Biomedical subjects
Publications and source records attributed to A J Crisp.
Recent publicity about osteoporosis has stimulated an enormous number of enquiries about treatment and prompted a surge of referrals to rheumatologists. In what circumstances should osteoporosis be considered a disease, how is it best monitored, what treatment would you advocate and for how long?
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The levels of a range of components were measured by 1H nuclear magnetic resonance (1H NMR) in samples of synovial fluid taken from three groups of patients: 10 with osteoarthritis (OA), 18 with rheumatoid arthritis (RA), and 11 with traumatic effusions. A large number of low molecular weight species were measured simultaneously in addition to triglycerides and glycoproteins. Large variations were found between individuals in any one disease group, and there was no measurable correlation between disease state and levels of any low molecular weight component. However, patients with traumatic effusions had high levels of saturated triglycerides, while those with OA had low levels. The chain length of the triglycerides found in OA synovial fluid appears to be shorter than that for the other groups. In RA the composition of triglycerides appears normal, while the overall level is slightly above normal. In a separate study, serial samples of synovial fluid drawn from the knees of two arthritic patients were examined, and the concentrations of glycoprotein, triglycerides and creatinine were found to show a reasonable correlation with each other and with systemic measures of disease activity. These data suggest the potential of synovial fluid triglycerides and creatinine as inflammatory markers.
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This study was undertaken to determine whether moderate increases in left ventricular systolic pressure in anaesthetized dogs result in changes in respiratory activity. Left ventricular systolic pressure was changed using a preparation in which the applied pressure did not distend the aortic arch and in which left atrial and carotid sinus pressures were held constant. The systemic circulation was perfused at constant flow and respiratory activity was assessed from the phrenic electroneurogram. Increases in aortic root and left ventricular systolic pressures resulted in a decrease in arterial perfusion pressure, no significant change in heart rate and a decrease in phrenic nerve activity. These responses differed from those to changes in carotid sinus pressure, which were decreases in perfusion pressure and heart rate but no significant steady-state change in phrenic activity. Responses to changes in ventricular pressure were obtained to each small step between 16 and 28 kPa (120 and 210 mmHg). Following cervical vagotomy, changes in ventricular pressure resulted in neither respiratory nor vascular responses. These results indicate that left ventricular receptors may play a role in the control of respiration.
The aim of this study was to determine whether the degree of stimulation of left ventricular receptors influenced the sensitivity of the carotid sinus baroreceptor reflex. In anaesthetized dogs, the stimulus to left ventricular receptors was changed by changing aortic root and hence ventricular systolic pressure, using a preparation in which the applied pressure did not distend the aortic arch and in which left atrial pressure was controlled. A large step increase in either carotid or left ventricular pressure resulted in vasodilatation both in a perfused hindlimb and in the remainder of the systemic circulation and resulted in a reduction in the response to a change in pressure in the other area. The stimulus-response curves, relating limb and systemic perfusion pressures to small step changes in carotid sinus pressure, were displaced downwards at high left ventricular pressures. However, the curves remained parallel indicating the absence of an interactive effect. These results indicate that the vascular responses to changes in carotid and ventricular pressures show simple additive summation.
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1. This study was undertaken to determine whether physiological changes in pressure localized to the right ventricle result in reflex cardiovascular or respiratory responses. 2. Right ventricular systolic pressure was changed using a preparation in which right atrial and carotid sinus pressures were held constant. The pulmonary and hence the systemic circulation were perfused at constant flow. Vascular resistance and respiratory activity were assessed from the systemic arterial pressure and the phrenic electroneurogram. 3. Changes in right ventricular systolic pressure did not result in any consistent changes in heart rate, systemic arterial blood pressure or phrenic nerve activity. 4. Expected responses occurred to changes in the stimuli to carotid baroreceptors and chemoreceptors, distension of pulmonary arterial baroreceptors, and injections of veratridine into the left ventricle and pulmonary circulation. This suggests that the absence of responses to right ventricular distension was unlikely to have been due to damage to nervous pathways. 5. These results indicate that it is unlikely that there are reflexes arising from the right ventricle which have a major role in cardiovascular or respiratory control.
Thirty-three patients with undiagnosed chronic knee pain had features of autonomic disturbance. Thermography is a useful imaging technique for demonstrating this abnormality. The patients lacked the thermographic symmetry observed in 16 normal controls but this returned with resolution of the pain. Recognized radiological and scintigraphic features of algodystrophy were found. The long duration of symptoms, high proportion of young females and the severity of the associated disability were notable. It is suggested that algodystrophy is a more frequent cause of chronic knee pain than previously recognized. Autonomic abnormalities may be less intense in disease at this site, particularly in young females and may be overlooked. This characteristic of algodystrophy of the knee may contribute to chronicity and subsequent disability.
Seventy-two patients with relatively early but progressive rheumatoid arthritis were treated with chloroquine sulphate, D-penicillamine or a combination of both drugs over 1 year. Chloroquine resulted in significantly fewer side-effects but combined treatment appeared to increase the risks of toxicity. Significant clinical improvements were seen with each regimen and these were indistinguishable between treatments. However, chloroquine had less impact on haemoglobin, ESR, rheumatoid factor levels and C-reactive protein than the other treatments. Furthermore, radiological deterioration was most frequent amongst those given chloroquine alone. Combination treatment with D-penicillamine and chloroquine thus offered no advantages. Chloroquine caused fewer side-effects than both D-penicillamine and combination treatment but appeared to have a less pronounced effect on the disease process as measured by laboratory and radiological indices.
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A quantitative mouse calvarial bone resorption assay was employed to investigate the effects of the mast cell products, heparin and histamine, and of salmon calcitonin. 'Amorphous' heparin, containing a range of molecular weight fractions, inhibited resorption by 15-20% at concentrations of 0.75-5.0 mg/ml. A 'defined' heparin species of mol.wt 13 500 inhibited resorption by 14-28% at 10(-5)-10(-4) mol/l. Histamine inhibited resorption by 19-55% at 10(-3)-10(-2) mol/l. It is proposed that heparin and histamine depress coupled bone resorption and formation and may lead to net loss of bone. Salmon calcitonin inhibited resorption at concentrations as low as 10 pg/ml. 'Amorphous' (but not 'defined') heparin blunted calcitonin induced inhibition of bone resorption and may derepress osteoclasts.
The number and distribution of mast cells were assessed in 116 synovial membranes from patients with rheumatoid arthritis and in 30 control specimens. Rheumatoid synovial membranes contained a mean of 48.5 mast cells per 20 high-power fields (HPF) (range 0-252), and control synovial membranes had a mean of 3.9 mast cells per 20 HPF (range 0-13) (P less than 0.001). In a comparison of high and low mast cell subgroups in rheumatoid arthritis, counts were directly related to the intensity of clinical synovitis in the affected joint, but not to hemoglobin concentration or erythrocyte sedimentation rate. Joints excised from 5 patients with rheumatoid arthritis were characterized by active bone remodeling with increased osteoid, active resorption by osteoclasts, and trabecular osteoporosis. Mast cells were prominent in both extraosseous pannus and intraosseous invasive tissue. The possible roles of mast cells in the pathogenesis of rheumatoid arthritis are discussed.
Fragments of synovial membranes from three patients with rheumatoid arthritis were incubated in Dulbecco's modified Eagle's medium (DMEM). Histamine was released into the medium at rates up to 649.3 ng/g synovium/day. To investigate whether histamine in synovial fluid may have more than a vasoactive role, cells cultured from human trabecular bone adjacent to a rheumatoid joint and human adherent rheumatoid synovial cells were incubated with different concentrations of histamine for 5 min. Histamine increased the intracellular content of cyclic AMP up to three fold in a dose-related manner but had no effect on synovial cells. This offers preliminary evidence that cells grown from human trabecular bone have histamine receptors.