Considerations in selecting a mobile master medication cart.
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Biomedical subjects
Publications and source records attributed to E Superstine.
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Two epimeric aldehydes [(R)- and (S)-quinidinals] and the corresponding acids[(R)- and (S)-norhydroquinidinoic acids] were prepared by the oxidation of quinidine. The alpha-alpha interactions of the carbonyl group and the aromatic moiety, as reflected in the NMR spectra, were compared with those of quinidine. NMR spectroscopic analyses made it possible to assign both the stable conformation and their configuration at C-3 to these molecules. The free hydroxyl group at C-9 must be present for the chemical shift values to be concentration dependent. These findings provide more information on association in the parent molecules.
NMR analyses of quinidine and other cinchona alkaloids and their monoprotonated salts in deuterium oxide and in deuterochloroform revealed that the molecules assume new conformations in polar and nonpolar media, affecting the protonation site and hydrophilic-lipophilic characteristics. The ion-pair feature of the salts is lost and the molecules assume a neutral feature when they are transferred from an aqueous to a lipoid phase. Hydrophobic bonds between the molecules and their environment and within the molecule itself may affect the binding of cinchona alkaloids to membranes in biological fluids.
1,3,4,14b-Tetrahydro-2,7-dimethyl-2H-dibenzo(b,f)pyrazino-(1,2-d)-(1,4)-oxazepine hydrogen maleate (Org GC 94) is an oral "antamine" preparation with anti-serotoninergic and anti-histaminic effects. Its lack of unpleasant side-effects permits protracted use for the preventive treatment of serotonin-migraine. Its chemical structure--tetracyclic ring, C-beta, C-alpha, amine in a secondary position--allows block of the receptors for serotonin and histamine. Preventive treatment with 3 x 5 mg/day of Org GC 94 for a period of 3 months can almost completely eliminate migraine attacks. 21 out of 30 patients (70%) profited from such a treatment, showing a drop from 5--30 attacks to 0--1 attack per month and normalization of high urinary serotonin, 5-HIAA or histamine levels. However, 30 patients receiving 3 x 0.5 mg or placebo daily reacted only rarely. The typical side-effects of anti-serotonin drugs, especially sedation or dizziness and hyperorexia were hardly observed. Randomization of the serotonin-migraine cases and double-blind methodology were applied throughout the trial.
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The effect of theophylline on serum uric acid measurements was studied. Serum uric acid levels were measured by the phosphotungstate method in eight healthy adults, three of whom received a single u.3-mg/kg oral theophylline dose (as aminophylline elixir) while fasting, and in 15 fasting nonuremic patients (age 14 to 51 years) on chronic oral aminophylline therapy. Uric acid levels also were measured in vitro for serum with known amounts of theophylline (0-49 microgram/ml). Serum theophylline levels were measured by high-pressure liquid chromatography for the patients receiving chronic theophylline therapy and spectrophotometrically for the subjects receiving a single oral dose. In the 15 chronic theophylline patients, actual total serum uric acid levels were not significantly different (p greater than 0.05) from those expected had they been a normal population (i.e., healthy, not receiving theophylline). Likewise, in vitro studies showed no difference in uric acid levels of serum exposed to various concentrations of theophylline. A positive correlation (r greater than or equal to 0.816) between serum theophylline and uric acid levels was found in two of the three single-dose studies, suggesting a pharmacological interaction. Therapeutic serum theophylline levels do not interfere with the measurement of serum uric acid levels by the phosphotungstate method.
The information reported in a variety of sources on drug interferences with routine laboratory tests (serum concentrations of sodim, potassium, carbon dioxide, chloride, glucose, BUN, cholesterol, total protein, albumin, total bilirubin, alkaline phosphatase, and SGOT) performed by a 12-channal autoanalyzer was reviewed. A determination was made whether or not the information was based on an evaluation of original articles, if the study was done in vitro or in vivo, what medium was used, if the drug level causing the interference would be encountered in a patient's serum, and if the reported conclusions were clinically significant. The review narrowed considerably the list of drug interactions with laboratory tests performed by 12-channel autoanalyzer methods. Clinically significant interactions were found for (1) aminosalicylic acid and the test for serum glucose; (2) gamma globulins and cholesterol measurement; (3) sulfonamides and paramethadione and the test for albumin; (4) albumin from placental sources and alkaline phosphatas measurement; (5) erythromycin estolate and aminosalicylic acid and the determination of SGOT; and, possibly (5) medications releasing bromide ions and the measurement of serum chloride. The study showed the need to determine the relevancy of drug interactions to the specific methods used in the laboratory of each medical institution.
NMR spectra of quinidine (I), hydroquinidine (II), and their respective acetyl derivatives (III and IV) were compared. The chemical shifts of some protons in I differed from those of their counterparts in II. These values were concentration dependent in I and II; they were similar in III and IV but not concentration dependent. The implications of these findings and the correlation of the NMR data with the preferred conformations are discussed.
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The hemodynamic effects of dopamine were studied in 19 patients following intracardiac operation or myocardial revascularization using extracorporeal circulation. The heart rate, mean blood pressure, central venous pressure, left atrial and pulmonary artery pressures, cardiac output, and urine output were recorded before and at the end of one-hour infusions of dopamine at 5, 10, and 15 mug/kg/min. Infusion of 5 mug/kg/min of dopamine resulted in the highest gain in cardiac output and stroke work without an increase in myocardial oxygen consumption, as evidenced by lack of significant rise in heart rate. In addition, this dosage was not accompanied by an increase in pulmonary or systemic vascular resistance, nor were other untoward effects observed after administration of 5 mug/kg/min of dopamine.
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