Drugs online research references
Jpn Circ J. 1984 Sep;48(9):988-93.
Acute effect of atenolol on hemodynamic, plasma renin activity and plasma aldosterone concentration in the once daily oral administration.
Sasaki Y, Arakawa K.
A new beta-blocking agent, atenolol was studied on the supposition that it was a beta-blocker without any action on central nervous system. Atenolol was orally given to 10 patients with essential hypertension once a day and changes in various parameters were observed through 24 hours. As the results, hypotensive effect was accompanied by marked reduction of heart rate, systemic vascular resistance, plasma renin activity and blood aldosterone level over 24 hours. It was a decrease in systemic vascular resistance that showed best correlation with hypotensive effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6384568&dopt=Abstract
J Chromatogr B Biomed Appl. 1996 Jun 7;681(2):291-8.
Determination of sotalol in human cardiac tissue by high-performance liquid chromatography.
Laer S, Neumann J, Scholz H, Uebeler P, Zimmermann N.
Abteilung Allgemeine Pharmakologie, Universitats-Krankenhaus Eppendorf, Hamburg, Germany.
A sensitive and quantitative reversed-phase HPLC method for the analysis of D,L-sotalol in human atria, ventricles, blood and plasma was developed. Sotalol was determined in about 100 mg of human right atria, left ventricles, and in 500 microliters of blood and plasma samples of patients undergoing coronary bypass surgery or heart transplantation. Patients were taking 80-160 mg of sotalol as an antiarrhythmic agent. Atenolol was used as an internal standard certifying high precision of measurement. Sotalol blood and plasma concentrations correlated linearly to the obtained signals from 26.5 ng/ml to 2.12 micrograms/ml. Sotalol tissue concentrations showed linearity between 0.27 ng/mg and 10.6 ng/mg wet weight. The limit of quantitation was 0.27 ng/mg at a signal-to-noise ratio of 10. Sotalol was extracted from homogenized tissue with a buffer solution (pH9) and the remaining pellet was extracted with methanol. The methanol extract was evaporated under nitrogen and reconstituted in buffer (pH3). The whole extract was cleaned by solid-phase column extraction, eluted with methanol, evaporated again, reconstituted in the mobile phase (acetonitrile-15 mM potassium phosphate buffer pH3, 17:83, v/v) and injected onto the HPLC column (Spherisorb C6 column, 5 microns, 150 x 4.6 mm I.D.). For the detection of sotalol, the UV wavelength was set to 230 nm. Recoveries of sotalol and atenolol in atria and ventricles were 65.6 and 75.0%, respectively. Intra- and inter-assay coefficients of variation for tissue concentrations were 3.38 and 6.14%, respectively. Intra- and inter-assay accuracy for determined tissue sotalol concentrations were 94.9 +/- 6.3 and 99.6 +/- 4.1%.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8811439&dopt=Abstract
G Ital Cardiol. 1997 Nov;27(11):1113-20.
Abnormal myocardial glucose handling in patients with syndrome X: effect of beta-adrenergic blockade.
Fragasso G, Chierchia SL, Rossetti E, Landoni C, Lucignani G, Fazio F.
Division of Cardiology, INB/CNR, Istituto Scientifico H San Raffaele, University of Milan.
The present study was designed to test the hypothesis that patients with angina, positive exercise test and angiographically smooth coronary arteries (syndrome X), may exhibit abnormal myocardial glucose handling, as assessed by fluorodeoxyglucose (FDG) and positron emission tomography (PET) and to investigate the possibility that this abnormality could be reversed by treatment with betablockers, the drugs of choice in most patients with syndrome X. Eight consecutive patients (4 females, age 53 +/- 4 yrs) with syndrome X were studied. Off therapy, they underwent stress/rest 99m-TcMIBI SPET (360 degrees) and assessment of resting glucose metabolism by PET. PET studies were again performed after a 10 day treatment period on oral atenolol (100 mg/o.d.). All patients exhibited significant fasting FDG uptake in 2 or more myocardial regions. Overall, there were 28 of 48 segments (58%) with abnormal tracer uptake. On atenolol, there were only 5 segments with persistent FDG uptake (10%) in 2 patients. At rest, 7 patients exhibited perfusion defects in 14 myocardial segments. With stress performed in pharmacological wash-out, 5 patients developed perfusion defects in 10 myocardial segments. Eight of these segments were already underperfused at rest, and showed further reduction in perfusion after stress. All hypoperfused segments showed abnormal FDG uptake when the PET study was performed off therapy. The results suggest that, in patients with syndrome X, imbalance of the demand/supply ratio, either caused by limited coronary flow reserve or by primary vasoconstriction with reduction in myocardial perfusion, may determine a sustained metabolic shift towards anaerobic glycolysis. The mechanism by which atenolol improves metabolism in these patients could be simply related to reduction in O2 consumption.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9419821&dopt=Abstract
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