Anti-SP65 of all isotypes was increased in RA, but achieved significance (P less than 0.01) for IgA only. Adjusting specific antibody results for elevations in total serum Ig levels reduced AS and RA anti-SP65 to near normal levels, suggesting that a major component of the increased anti-SP65 may be secondary to polyclonal activation.

Antibodies↗
PubMed1989

A neurogenic mechanism for symmetrical arthritis.

Human synovium is richly innervated by autonomic and sensory nerve fibres, many of which contain neuropeptides. The hypothesis is that, in addition to a sensory role, some of these fibres modulate the response of the synovial membrane to a variety of noxious stimuli by releasing these peptides. Synovial damage results in acute inflammation in the damaged joint and a neurogenically mediated infiltrate of inflammatory cells in the contralateral joint. These cells might protect the contralateral synovium from injury similar to that in the damaged joint. An increased response would lead to synovitis and symmetrical disease.

Arthritis↗
PubMed1989

Hypoxic-reperfusion injury in the inflamed human joint.

A series of experiments showed that, on exercise of the inflamed human knee, intra-articular pressure rises above synovial capillary perfusion pressure, causing intra-articular hypoxia; and that, on cessation of exercise, there is oxidative damage to lipids and IgG within the joint. These findings are consistent with the hypothesis that persistence of synovial inflammation can be due to exercise-induced hypoxic-reperfusion injury mediated by reactive oxygen species.

Adult↗
PubMed1989

Immunohistological features of synovitis in ankylosing spondylitis: a comparison with rheumatoid arthritis.

The immunohistological features of the synovial membrane in ankylosing spondylitis, HLA-B27 associated oligoarthritis, and rheumatoid arthritis wer examined with particular reference to T lymphocyte subsets. T helper (CD4+) cells clearly outnumbered T suppressor/cytotoxic (CD8+) cells in rheumatoid arthritis, whereas both cell types were present in equal numbers in ankylosing spondylitis. A reduction of CD4+/CD45R+ suppressor/inducer cells relative to CD4+/UCHL1+ helper/inducer cells was apparent in all diagnostic groups. The observations were suggestive of disease specific inflammatory responses within synovial membrane.

Adult↗
PubMed1989

Use of laser Doppler flowmetry and transcutaneous oxygen tension electrodes to assess local autonomic dysfunction in patients with frozen shoulder.

The laser Doppler flowmeter (LDF), which measures changes in cutaneous blood flow, and the transcutaneous oxygen electrode which measures cutaneous perfusion, were used to study reflex changes in the microcirculation of the shoulder in 38 patients with frozen shoulder and 10 normal controls. In all controls and 22 patients with frozen shoulder, a normal LDF response to inspiration/expiration was observed. In 16 patients with frozen shoulder, LDF responses were either unilaterally or bilaterally absent. Comparison between the two patient groups showed a significant association (chi 2 = 6.43, P less than 0.02) between abnormality of response and the persistence of pain. TcPO2 was in the normal range in all patients and controls. These findings suggest that the LDF together with the TcPO2 may be a useful method of studying the skin microcirculation over the shoulder.

Adult↗
PubMed1988

Delay in diagnosis of spondarthritis.

A survey was made of referral patterns and investigative procedures in 125 patients with HLA-B27 related spondarthritic diseases reviewed in the rheumatology department of a district general hospital. At the time of referral a large proportion of the patients had already been seen by other hospital departments for the same complaint although in many cases such referrals did not result in a correct diagnosis. Multiple referrals had often resulted in prolonged diagnostic delay during which time unnecessary and invasive investigations were performed. The data indicate the need for improved diagnostic awareness of common rheumatic conditions by all clinicians dealing with musculoskeletal disease.

Diagnostic Errors↗
PubMed1988

Mechanisms of persistent synovitis.

Rheumatoid arthritis is characterised by persistent and symmetrical synovitis. In this article we propose two linked hypotheses to explain these observations. A mechanism to explain symmetry of synovitis is described whereby fine afferent nerve fibres from joints become bilaterally sensitized to movement with resultant release of neuropeptides promoting an inflammatory response. Clinical and experimental evidence is reviewed and shows that movement and resulting hypoxic reperfusion injury leads to a persistent synovitis.

Animals↗
PubMed1986

Admission thyroid function testing in elderly patients.

The free thyroxine index (FTI) was measured in 307 elderly patients admitted to two geriatric units. The initial FTI was abnormal in 41 (13.3%), being raised in 27 and low in 14 patients. On further testing, these abnormalities were found to be either transient or of no clinical significance in 36 of the 41 patients (88%). Only five of the 307 patients (1.6%) were finally treated for previously undiagnosed thyroid disease and of these three improved (1%). Thyroid disease identified by routine screening, and not suspected from the history and clinical findings, was present in only two patients (0.7%). In view of these findings we suggest that thyroid screening is no more justified in the elderly than in younger hospitalised patients.

Aged↗