Life-threatening pseudophaeochromocytoma after toloxatone, terbutaline, and phenylephrine.
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Biomedical subjects
Publications and source records attributed to N Moore.
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A solid-phase enzyme-linked immunosorbent assay (ELISA) has been developed to detect and quantify the K88 fimbrial adhesin antigen. The assay was used to detect cell-bound antigen present in bacterial suspensions and cell-free K88 antigen present in extracts. Comparable amounts of K88 antigen were detected with whole bacteria and in the equivalent extracts. The assay was used to compare the expression of the K88 antigen by one laboratory strain (K12:K88ab) and three wild-type strains (O8:K87:K88ab:H19, O8:K87:K88ac:H19 and K88ad) of enterotoxigenic Escherichia coli (ETEC) during cultivation with eight medium types and two medium forms. Determination of the expression of K88 during unshaken batch culture revealed a correlation between growth phase and expression, with maximal concentrations being detected during late log to early stationary phase. Colony blotting experiments demonstrated that expression of the K88 antigen was under quantitative and not qualitative control.
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Antacids can modify the pharmacokinetic parameters of sustained-release preparations of theophylline by changing the gastric pH. Though this has been studied with various theophylline/antacid combinations, the specific preparations investigated here have not previously been tested. The objective of the study was to assess any change in the availability of theophylline from a sustained-release preparation (SR), induced by the coadministration with an antacid. The study was designed as a double-blind randomized crossover trial in the Pneumology Departments of three general hospitals. Fifteen patients were studied. They all had stable asthma treated with theophylline and no major organ failure or gastro-intestinal lesions requiring the use of antacids. The antacid (aluminium hydroxide 800 mg and magnesium hydroxide 800 mg), or placebo, tid, was added to a stable regimen of theophylline SR bid, for 4 days, in crossover fashion. Plasma theophylline concentrations were measured before and 1, 2, 3, 4, 6, 8, 10, 12, 16 and 24 h after the morning dose of Armophylline on the fourth day of each treatment period; the maximum plasma concentration (Cmax), and time to Cmax (tmax) were noted, and the area under the 24-h time-concentration curve (AUC0-24) and mean plasma concentration (Cmean) were computed. Peak expiratory flows on the same day, before and 3, 6 and 12 h after the morning dose of Armophylline were also measured. There was no change in any of the parameters studied. The addition of the antacid to theophylline, each given according to standard clinical practice, did not modify the pharmacokinetics of the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic hyperglycaemia results in glycation of serum albumin and might affect the binding of drugs. The aim of the present study was to compare, using an equilibrium dialysis method, the protein binding of therapeutic concentrations digitoxin, valproate and phenytoin in sera from 70 insulin-dependent diabetics and 25 controls. Drug concentrations were measured by fluorescence immunopolarisation. Glycated albumin was measured by laser nephelometry after affinity chromatography. In sera from diabetics, protein binding of digitoxin (88.8 versus 89.9%) was unchanged; the protein binding of valproate (75.2 versus 80.7%) and phenytoin (67.9 versus 75.3%) was significantly decreased, but with no correlation with the concentration of glycated albumin. We conclude that the difference in protein binding between diabetic and control sera is due to glucose-independent modification of albumin in diabetics.
Sexually receptive, intact, proestrous rats were infused bilaterally into the ventromedial nucleus of the hypothalamus with one of several serotonin (5-HT) agonists and with the endogenous ligand, 5-HT. Serotonin (2000 ng) and the 5-HT1A agonists, 8-hydroxy-2-(di-n-propylamino)tetralin [8-OH-DPAT (200 ng)], 5-methoxy-3-(di-n-propylamino)chroman [5-MEO-DPAC (200-2000 ng)] and 5-hydroxy-3-(N-di-n-propylamino)chroman [5-OH-DPAC (200-2000 ng)] inhibited female lordosis behavior within 10 min of the infusion. The rank order of the effectiveness of these compounds was 8-OH-DPAT > 5-OH-DPAC > or = 5-MEO-DPAC > 5-HT. The nonselective 5-HT agonist, 1-(m-trifluoromethyl) piperazine [TFMPP (2000 ng)], did not reduce lordosis behavior. In addition to their reduction of lordosis behavior, the 5-HT1A agonists elicited resistive behavior toward the male's attempts to mount. There were minimal effects of the 5-HT1A agonists on either quality of the lordosis reflex or on proceptivity. However, rats pretreated with TFMPP and infused with 8-OH-DPAT 1 hr later, did show a transient suppression of lordosis quality. These results provide further evidence that the ventromedial nucleus of the hypothalamus contains 5-HT1A sites, the activation of which reduces lordosis behavior in regularly cycling, proestrous rats.
Sixteen patients who had undergone abdominal aortic surgery were allocated randomly to receive either propofol (total dose 3.2 (SEM 0.3) mg kg-1 h-1) or flunitrazepam (total dose 15 (2) micrograms kg-1 h-1) for 16 h after operation. Metabolic effects of sedation were assessed using a Deltatrac metabolic monitor. Initiation of sedation induced a 25% decrease in VO2 in both groups. The decrease was about 40% at 16 h. VO2 increased within 30 min after discontinuation of propofol and stabilized at values considerably less than the immediate postoperative value. A similar but slower increase was noted with flunitrazepam. While the propofol loading dose reduced the Buffington index and should therefore be avoided, no cardiovascular side effects were noted with the maintenance infusion. Weaning from ventilatory support was achieved within 15 (2) min and 264 (108) min after discontinuation of propofol and flunitrazepam, respectively.
The thoracic outlet syndromes encompass the diverse clinical entities affecting the branchial plexus or subclavian artery including cervical ribs or bands. Thoracic outlet syndrome are often difficult to diagnose on existing clinical and electrophysiological criteria and new diagnostic methods are necessary. This study reports our experience with magnetic resonance imaging (MRI) of the brachial plexus in 20 patients with suspected thoracic outlet syndrome. The distribution of pain and sensory disturbance varied widely, weakness and wasting usually affected C8/T1 innervated muscles, and electrophysiology showed combinations of reduced sensory nerve action potentials from the fourth and fifth digits, and prolonged F-responses or tendon reflex latencies. The MRI study was interpreted blind. Deviation of the brachial plexus was recorded in 19 out of the 24 symptomatic sides (sensitivity 79%). Absence of distortion was correctly identified in 14 out of 16 asymptomatic sides (specificity 87.5%). The false positive rate was 9.5%. Magnetic resonance imaging demonstrated all seven cervical ribs visible on plain cervical spine radiographs. Magnetic resonance imaging also showed a band-like structure extending from the C7 transverse process in 25 out of 33 sides; similar structures were detected in three out of 18 sides in control subjects. These MRI bands often underlay the brachial plexus distortion observed in our patients. We also observed instances of plexus distortion by post-traumatic callus of the first rib, and by a hypertrophied serratus anterior muscle. If they did not demonstrate a cervical rib, plain cervical spine radiographs had no value in predicting brachial plexus distortion. We believe MRI to be of potential value in the diagnosis of thoracic outlet syndrome by: (i) demonstrating deviation or distortion of nerves or blood vessels; (ii) suggesting the presence of radiographically invisible bands; (iii) disclosing other causes of thoracic outlet syndrome apart from ribs or bands.
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An evaluative survey, actualized until june 1991 is presented of instruments measuring alcohol problems. It is argued that in international comparative studies into the quality of alcohol treatment, scientists must agree on using identical measuring instruments and procedures.
Mortality studies demonstrate that, in all the Countries evaluated, alcoholics die twenty years earlier than expected. Causes of death vary according to drinking patterns. Though mortality data seem crude, they can detect changes due to clinical intervention. Alcoholism studies should benefit by improvement of research methodologies as already applied to other chronic diseases.
Although it was usually admitted that hypertension is associated with a reduction in conduit artery compliance and distensibility, recent experiments using newly developed high precision echo-tracking devices allowing simultaneous, non-invasive measurements of blood pressure and arterial diameter have suggested that compliance and distensibility, when calculated at equal transmural pressure, could indeed be maintained, or even increased, in hypertensive subjects. Such a maintained arterial compliance could be explained best by a decrease in wall stress despite the increase in arterial blood pressure, through either an increase in wall thickness or a decrease in arterial wall elastic modulus. Thus, the goal of the present study was to assess the role of the changes in these determinants of vessel compliance in the arterial response to an acute increase in arterial pressure in 7 healthy volunteers. Arterial pressure (AP, Finapress) as well as right radial artery internal diameter and wall thickness (Echo-Tracking, NIUS 2, Asulab) were measured continuously before and after a 2 min cold pressor test (CPT). The following parameters were then calculated at fixed (105 mmHg) pressure from the pressure/diameter curve: compliance (mm2/mmHg) and distensibility (mmHg-1) mid-wall stress (dynes/cm2) and incremental elastic modulus (dynes/cm2). During CPT, mean AP increased (from 83 +/- 4 to 106 +/- 8 mmHg; p < 0.01), compliance distensibility; and mean internal diameter (mm) decreased, mean wall thickness (mm) increased, whereas wall stress and elastic modulus remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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Four patients with primary hyperaldosteronism were treated with nadroparin 4100 or 6150 antiXa IU daily for 4 days. Plasma and urine sodium and potassium, and plasma aldosterone and renin were monitored before, during and after the study. After four days of treatment, and for the following two days, plasma aldosterone was decreased (by a mean of 49% on Day 6), and urinary Na/K was increased (3.7-fold). The direction of the changes was reversed on Day 8. The study has confirmed the effect of low molecular weight heparin on aldosterone, and makes it unlikely that it is related to inhibition of angiotensin II stimulation in these patients, as renin could not be detected in their plasma.
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