Assessment of ankylosing spondylitis.
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Humans↗
Biomedical subjects
M J Davis
Publications and source records attributed to M J Davis.
The safety and economic advantages of day case electrophysiologic studies.
Electrophysiologic Studies (EPS) have been performed as 'day case' procedures in selected patients at Royal Perth Hospital since April 1987. Previously, EPS had involved hospitalisation for two to ten days. During the 51 month period to June 1991, 484 EPS were performed in total. Of these, 153 (105 males and 48 females aged 46 +/- 31y) were day case procedures. Studies were baseline in 60 cases and included drug evaluation in 30. Sixty-one additional studies were performed solely to evaluate therapy. Twenty-one patients required cardioversion. One hundred and fifty one patients were discharged on the same day and two required prolonged observation. The financial cost savings to the hospital for day case EPS is estimated to be $115 per patient and to the community potentially a further $108 per patient. This study demonstrates that in selected patients undergoing elective EPS, day case management is a safe and economic alternative to hospital admission.
Adolescent↗
Radiofrequency catheter ablation of the AV node to improve the function of an antitachycardia implantable defibrillator.
A case of coexisting atrial fibrillation and ventricular tachycardia in a patient with an implantable cardioverter defibrillator is described. Despite careful reprogramming, the device was not always able to distinguish between the two arrhythmias and continued to deliver inappropriate antitachycardia therapy including DC shocks. Attempts to pharmacologically control the atrial fibrillation were unsuccessful so radiofrequency ablation of the atrioventricular node was performed. Following successful ablation, there have been no further false detections no episodes of further ventricular tachycardia.
Aged↗
Dual chamber rate responsive pacing to allow sotalol therapy for ventricular tachycardia.
In order to allow the use of sotalol to control ventricular tachycardia (VT), dual chamber rate responsive (DDDR) pacemakers were implanted in ten patients aged 6 to 73 years (mean 50 years). Nine presented with monomorphic VT (seven inducible at baseline electrophysiological study [EPS]) and one with syncope (monomorphic VT at EPS). On sotalol, VT was initiated in only one. This patient received sotalol in the absence of an effective alternative agent. The mean dose was 468 +/- 269 mg/day. Indications for pacing were symptomatic sotalol induced bradycardia (7), sinus node dysfunction (1), postoperative complete heart block (1), and infra-His block at baseline EPS (1). At least five of these patients would have been candidates for an implantable cardioverter defibrillator had sotalol required discontinuation. Initially, nine patients were paced in DDDR mode and one, with normal AV conduction on sotalol, in AAIR. One patient was unable to tolerate sotalol despite pacing. One patient died suddenly after 35 months of symptom-free follow-up. There was a significant improvement in symptomatic status (P = 0.03) after pacing among the other eight patients with no recurrence of VT. The implantation of a DDDR pacemaker may be indicated in selected patients with serious cardiac arrhythmias. With such a device programmed to an appropriate mode, sotalol can be used successfully where otherwise contraindicated by bradycardia or preexisting conduction disease. For some patients this may obviate the expense, inconvenience, and attendant risks of implantable cardioverter defibrillator implantation.
Bradycardia↗
Pityriasis rosea and discoid eczema: dose related reactions to treatment with gold.
Sixteen cases of either a pityriasiform or discoid eczematous rash occurring in patients with rheumatoid arthritis receiving treatment with gold (sodium aurothiomalate and auranofin) were studied. The results suggest that this is a dose related, not allergic, reaction to gold. The development of this rash is not an absolute indication to stop treatment with gold. Control can often be effected with potent topical steroids or a reduction in the dose or frequency of treatment with gold.
Arthritis, Rheumatoid↗
Stretch-activated single-channel and whole cell currents in vascular smooth muscle cells.
Mechanosensitive ion channels may play a key role in transducing vascular smooth muscle (VSM) stretch into active force development. To test this hypothesis, we recorded single-channel and macroscopic currents during mechanical stimulation of enzymatically dispersed vascular smooth muscle cells. Patch pipette suction activated a nonselective cation channel that was permeable to K+, Na+, and Ca2+. Whole cell stretch was accomplished using two patch-type micropipettes attached to the cell ends with suction. Stretch elicited a sustained depolarization with a magnitude similar to that observed in pressurized arteries. Under whole cell voltage clamp, stretch activated an inward current with a reversal potential near -15 mV. In another series of experiments, whole cell stretch failed to modify the current-voltage relationship for voltage-gated calcium currents. Thus, in VSM, both single-channel and whole cell data are consistent with activation of a nonselective cation channel by stretch. This mechanism may, in part, account for pressure-induced activation of intact blood vessels.
Animals↗
Modulation of bat wing venule contraction by transmural pressure changes.
We tested the hypothesis that the frequency and amplitude of spontaneous venular contractions in the bat wing could be modulated by changes in transmural pressure. In one series of experiments, venous pressure in the wing was elevated by pressurizing a box containing the body of the animal while the wing was exposed to atmospheric pressure. During this time, venular diameters were continuously recorded using intravital microscopic techniques while venular pressures were measured through servo-null micropipettes. In another series of experiments, single venular segments were dissected from the wing, cannulated, and pressurized in vitro. The results from both experimental protocols were qualitatively similar; alterations in venous pressure over a narrow range (+/- 5 cmH2O from control) produced substantial changes in contraction frequency and amplitude. The product of frequency and cross-sectional area was maximal over the venous pressure range between 10 and 15 cmH2O. Venules demonstrated a rate-sensitive component in their reaction to rapid pressure changes, because contraction bursts occurred immediately after positive pressure steps and quiescent periods often occurred after negative pressure steps. We conclude that venular vasomotion in the bat wing is modulated by intraluminal pressure and involves a bidirectional, rate-sensitive mechanism. In addition, comparisons with arteriolar vasomotion studies suggest that venules are more sensitive to luminal pressure changes than arterioles.
Animals↗
Endotoxin impairs flow-induced vasodilation of porcine coronary arterioles.
The purpose of this study was to test the hypothesis that endotoxemia impairs endothelium-dependent (both receptor-mediated and flow-induced) vasodilation in porcine coronary arterioles. Coronary arterioles were isolated from three groups of 4- to 8-wk old (10.3 +/- 0.8 kg) pigs: endotoxemic (E; 250 micrograms/kg endotoxin iv), control (C; equal volume of saline), and untreated pigs (UT). Subepicardial arterioles (60-120 microns) were isolated and cannulated with two micropipettes that were connected to two independent reservoir systems. Intraluminal pressure was set at 60 cmH2O throughout the experiments. All C vessels developed spontaneous tone and exhibited flow-induced vasodilation from 65 to 95% maximal diameter. Spontaneous tone developed in only three of five arterioles from E pigs, and flow-induced vasodilation was not observed in any arteriole from E pigs. Spontaneous tone developed in all six arterioles isolated from UT pigs but disappeared in four of these vessels as a result of 1 h of in vitro incubation with endotoxin (2.5 micrograms/ml). Flow-induced vasodilation was also abolished in these vessels after 1 h of endotoxin exposure. Incubation with 3 mM L-arginine, in vitro, restored flow-induced vasodilation in E arterioles and endotoxin-treated UT arterioles. Vasoconstriction induced by acetylcholine (ACh) and vasodilation induced by nitroprusside (NP) and bradykinin (BK) were similar in arterioles from all groups. In contrast, endotoxin impairs flow-induced vasodilation of coronary arterioles. The mechanism responsible for the impairment of flow-induced vasodilation seems to reside in disruption of the L-arginine/nitric oxide pathway.
Acetylcholine↗
Cellular mechanisms involved in the vascular myogenic response.
By definition, the myogenic response is the contraction of a blood vessel that occurs when intravascular pressure is elevated and, conversely, the vasodilation that follows a reduction in pressure. Over the last several decades numerous investigators have demonstrated the importance of the myogenic response in the local regulations of blood flow, capillary pressure, and in the generation of basal vascular tone. Despite the considerable information obtained from these investigations, information about the cellular mechanisms that underlie this response has been slow to accumulate. Because of the physiological significance of the myogenic response, its mechanistic basis represents an important subject for research. Currently, there are several broad hypotheses concerning the sequence of events that couple changes in intravascular pressure or stretch with alterations in vascular smooth muscle activation. These hypotheses include 1) altered membrane properties leading to activation of ion channels; 2) modulation of biochemical cell-signaling pathways within vascular smooth muscle; 3) length-dependent changes in contractile protein function; and 4) endothelial-dependent modulation of vascular smooth muscle tone. This review summarizes current work relative to each of these hypotheses and describes a possible sequence of events to account for myogenic activation of vascular smooth muscle.
Animals↗
Stretch-induced increases in intracellular calcium of isolated vascular smooth muscle cells.
Vascular smooth muscle responds to stretch with an increase in active force development. To investigate the role of Ca2+ in this response, we used the fluorescent dye fura-2 to quantitate changes in cytosolic Ca2+ in single, vascular smooth muscle cells during rapid stretch. Cells were enzymatically dispersed from pig coronary arteries, loaded with fura-2/AM, and studied using a digital-imaging microscope. Stretch of individual cells was accomplished by attachment with suction to two patch-type micropipettes to apply force to the ends of the cell. Stretch induced the release of Ca2+ from intracellular stores as well Ca2+ influx across the plasma membrane. In physiological saline solution containing 1.5 mM Ca2+, intracellular calcium increased with cell stretch in a sigmoidal fashion. This relationship was shifted upward in 10 mM Ca2+ bath solution and abolished after several minutes in Ca(2+)-free solution. The dihydropyridine Ca2+ channel blocker nifedipine, in doses sufficient to completely block inward Ca2+ current, produced only a partial block of the sustained stretch-induced intracellular Ca2+ response. It is concluded that in isolated pig coronary arterial smooth muscle cells, stretch-induced Ca2+ influx occurs in part via a nifedipine-resistant pathway, which may be a stretch-activated cation channel.
Animals↗
Pathophysiological consequences of atherosclerosis extend into the coronary microcirculation. Restoration of endothelium-dependent responses by L-arginine.
The goals of this study were 1) to quantitate the effects of atherosclerosis on physiological and pharmacological endothelium-dependent vasoactive responses in coronary arterioles downstream from arterial lesions and 2) to determine if administration of L-arginine, the precursor for endothelium-derived was induced in pigs, and vasomotor responses of isolated, cannulated coronary arterioles (30-70 microns in diameter) were assessed by measuring diameter changes in vitro. To assess pharmacological alterations of endothelium-dependent responses, dose-response curves were constructed to ADP, serotonin, and histamine. To assess physiological alterations in endothelial function, different flow rates were established across the vessel. Arteriolar diameters were measured in vessels from normal and atherosclerotic pigs under control conditions, after administration of L-arginine, and after endothelial denudation. In arterioles from normal pigs, administration of serotonin, histamine, or ADP produced dose-dependent vasodilation, which was abolished by endothelial denudation. In arterioles from atherosclerotic pigs, administration of histamine, serotonin, and ADP produced dilation at only the highest doses (10(-6)-10(-7) M), and the extent of dilation was only 20-30% of that observed in arterioles from normal pigs. Initiation of flow also produced vasodilation in arterioles from normal pigs that was completely abolished after endothelial denudation. In arterioles from atherosclerotic pigs, flow-induced responses were absent. These abnormal physiological and pharmacological responses (i.e., blunted vasodilation to pharmacological stimulation and to flow) were restored after administration of L-arginine for 40 minutes. The vascular responses after administration of L-arginine were not different from those observed under control conditions in arterioles from normal pigs. In addition, L-arginine did not restore vasodilation to the endothelium-dependent agonists in denuded segments. From these data in arterioles downstream from atherosclerotic lesions, we conclude that 1) the ED50 and maximal responses of endothelium-dependent vasodilation to ADP, histamine, and serotonin are attenuated; 2) the physiological response to flow, that is, flow-mediated endothelium-dependent vasodilation, is absent; and 3) the abnormality in arteriolar responsiveness during large vessel disease involves an impairment of the synthesis and/or release of endothelium-derived relaxing factor.
Animals↗
Rheumatoid arthritis: an association with pemphigus foliaceous.
We have observed a high incidence of pemphigus foliaceous, in the absence of therapy with penicillamine, within a small population of patients with rheumatoid arthritis. We suggest that penicillamine as well as inducing autoimmune disease might exacerbate subclinical pemphigus foliaceous in this group, accounting for those few patients whose skin disease fails to resolve following drug withdrawal. Pemphigus and rheumatoid arthritis have both been associated with HLA DR4, which was present in all three of our patients who were tested.
Adult↗
Hairy cell leukaemia and rheumatoid arthritis.
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Arthritis, Rheumatoid↗
Should disease-modifying agents be used in mild rheumatoid arthritis?
A 12-month double-blind controlled study comparing hydroxychloroquine 400 mg daily with placebo in 104 patients with mild RA was conducted to see whether patients with mild rheumatoid arthritis (RA) benefit from treatment with disease-modifying agents. Mild RA was defined as synovitis limited to the hands and feet, an ESR less than 30 mm/h and C-reactive protein less than 20 mg/l, a situation where accepted clinical practice is to use a non-steroidal anti-inflammatory agent alone. By 6 months, the improvement of clinical and laboratory parameters in the hydroxychloroquine treated patients was significant compared with pretreatment levels and significantly greater than the control group. This improvement was maintained at 12 months. In addition, fewer patients withdrew through lack of efficacy, eight on hydroxychloroquine versus 18 on placebo. The implications of treating this well defined group of patients is discussed.
Arthritis, Rheumatoid↗
Sino-atrial arrest due to temporal lobe epilepsy.
A case of sino-atrial arrest due to temporal lobe epilepsy is described and compared with previously documented such cases in the literature. The rarity of bradycardias and sinus arrest due to arrhythmogenic seizures is discussed, as is the role of prospective ambulatory electroencephalographic and electrocardiographic studies in evaluating this association.
Adult↗
Endothelial independence of myogenic response in isolated skeletal muscle arterioles.
The goal of this study was to determine whether the endothelium played a role in the myogenic response of skeletal muscle arterioles. First-order arterioles (n = 15) were isolated from the rat cremaster muscle and cannulated for in vitro study. The development of spontaneous tone reduced the diameter of the isolated arterioles from 166.7 +/- 7.6 microns to 89.2 +/- 7.2 microns. The arterioles were exposed to step changes in intraluminal pressure over a range of 10-170 cmH2O and had no flow through their lumen. The vessels exhibited active constriction to step increases or active dilation to step decreases in pressure (50-150 cmH2O). At 90 cmH2O, arterioles dilated by 89.2 +/- 6.0% in response to the endothelium-dependent vasodilator acetylcholine (10(-6) M; ACh) and 89.6 +/- 10.9% in response to endothelium-independent dilator adenosine (10(-4) M; Ado). The endothelium was physically denuded by rubbing the vessel lumen. After denudation, the arteriolar dilation to ACh was abolished, whereas the dilation to Ado was unaltered. The absence of endothelium was verified by electron microscopy. Basal tone and the response to changes in pressure were not significantly different from endothelium-intact vessels. These studies indicate that the endothelium is not responsible for myogenic activity or development of spontaneous tone in skeletal muscle arterioles.
Acetylcholine↗
Interaction of pressure- and flow-induced responses in porcine coronary resistance vessels.
Pressure-induced myogenic responses and flow-induced vasodilatory responses have been documented in coronary resistance arterioles, but the interaction of these two mechanisms and the nature of the flow-mediated response are not well understood. Experiments were designed to quantitatively study the interaction of pressure- and flow-induced responses and to characterize the nature of the substance responsible for flow-mediated dilation in isolated coronary arterioles. Subepicardial arterioles (40-80 microns) were isolated from pigs and cannulated with two glass micropipettes and then pressurized via independent reservoir systems. Flow was initiated by simultaneously moving the reservoirs in equal and opposite directions thus generating a pressure gradient (delta P) without changing the mean intraluminal pressure (IP). IP was changed by moving both reservoirs in the same direction to alter myogenic tone in the absence of flow (delta P = 0). Flow-mediated dilation competed with myogenic constriction when flow and pressure were elevated. Also, flow potentiated myogenic dilation when IP was decreased. The magnitude of flow-induced dilation was greatest at an intermediate level of vascular tone (IP = 60 cmH2O) but was attenuated at higher and lower levels of tone. In the presence of flow (delta P = 4 cmH2O), pressure-diameter relationships were shifted upward, and the magnitude of myogenic responsiveness was attenuated. Double-vessel bioassay studies indicated that a transferable substance was released from intact endothelium in response to flow. Flow-induced dilation was not affected by indomethacin but was abolished by NG-monomethyl-L-arginine or by mechanical removal of endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The association and predictive value of the complex immunoglobulin A-alpha 1-antitrypsin in the development of erosions in early rheumatoid arthritis.
Immunoglobulin A-alpha 1 antitrypsin complex (IgA-AT), its constituent components and nine other clinical or laboratory variables were measured in thirty-three patients with early, non-erosive rheumatoid arthritis (RA) in order to assess their value in predicting the subsequent development of erosions. After 12 months, eighteen patients had developed erosions. Comparison of variables measured at outset between the group of patients subsequently developing erosions and those not, showed only the complex IgA-AT level to be significantly different, the mean being higher in the erosive group. In the subgroup of patients with high IgA-AT levels (greater than 3.0 arbitary units) all developed erosions. The possible therapeutic implications of these findings are discussed.
Arthritis, Rheumatoid↗