[Spinal arteriovenous malformation: assessment with magnetic resonance imaging and angiography].
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Adult↗
Biomedical subjects
T Wang
Publications and source records attributed to T Wang.
Spectrum of antiarrhythmic response to encainide.
Encainide is effective in suppressing non-life-threatening ventricular arrhythmias; however, inconsistent results have been noted in patients with more serious ventricular arrhythmias. Thirty-seven patients with drug-resistant ventricular arrhythmias were studied. Patients in group I (n = 11) has sustained ventricular tachycardia and those in group II (n = 26) had nonsustained ventricular arrhythmias. In group I, 8 patients had remote myocardial infarction, congestive heart failure and sustained ventricular tachycardia requiring repeated cardioversion (group Ia). None of these patients responded to encainide treatment, but 6 did have an antiarrhythmic response (complete in 3 and only partial in 3) to other investigational antiarrhythmic agents. Three patients in group I, all without ischemic heart disease (group Ib), had an excellent antiarrhythmic response to encainide, as did 21 of 26 patients in group II. In 4 of 5 patients in group II who did not respond, the dosage was limited due to the development of sinus pauses, atrioventricular block or bundle branch block, and in 3 of these 4 patients preexisting conduction disease was evident (PR longer than 0.2 second or QRS longer than 0.12 second). Diplopia occurred while taking the maximal oral dosage in the fifth patient. At 21.5 months of follow-up, 14 of the original 24 patients who responded to encainide continue to receive it; 3 have died (all due to natural progression of left ventricular dysfunction) and encainide was discontinued in 7: in 2 because of syncope, in 2 because of new-onset atrial fibrillation, in 1 patient because of exercise-induced polymorphic ventricular tachycardia, in 1 because of diplopia and in 1 because of skin exanthem.(ABSTRACT TRUNCATED AT 250 WORDS)
Anilides↗
Caffeine elimination: a test of liver function.
Fasting plasma caffeine concentration and various parameters of caffeine elimination from plasma obtained after a standardized oral dose of 140 mg caffeine have been compared in nine patients with liver cirrhosis, eight patients with non-cirrhotic liver disease and ten healthy volunteers with regard to their ability to discriminate between the different groups. Fasting plasma caffeine concentrations were significantly higher in cirrhotics (11.1 +/- 10.5 mumol/l) than in healthy volunteers (1.5 +/- 0.8 mumol/l). The respective values measured in patients with non-cirrhotic liver disease (3.1 +/- 3.1 mumol/l) did not differ significantly from the controls. Plasma disappearance rate and clearance of caffeine were significantly decreased in cirrhotics (0.11 +/- 0.02 h-1; 1.0 +/- 0.3 ml/min per kg) and in patients with non-cirrhotic liver disease (0.18 +/- 0.04 h-1; 2.2 +/- 0.7 ml/min per kg) as compared to healthy volunteers (0.23 +/- 0.04 h-1; 3.1 +/- 0.9 ml/min per kg). Plasma caffeine concentration determined 12 h after administration of the test dosage discriminated best between patients with cirrhosis (5.4 +/- 1.6 mumol/l), patients with non-cirrhotic liver disease (2.0 +/- 1.4 mumol/l) and healthy volunteers (0.8 +/- 0.2 mumol/l). These results, the safety of the test compound and the simplicity of a single caffeine determination in plasma 12 h after a standardized dose of caffeine make this test attractive for evaluation of liver function.
Adult↗
Homology of ATP binding sites from Ca2+ and (Na,K)-ATPases: comparison of the amino acid sequences of fluorescein isothiocyanate labeled peptides.
Ca2+ and (Na,K)-stimulated ATPases from various species and tissues were labeled with fluorescein isothiocyanate (FITC). Labeled peptides were solubilized by tryptic digestion and purified by reverse phase high pressure liquid chromatography. The amino acid sequences of the labeled peptides reveal considerable homology between sarcoplasmic reticulum Ca2+-ATPases from various sources. These Ca2+-ATPases also contain a region of homology with all other ATPases thus far sequenced. A difference was demonstrated between dog skeletal and cardiac Ca2+-ATPases. These results demonstrate homology of the putative ATP binding site of ATPases, which extends over tissue, species, and cation specificity, including the completely conserved amino acid sequence: lys-gly-ala-pro-glu.
Adenosine Triphosphate↗
Bretylium: relations between plasma concentrations and pharmacologic actions in high-frequency ventricular arrhythmias.
Although it is widely assumed that the early arrhythmogenic and pressor responses to bretylium are caused by catecholamine release from the adrenergic neuron, this assumption has not been systematically studied in humans. Pharmacologic responses to a placebo infusion and 3 separate bretylium infusions (2.5, 5.0, 10 mg/kg over 60 minutes) were assessed in 6 patients with recurrent, nonsustained ventricular tachycardia. Plasma bretylium concentration, blood pressure (BP), plasma norepinephrine (NE) concentration, arrhythmia frequency and adrenergic neuronal blockade (assessed by the presence or absence of reflex venoconstriction) were measured. Adrenergic blockade was seen with every bretylium infusion and at a time when relatively small amounts of bretylium had been administered (range 160 to 750 mg, median 252). Temporal relations (p less than 0.03) were noted among the time of onset of adrenergic neuronal blockade, onset of the pressor response, increase in NE plasma concentration and increase in ventricular arrhythmia frequency. BP responses during the infusions were linearly related to change in plasma NE at the time of development of adrenergic neuronal blockade. Bretylium plasma concentrations higher than 3 micrograms/ml were frequently associated with a short-lived pressor response. There was a significant relation (p less than 0.06) between the increase in plasma NE during the infusion and an increase in ventricular arrhythmia frequency. Reduction in arrhythmia frequency was seen in only 1 patient, beginning 6 hours after the development of adrenergic neuronal blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Complete amino acid sequence of the ubiquinone binding protein (QP-C), a protein similar to the 14,000-dalton subunit of the yeast ubiquinol-cytochrome c reductase complex.
The amino acid sequence of the ubiquinone binding protein (QP-C) in the cytochrome bc1 region of the mitochondrial electron transfer chain was determined by analysis of peptides obtained by cyanogen bromide cleavage and staphylococcal protease digestion of succinylated derivatives. It was found to consist of 110 amino acid residues and its amino terminus to be blocked by an acetyl group, as determined by mass spectrometry of the amino-terminal peptide and a comparison with peptides chemically synthesized on high-performance liquid chromatography. The molecular weight of this ubiquinone binding protein including the acetyl group was calculated to be 13,389. The predicted secondary structure of QP-C has alpha-helical content of about 50% and QP-C was classified as an "all-alpha" or "alpha + beta" protein. This is the first report describing the amino acid sequence of the ubiquinone binding protein. A comparison of this sequence with that of the 14-kDa subunit of the yeast ubiquinol-cytochrome c reductase complex from the nucleotide sequence showed these two sequences to be quite similar.
Amino Acid Sequence↗
Impact of trichloroethylene contaminated groundwater discharged to the main canal and Indian River lagoon, Vero Beach, Florida.
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Animals↗
Comparison of the rat microsomal Mg-ATPase of various tissues.
The microsomal Mg-ATPase from various rat tissues was compared. After fractionating the microsomal vesicles by sucrose gradient centrifugation, the highest specific activity of the Mg-ATPase was found in the low-density vesicles which contained plasma membrane. A large fraction (25-90%) of the microsomal Ca-independent Mg-ATPase found in each tissue had the following properties: (1) the Km for ATP was 0.2 mM; (2) the rate of ATP hydrolysis by the Mg-ATPase was nonlinear due to an ATP-stimulated inactivation of the enzyme; (3) wheat germ agglutinin, concanavalin A, glutaraldehyde, and antiserum prevented inactivation induced by ATP or AdoPP[NH]P; (4) detergents at relatively low detergent:protein ratios increased the rate of inactivation with little change in the initial rate of ATP hydrolysis; (5) the Mg-ATPase was inactivated by irradiation in the presence of 8-azido ATP. (6) in addition to ATP, the Mg-ATPase was able to hydrolyze CTP, GTP, UTP, ITP, and GTP but was unable to hydrolyze any of the 10 nonnucleotide phosphocompounds which were tested; (7) the bivalent cation requirement of the Mg-ATPase could be provided by Mg2+, Ca2+, Mn2+, Zn2+, or Co2+ but the enzyme was inactive in the presence of Cu2+, Sr2+, Ba2+, or Be2+; (8) the Mg-ATPase activity was not altered by ionophores or inhibitors of the Na,K-ATPase, the Ca,Mg-ATPase or the mitochondrial F1ATPase. These data suggest that a major portion of the microsomal, basal Mg-ATPase activity is due to one unique enzyme found in most if not all tissues.
Adipose Tissue↗
Pharmacokinetics and nondialyzability of mexiletine in renal failure.
Mexiletine is an investigational antiarrhythmic drug eliminated primarily by hepatic metabolism. To evaluate its pharmacokinetics in patients with renal failure, we gave 14 subjects (creatinine clearance from 0 to 68.9 ml/min, including five subjects who required maintenance dialysis) a single, 200 mg dose of mexiletine. Serial blood samples were drawn and analyzed for mexiletine concentration by gas chromatography. The elimination t1/2 was 18.9 +/- 7.4 hours and oral clearance was 378 +/- 109 ml/min (means +/- SD). There was no correlation between these parameters and creatinine clearance. In subjects receiving dialysis, the study was also repeated during dialysis 1 week later. There was no significant difference between the AUCs either while receiving dialysis or when calculated on a day when the subject was not receiving dialysis. Thus dosing adjustments for mexiletine should not be necessary in patients with creatinine clearance values as low as 10 ml/min or in patients receiving dialysis. Furthermore, supplemental doses of mexiletine are not likely to be needed after dialysis. Evaluation of the kinetics at steady state are necessary to extrapolate further our observations after a single oral dose.
Administration, Oral↗
Effects of riboflavin deficiency on metabolism of nitrosamines by rat liver microsomes.
The effects of riboflavin deficiency on the metabolism of N-nitrosodimethylamine [(DMN) CAS: 62-75-9] and other nitrosamines were examined in rats. After weanling rats were put on a riboflavin-deficient diet, the development of the deficiency was monitored by the growth rate and the erythrocyte glutathione reductase activation coefficient. In the riboflavin-deficient rats, the liver microsomal NADPH-cytochrome c reductase activity was lower but the cytochrome P450 content was higher than that of the control. The metabolism of DMN was dependent on the severity of the deficiency. During mild deficiency, which was observed mainly with Sprague-Dawley rats, the microsomal DMN demethylase (DMNd) activity was elevated 30-80%, but the metabolism of N-nitrosomethylbenzylamine (CAS: 937-40-6) and three other nitrosamines was slightly decreased. Dietary restriction in the pair-fed group also caused an elevation of DMNd activity above that of the ad libitum control group due to a partial fasting effect. During severe deficiency, which was observed mainly with Wistar rats, however, the metabolism of DMN, as well as the oxidation of benzo[a]pyrene, was decreased. Preincubation with flavin adenine dinucleotide and flavin mononucleotide enhanced the DMNd activity of the microsomes from riboflavin-deficient rats but not that from control rats. The results suggest that, depending on the alterations of the monooxygenase enzyme system during the development of the deficiency, riboflavin deficiencies may have different effects on the metabolism of DMN and some other carcinogens.
Animals↗
[Fetal membranes of the human. Electron microscopy study].
The structure of the human fetal membranes was examined after normal and pathological pregnancy. The cellular junctions are desmosomes and gap junctions in the amniotic epithelium, whereas in the chorionic epithelium tight junctions in the form of maculae occludentes are found occasionally in addition to desmosomes and gap junctions. The absence of zonulae occludentes, which could act as an effective permeability barrier, in the fetal membranes indicates that the intercellular spaces of the fetal membranes represent an extracellular route for paraplacental substance exchange. In pathological pregnancy such as diabetes mellitus, rhesus incompatibility and toxemia, the morphological variations of amniotic epithelium compared with normal amnion are manifold and greatly specific. On the contrary, the morphological changes of chorionic epithelium in pathological pregnancy seem nonspecific. They differ in various pathological pregnancies only in quantity. In addition to fibroblasts and Hofbauer cells, the connective tissue of the fetal membranes contain myofibroblasts. Since myofibroblasts possess the ability to contract, we assume that they may contribute to protection of the fetal membranes from overdistension.
Epithelium↗
Effects of verapamil, diltiazem, nisoldipine and felodipine on sarcoplasmic reticulum.
Verapamil, diltiazem, nisoldipine and felodipine, calcium antagonist drugs with different chemical structures, were studied for their effects on activities of sarcoplasmic reticulum (SR) isolated from dog cardiac and rabbit skeletal muscles. Nisoldipine and felodipine exerted biphasic actions on both cardiac and skeletal SR Ca2+-ATPase with maximum activation of 40-60% occurring at 20-40 microM for nisoldipine and 30-40% occurring at 15-30 microM for felodipine. At higher drug concentrations, Ca2+-ATPase was inhibited. In the presence of oxalate the maximum activation of the Ca2+ uptake rates at 5-20 microM nisoldipine were 30-50% for cardiac SR and at 80-100 microM of the drug were 300-500% for skeletal SR. Felodipine inhibited the rate of Ca2+ uptake by dog cardiac SR, but activated Ca2+ uptake by rabbit skeletal SR with a maximum of 30-50% at 12-25 microM. At higher concentrations of the two drugs the rate of Ca2+ uptake was inhibited. In the absence of oxalate, i.e., limited transport, nisoldipine shortened the duration of time that Ca2+ was bound to the cardiac and skeletal SR, while the rate of release of Ca2+ from skeletal SR was stimulated. Felodipine at low concentrations similarly caused a premature release of Ca2+ from skeletal SR at a rapid rate; at high concentrations both drugs did not alter Ca2+ binding but delayed Ca2+ release. Unlike nisoldipine and felodipine, verapamil and diltiazem inhibited the rates of Ca2+ transport both in cardiac and skeletal SR. The two drugs inhibited Ca2+-ATPase in cardiac SR but activated the enzyme in skeletal SR.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Epithelium of the human chorion laeve in diabetes mellitus. Light and electron microscopic examination.
The epithelium of human chorion laeve from pregnancies complicated by diabetes mellitus was examined under the light and electron microscopy. In comparison with normal chorion laeve, the epithelium of chorion laeve in diabetes mellitus shows the following morphological changes: The trophoblast cells display more microvilli and cell processes on their surface. Trophoblast cells with different cytoplasmic characteristics can be seen. Some display few organelles and large glycogen depositions; other are rich in organelles. Furthermore, some cells with electron dense filaments and few cell organelles can be found. Necrotic cells are frequently present in the outer epithelial layers. The intercellular spaces in the epithelial layers near the basement membrane are narrower. Since vasculopathy of the decidual arteries with disturbance of blood circulation is often found in pathological pregnancies, we assume that the morphological changes found are due to deficiency in nutrient and oxygen supply.
Chorion↗
Determination of volatile halocarbons in water by purge-closed loop gas chromatography.
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Chromatography, Gas↗
Pharmacology, electrophysiology, and pharmacokinetics of mexiletine.
Mexiletine is a class I antiarrhythmic agent that is active after both oral and intravenous administration and similar in structure and activity to lidocaine. It decreases phase O maximal rate of depolarization (Vmax) by fast sodium channel blockade. The marked rate dependence of Vmax depression may explain mexiletine's lack of effect on normal conduction and its efficacy against ventricular tachyarrhythmias. Mexiletine significantly decreases the relative refractory period in His-Purkinje fibers without changing the sinus rate or atrioventricular and His-Purkinje conduction times. Action potential duration is usually shortened. Mexiletine may aggravate preexisting impairment of impulse generation and conduction. Uptake and distribution of mexiletine are rapid, systemic bioavailability is about 90%, and tissue distribution is extensive. Mexiletine is primarily metabolized in the liver; 10% to 15% is excreted unchanged in the urine. Elimination half-life is 9 to 11 hours after intravenous or oral administration. Microsomal enzyme induction shortens mexiletine's elimination half-life, whereas hepatic disease and acute myocardial infarction prolong it. Renal disease has little effect, although hemodialysis increases mexiletine clearance. Plasma concentrations from 0.75 to 2.0 mg/L are usually associated with a desirable therapeutic response.
Absorption↗
Encainide and its metabolites. Comparative effects in man on ventricular arrhythmia and electrocardiographic intervals.
To assess the relative contributions of encainide and its putatively active metabolites, O-demethyl encainide (ODE) and 3 methoxy-O-demethyl encainide (3MODE), to the drug's pharmacologic effects, we compared intravenous infusions and sustained oral therapy in two phenotypically distinct groups of patients, extensive and poor metabolizers of encainide. Unlike poor metabolizers, extensive metabolizers had appreciable quantities of both metabolites detectable in plasma and had fourfold shorter elimination half-lives for encainide. By quantitating electrocardiogram intervals, arrhythmia frequency, and plasma concentrations, we found that, in poor metabolizers, arrhythmia suppression and ventricular complex (QRS) prolongation were correlated positively with encainide concentrations (r greater than or equal to 0.570, P less than 0.014). In these two subjects, antiarrhythmic concentrations of encainide (greater than 265 ng/ml) were at least fivefold higher than those sustained in the six extensive metabolizers during steady state oral therapy. In extensive metabolizers, encainide concentrations were uncorrelated with effects. Arrhythmia suppression and QRS prolongation in extensive metabolizers correlated best with ODE (r greater than or equal to 0.816, P less than 0.001); QTc change correlated positively with both 3MODE and ODE. Arrhythmia suppression paralleled QRS prolongation; the relationship between them appeared similar in both phenotypic groups. In most patients, extensive metabolizers, encainide effects during oral therapy are mediated by metabolites, probably ODE.
Aged↗
Abrasion of acrylic veneers by simulated toothbrushing.
The abrasion responses were tested on four acrylic veneer materials, K + B Plus, K + B 75, Isosit, and Ivocron. The studies were performed in two independent research laboratories. Two different brushing machines were used with an abrasive slurry. The results were used for comparing the degree of abrasion for the resin materials. Three analytical methods of measuring the degree of abrasive wear were used: surface profile measurement, microscopic evaluation, and measurement of loss of volume. Isosit showed the best abrasion resistance of the four materials tested.
Acrylic Resins↗
Survival with total occlusion of left main coronary artery.
Complete occlusion of the left main coronary artery is considered to be a terminal event in most cases. We describe two patients with this lesion who underwent successful coronary bypass surgery with complete relief of symptoms and long-term survival. The angiographic findings and clinical management of the two patients are discussed.
Journal Article↗