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Biomedical subjects

P Roberts-Thomson

Publications and source records attributed to P Roberts-Thomson.

At least 19 recordsLinked to original sources
PubMed2003

A randomized placebo-controlled trial of arthroscopic lavage versus lavage plus intra-articular corticosteroids in the management of symptomatic osteoarthritis of the knee.

OBJECTIVE: To assess the efficacy of intra-articular steroid injections following arthroscopy and joint lavage in symptomatic OA of the knee. METHODS: Seventy-seven patients with OA of the knee were randomized to receive either 120 mg methylprednisolone acetate (MPA) or placebo following arthroscopy. Clinical assessments included severity of pain on movement and at rest, stiffness, the presence of joint effusions, range of movement, WOMAC (Western Ontario and McMaster Universities Osteoarthritis Index) score and Lequesne functional assessment. The outcome measures were evaluated at baseline and 2, 4, 8, 12 and 24 weeks. Further arthroscopies and synovial biopsies were performed at the time of clinical response and at relapse. RESULTS: An intention-to-treat analysis was performed on 71 patients (38 MPA, 33 placebo). Using the OARSI (Osteoarthritis Research Society International) response criteria, 58% of the steroid group vs 33% of the placebo group (adjusted relative risk = 2.38) (P = 0.004) responded at 4 weeks. At other time points, there were no significant differences between the treatment groups. There were no significant differences between the two treatment groups for pain, stiffness or WOMAC or Lequesne assessments at any time point. CONCLUSIONS: The response to intra-articular corticosteroids following joint lavage is short-lived (2-4 weeks), achievement of an OARSI response criterion being the only difference between the two groups.

Adrenal Cortex Hormones↗
PubMed2003

Risk of cancer in patients with scleroderma: a population based cohort study.

BACKGROUND: Previous studies have suggested an increased risk of cancer among patients with scleroderma. OBJECTIVE: To study a population based cohort of patients with scleroderma in South Australia. METHODS: Subjects with scleroderma were identified from the South Australian Scleroderma Registry established in 1993. All subjects on the scleroderma registry were linked to the South Australian Cancer Registry to identify all cases of cancer until 31 December 2000. Standardised incidence ratios (SIRs) for cancer for subjects with scleroderma were determined using the age- and sex-specific rates for South Australia. RESULTS: In 441 patients with scleroderma, 90 cases of cancer were identified, 47 of which developed after inclusion on the scleroderma registry. The SIRs for all cancers among these patients were significantly increased (SIR=1.99; 95% confidence interval (95% CI) 1.46 to 2.65) compared with the cancer incidence rates for South Australia. The SIRs for lung cancer (SIR=5.9; 95% CI 3.05 to 10.31) were also significantly increased. The SIRs for all cancers among the subgroups with diffuse scleroderma (SIR=2.73; 95% CI 1.31 to 5.02) and limited scleroderma (SIR=1.85; 95% CI 1.23 to 2.68) were significantly increased. CONCLUSIONS: This population based cohort study provides evidence that scleroderma is associated with cancer, and in particular, lung cancer. In addition, both diffuse and limited forms of scleroderma are associated with a similarly increased risk of cancer.

Adolescent↗
PubMed2000

Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea.

BACKGROUND: Patients with obstructive sleep apnea (OSA) experience repetitive episodic hypoxemia with consequent sympathetic activation and marked blood pressure surges, each of which may impair endothelial function. We tested the hypothesis that patients with OSA have impaired endothelium-dependent vasodilation, even in the absence of overt cardiovascular disease. METHODS AND RESULTS: We studied 8 patients with OSA (age 44+/-4 years) and 9 obese control subjects (age 48+/-3 years). Patients with OSA were newly diagnosed, never treated for OSA, on no medications, and free of any other known diseases. All obese control subjects underwent complete overnight polysomnographic studies to exclude occult OSA. Resistance-vessel function was tested by use of forearm blood flow responses to intra-arterial infusions of acetylcholine (a vasodilator that stimulates endothelial release of nitric oxide), sodium nitroprusside (an exogenous nitric oxide donor), and verapamil (a calcium channel blocker). Conduit-vessel function was also evaluated by ultrasonography. Brachial artery diameter was measured under baseline conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent vasodilator). Patients with OSA had a blunted vasodilation in response to acetylcholine (P:<0.007), but responses to sodium nitroprusside and verapamil were not significantly different from those of control subjects. No significant difference in conduit-vessel dilation was evident between OSA patients and obese control subjects. CONCLUSIONS: Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation. This may be implicated in the pathogenesis of hypertension and heart failure in this condition.

Acetylcholine↗
PubMed1999

The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation.

OBJECTIVE: There is limited information on the mechanisms mediating the deleterious effects of passive smoke exposure. Cross-sectional studies indicate that nonsmokers exposed chronically to passive smoke have impaired endothelium mediated vasodilation. We tested the hypothesis that acute exposure to sidestream (passive) smoke impairs endothelium-dependent vasodilation in healthy nonsmokers. METHODS AND RESULTS: We studied 12 healthy nonsmokers (aged 27 +/- 5 years, nine men and three women). We obtained measurements of blood pressure, heart rate, and bilateral forearm blood flow (FBF). Each individual was studied twice, following a randomized, placebo-controlled design. The effects of passive smoke were studied on one day and the effects of vehicle (room air) on a separate day. Acetylcholine (ACh) and sodium nitroprusside (SNP) were infused into the left brachial artery before and after 15 min of exposure to either passive smoke (carbon monoxide concentration between 20 and 40 p.p.m.) or vehicle (room air). The order of ACh and SNP, and smoke or vehicle, was randomized between individuals. Smoke exposure increased carboxyhemoglobin from 0.5 +/- 0.1 % to 0.8 +/- 0.1% (P= 0.002). Neither passive smoke nor vehicle changed baseline measurements of heart rate, blood pressure and forearm vascular resistance (FVR). The vasodilatory responses to ACh and SNP were very similar, both before and after exposure to passive smoke and before and after vehicle. CONCLUSION: Our data demonstrate that acute exposure to passive smoke does not alter either endothelium-dependent or independent vasodilatory responses in healthy nonsmoking individuals. Hence, impaired endothelial vasodilatory responses in nonsmokers chronically exposed to passive smoke most likely reflect chronic functional and/or structural changes in responses to cigarette smoke, rather than the acute effects of cigarette smoke toxicity on endothelial function.

Acetylcholine↗
PubMed1999

The clinical associations of mitotic spindle autoantibodies in a South Australian cohort.

BACKGROUND: The mitotic spindle apparatus (MSA) is a unique structure of microtubules and associated proteins involved in the segregation and reorganisation of chromosomes during cell division. Autoantibodies to the MSA (anti-MSA) are reported to occur rarely, but are easily identified during the immunofluorescent detection of anti-nuclear antibodies (ANA), and are generally reported as part of that investigation. AIMS: As the clinical significance of these antibodies is unknown, our aim was to identify the clinical features of subjects identified with anti-MSA, and in a subset investigate the co-association with organ specific anti-thyroid antibodies. METHODS: All ANA results from the three major immunology laboratories serving South Australia between January 1993 and June 1998 were retrospectively reviewed to identify anti-MSA subjects. Clinical details were extracted from hospital or general practice records using a standard proforma. Thyroid autoantibodies were measured using standard technique. A control group of consecutive ANA positive, anti-MSA negative individuals had anti-thyroid antibodies measured. Statistical comparison used chi2 test. RESULTS: Fifty-five subjects (43F) were identified with mean age 59.8 (range 17-91); 39 had specific diagnoses, with 16 identified as part of non-specific investigations. 'Arthritis' broadly accounted for the largest group, transient inflammatory arthritis n=7, degenerative joint disease n=6, rheumatoid arthritis n=5. Adenocarcinoma and mesothelioma accounted for one case each. Thirty-two subjects had anti-thyroid antibodies tested, with ten of 21 and two of 11 positive among the groups with anti-MSA titre >1:80 and <1:40 respectively, chi2=2.7, p=0.1. Anti-thyroid antibodies were detected more frequently among the high titre anti-MSA group (ten of 21) compared with high titre positive ANA, negative anti-MSA group (two of 11), RRisk 4.4, chi2=5.34, p=0.02. CONCLUSION: This study confirmed the relative rarity of anti-MSA and that its association is primarily with rheumatic diseases. The coincidence of mesothelioma is novel with only two previous reports of malignancy and anti-MSA. The co-association of high titre anti-MSA and thyroid autoantibodies suggest that the latter should be a follow up investigation if the former is identified as part of an investigative screen.

Adolescent↗
PubMed1999

Cytokines and cell adhesion molecules in musculoskeletal disorders.

This paper reviews the cytokine profiles and various cell adhesion molecules expressed in the more common inflammatory joint conditions such as rheumatoid arthritis, psoriatic arthritis, the spondyloarthropathies (Reiter's syndrome, ankylosing spondylitis), as well as systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, giant cell arteritis and polymyositis. Knowledge of the broad range of cytokines produced in these conditions and the expression of cell adhesion molecules that result from cytokine production will assist in the understanding of the pathogenesis of these conditions and may lead to new therapeutic interventions.

Journal Article↗
PubMed1997

Synovial membrane cytokine profiles in reactive arthritis secondary to intravesical bacillus Calmette-Guérin therapy.

We describe the cellular infiltrate and cytokine profile in sequential synovial membrane biopsies from a patient with acute followed by chronic synovitis after intravesical bacillus Calmette-Guérin (BCG) therapy for an in situ transitional cell carcinoma of the bladder. Histological and immunohistochemical analysis of 3 synovial biopsies were done sequentially over a 9 month period. The patient was HLA-B27 positive, but HLA-DR4 negative, and did not have the "shared epitope." Unlike other cases, this patient's arthritis did not respond initially to nonsteroidal antiinflammatory drugs and was exacerbated by corticosteroid therapy. The synovitis took a neutrophilic form, with marked synovial membrane content of interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha). It subsequently developed into chronic lymphoplasmacytoid synovitis, similar to rheumatoid arthritis (RA), with decreased IL-8 but continuing IL-1 and TNF-alpha production in the synovial membrane. The synovitis resolved to a fibrotic synovium with residual thickening of the synovial lining layer and continued production of TNF-alpha. Thus, during the evolution of this arthritis, the synovial layer and continued production of TNF-alpha. Thus, during the evolution of this arthritis, the synovial membrane yielded a cellular infiltrate and cytokine content that had marked similarities with that seen in RA; however, the arthritis eventually remitted spontaneously.

Aged↗
PubMed1996

Clinical associations of anti-lamin autoantibodies.

BACKGROUND: The clinical associations of anti-lamin autoantibodies were first described in 1973. Since then a number of individual case reports and two small series have been published. These have suggested an association with connective tissue disorders and autoimmune liver disease. AIMS: To identify the clinical and laboratory associations of anti-lamin autoantibodies in an Australian population. METHODS: Retrospective review of routine antinuclear antibody testing between 1990-1994 for characteristics linear staining of nuclear envelope on indirect immunofluorescence on HEp-2 cells with clinical status defined by retrospective review of case records. RESULTS: Twenty-eight patients were identified and the clinical status of 27 patients defined. Eleven patients had associated IgG anti-cardiolipin antibodies; anti-phospholipid syndrome was present in nine. Seven further patients had liver disease; five had autoimmune liver disease, with associated autoantibodies. The remaining nine patients had a diverse group of diseases. There was no correlation between the titre of the autoantibody and clinical status. An association with anti-cardiolipin antibodies was found although the cause remains obscure. CONCLUSION: Anti-lamin autoantibodies, as identified by indirect immunofluorescence, are associated with a diverse group of diseases but particularly with anti-phospholipid syndrome and liver disease. Testing for anti-phospholipid antibodies and more specific markers of systemic lupus erythematosus and autoimmune disease, for example anti-dsDNA antibodies, anti-smooth muscle antibodies and anti-mitochondrial antibodies should be pursued when anti-lamin autoantibodies are detected.

Adult↗
PubMed1996

Endothelin-1 produces heterogeneous regional haemodynamic effects in conscious rabbits.

Blood flow in the renal artery, superior mesenteric artery and infra-renal abdominal aorta of conscious rabbits was measured by Doppler ultrasound. Arterial pressure, heart rate and blood flow responses were assessed following 0.2 and 0.8 nmol/kg intravenous endothelin-1. The effects of the following antagonists on these responses were examined: phentolamine, propranolol, scopolamine, captopril, nifedipine, indomethacin, the V1-vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP and the competitive nitric oxide (NO) synthase inhibitor NG-nitro L-arginine (NOLA). Hindlimb resistance and arterial pressure responded in two phases, initial vasodilatation followed by vasoconstriction. Renal and mesenteric vasoconstriction occurred without initial vasodilatation. Following 0.2 nmol/kg endothelin-1, arterial pressure decreased by 18.5 +/- 0.8 mmHg, then increased by 25.2 +/- 1.7 mmHg (n = 27). Heart rate changed reciprocally. Renal resistance increased by 533 +/- 73% (n = 12). Mesenteric resistance increased by 420 +/- 34%. Hindlimb resistance decreased 54 +/- 2% (n = 12, all P < 0.01) then increased slightly (P < 0.05). All changes were greater at 0.8 nmol/kg, particularly the hindlimb vasoconstriction. The only antagonist to alter significantly these responses was NOLA, which in the hindlimb attenuated the vasodilatation and accentuated the vasoconstriction. We conclude that most of the haemodynamic effects of endothelin-1 are direct, but that NO generated by NO synthase causes part of the hindlimb vasodilatation, and that endothelin-1-induced vasoconstriction is attenuated by release of NO.

Animals↗
PubMed1995

Pulse methylprednisolone in rheumatoid arthritis: effects on peripheral blood and synovial fluid neutrophil surface phenotype.

OBJECTIVE: To determine the effects of a 1000 mg intravenous pulse of methylprednisolone (MP) on the expression of cell adhesion molecules on peripheral blood and synovial fluid (SF) neutrophils in rheumatoid arthritis. METHODS: Fluorescent flow cytometric analysis was performed on peripheral blood neutrophils (n = 13 patients) and knee joint SF neutrophils (n = 7 patients) prior and at 4 and 24 h after MP. Clinical and laboratory assessments of disease activity were performed. RESULTS: There was marked improvement in all clinical stores at 24 h including a decrease in pain score (p < 0.0005), stiffness (p < 0.00005), joint tenderness score and modified Health Assessment Questionnaire (HAQ) (p < 0.005), and an increase in well being (p < 0.001). At 24 h there was a significant decrease in SF neutrophil counts to mean (SEM) of 31.5% (15%) of baseline and an increase in peripheral blood neutrophils to a mean (SEM) of 199% (25%) of baseline. Furthermore, a significant decrease was observed in the expression of both structural and functional epitopes of CD11b (p < 0.05) and CD18 (p < 0.05) on SF neutrophils at both 4 and 24 h post-MP. There was also an increase in the expression of L-selectin (CD62L), which approached significance (p = 0.01), but no significant effect on CD11a, CD44 and sialyl Lewisx (CD15s). Peripheral blood neutrophils showed decreased expression of CD11b (p = 0.1), CD18 (p = 0.07), and L-selectin (p = 0.09), which approached statistical significance without any associated effects on CD11a, CD15s, or CD44. CONCLUSION: MP is associated with a marked decrease in CD11b and CD18 expression on SF neutrophils and, to a lesser extent, peripheral blood neutrophils. This may be due to decreased neutrophil activation as these cells traffic from the vasculature through the synovial membrane or to decreased activation in the synovial space.

Aged↗
PubMed1994

Endothelin-1 causes a biphasic response in systemic vasculature and increases myocardial contractility in conscious rabbits.

We studied the effects of an intravenous (i.v.) bolus of endothelin-1 (ET-1, 0.2 nmol/kg) in conscious rabbits, measuring arterial blood pressure (BP), heart rate (HR), myocardial contractility, and cardiac output and evaluating direct and indirect effects of ET-1 with pacing and pharmacologic antagonists. ET-1 caused a brief initial decrease in BP of 18 +/- 1 mm Hg, followed by a sustained increase of 26 +/- 3 mm Hg (n = 16, p < 0.001). HR increased initially by 60 +/- 11 beats/min and then decreased by 68 +/- 6 beats/min (n = 16, p < 0.001). Left ventricular (LV) dP/dt increased by 2,120 +/- 380 mm Hg/s (n = 5, p < 0.01). LV end-diastolic pressure (LVEDP) increased by 4 +/- 1 mm Hg (n = 5, p < 0.05). Cardiac output (CO) increased initially by 34 +/- 4% and then decreased by 28 +/- 3% (n = 16, p < 0.001). Total peripheral resistance (TPR) decreased initially by 34 +/- 3% and then increased by 72 +/- 13% (n = 16, p < 0.001). Pacing did not alter the effect of ET-1 on arterial BP, LVdP/dt, or LVEDP. The combination of propranolol and scopolamine significantly reduced the increase and decrease in HR and the increase in LVdP/dt. None of the antagonists significantly altered the effect of ET-1 on TPR. ET-1 causes brief initial vasodilation and increased myocardial contractility, followed by sustained vasoconstriction. The vascular effects appear to be of greater significance than the cardiac effects at the dose used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Comparative haemodynamic effects of verapamil, flecainide, amiodarone and sotalol in the conscious rabbit.

1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.

Amiodarone↗
PubMed1994

Effects of endothelin-1 on arterial pressure: a comparison of intravenous and intra-arterial administration in conscious rabbits.

1. Intravenous endothelin-1 releases endothelium-derived relaxing factor (EDRF) and prostacyclin from the lungs, and substantial pulmonary clearance is claimed. Since these vaso-active substances could alter the haemodynamic effects of endothelin-1, the effects of boluses of endothelin-1 injected intravenously and into the left ventricle (intra-arterial) were compared, measuring arterial pressure and heart rate in conscious male New Zealand rabbits. The pulmonary clearance of endothelin-1-like immunoreactivity (Et-1LI) and initial plasma half-life were measured in anaesthetized rabbits during and after intravenous infusion of endothelin-1. 2. The effects of intravenous and intra-arterial routes of administration were not significantly different. Arterial pressure decreased (intravenous: 21.6, intra-arterial: 24.2 mmHg, P = 0.12, n = 10, t-test, 9 d.f.), then increased (intravenous: 21.2, intra-arterial: 16.4 mmHg, P = 0.33), while heart rate increased (intravenous: 66, intra-arterial: 53 beats/min, P = 0.09), then decreased (intravenous: 50, intra-arterial: 54 beats/min, P = 0.30). 3. Arterial and venous plasma levels of Et-1LI were not significantly different, venous levels increasing from 30 +/- 3 pg/mL (12 +/- 1 pmol/L) at 1 pmol/kg per min to 770 +/- 78 pg/mL (308 +/- 31 pmol/L) at 16 pmol/kg per min (n = 5). Mean initial plasma half-life was 0.6 min (range: 0.25-1.1 min). 4. It was concluded that there is no significant net pulmonary clearance of exogenously administered endothelin-1 in the conscious rabbit, and that any vaso-active factors released in the lungs by endothelin-1 do not have a significant effect on systemic arterial pressure.

Animals↗
PubMed1994

Experimental hypertension produces diverse changes in the regional vascular responses to endothelin-1 in the rabbit and the rat.

OBJECTIVE: To examine the effects of hypertension on systemic and regional haemodynamic responses to endothelin-1. DESIGN: Comparison of responses between age-matched control and hypertensive rabbits (two-kidney, two wrapped), and between spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats. METHODS: Arterial pressure, heart rate and blood flow responses to 0.2 nmol/kg intravenous endothelin-1 were measured in conscious animals. Blood flow was measured by pulsed ultrasound Doppler in the ascending aorta, distal abdominal aorta, left renal artery and superior mesenteric artery. RESULTS: Endothelin-1 produced qualitatively similar effects in the hypertensive and control animals. In the systemic circulation, brief initial vasodilation preceded sustained vasoconstriction. In the hindlimb, marked vasodilation preceded relatively minor vasoconstriction, and profound vasoconstriction occurred in the renal and mesenteric vascular beds. In the rats but not the rabbits, fleeting vasodilation preceded the renal and mesenteric vasoconstriction. Significant differences between hypertensive and control animals were: accentuation of the pressor effect and heart rate responses in hypertensive animals of both species, and accentuation of hindlimb vasodilation in hypertensive rabbits but not SHR; and attenuation of the depressor effect in SHR but not hypertensive rabbits, attenuation of the mesenteric vasoconstriction in both hypertensive rabbits and rats, and attenuation of renal vasoconstriction in SHR. CONCLUSIONS: The increased responses to endothelin-1 of some variables in the hypertensive animals may involve structural changes in the resistance vessels. However, the reduced responses in the mesenteric vasculature of both species and the renal vasculature of the SHR are due to some mechanism other than structural change.

Animals↗
PubMed1993

Comparative hemodynamic effects of amiodarone, sotalol, and d-sotalol.

The effects of intravenous boluses of amiodarone (5 mg/kg), racemic sotalol (enantiomeric ratio d/l-sotalol 1:1;1.5 mg/kg), and d-sotalol (0.75 mg/kg) on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), left ventricular end-diastolic pressure (LVEDP), and peak rate of change of left ventricular pressure (LV dp/dt) were assessed in conscious rabbits. Amiodarone and sotalol had a modest negative inotropic effect: amiodarone reduced peak LV dp/dt by 8 +/ 2% (mean +/- SEM) (p < 0.05) and sotalol by 6 +/- 2% (p < 0.05). These two drugs had quite different effects on CO as a result of differences in their actions on peripheral blood vessels: amiodarone caused a 13 +/- 3% (p < 0.05) increase in CO associated with a substantial vasodilatory effect (TPR reduced 25 +/- 3%; p < 0.01); sotalol did not produce any substantial change in either CO or TPR. Bolus intravenous injection of amiodarone was associated with a significant increase in HR (12 +/- 3%; p < 0.01), whereas sotalol reduced HR by 7 +/- 1% (p < 0.05). In contrast, administration of the dextro-rotatory optical isomer, d-sotalol, produced no significant change in peak LV dp/dt, LVEDP, CO, TPR, or HR. These results confirm that amiodarone and racemic sotalol have a comparatively weak cardiodepressant action. The experiments also show that the reduction in cardiac performance associated with racemic sotalol is mediated predominantly through the beta-adrenoreceptor blocking action of the levo-rotatory isomer (l-sotalol) rather than any substantial cardiodepressant effect of the dextro-rotatory isomer.

Amiodarone↗
PubMed1991

Effects of endothelin-1 on arterial pressure and myocardial contractility in the conscious normotensive rabbit.

1. We studied the effects of an intravenous bolus of endothelin-1 on arterial pressure and myocardial contractility in the conscious rabbit. 2. Endothelin produced an initial fall in arterial pressure accompanied by an increase in heart rate. This was followed by a dose-dependent increase in arterial pressure, peaking about 7 min after injection, accompanied by a reciprocal fall in heart rate. 3. Left ventricular rate of change of pressure (LV dP dt) increased with endothelin except at higher doses (0.8 and 1.6 nmol/kg), where in some animals it decreased.

Animals↗
PubMed1991

Quality assurance of immunodiagnostic tests in Australasia.

A Royal College of Pathologists of Australasia (RCPA) sponsored Quality Assurance Program (QAP) in Clinical Immunology, involving 128 laboratories over a 1 yr period, revealed the following: successful participation in the program by 16 overseas laboratories (distant from Australia); only 30% of laboratories succeeded in returning their results by the scheduled date on every occasion; quantitation of urinary total protein and Bence Jones protein was poor and varied over a log scale; immunofixation was more successful in characterizing urinary paraprotein than immunoelectrophoresis; densitometry of protein electrophoresis appeared the method of choice in quantitating serum paraproteins accurately; nephelometric techniques gave better concordance between laboratories than turbidometric, radial immunodiffusion or agglutination techniques; poor concordance between laboratories in detecting weakly positive antinuclear antibodies (ANA); some laboratories had difficulties in identifying ANA patterns (only 60% of laboratories correctly identified the anticentromere pattern); few laboratories could correctly identify antibodies to extractable nuclear antigens (ENA); flow cytometry gave a smaller dispersion of lymphocyte subpopulation percentages than microscopy. A method was established to rank laboratory performance of selected tests over the 1 yr period. Such a comparative ranking scheme may alert laboratories in identifying specific or generalized deficiencies in performance.

Antibodies, Antinuclear↗