Drugs online research references
Cardiologia. 1990 Oct;35(10):851-6.
[Acute coronary vasomotor effects of nifedipine and its therapeutic efficacy in syndrome X]
[Article in Italian]
Montorsi P, Cozzi S, Loaldi A, Fabbiocchi F, Annoni L, De Cesare N, Polese A, Guazzi MD.
Istituto di Cardiologia, Universita degli Studi, Milano.
In 18 patients (12 females) presenting with effort-induced chest pain and normal coronary angiograms (syndrome X), 10 mg sublingual nifedipine increased the lumen of major coronary arteries (quantitative angiography) by 13% +/- 10 (p less than 0.01), coronary blood flow (thermodilution) by 23% +/- 26 (p less than 0.05), norepinephrine plasma concentration by 60% +/- 42 (p less than 0.01), and reduced the global ST segment shift during the effort stress test from 8.8 +/- 4.1 to 7 +/- 6.8 mm (p less than 0.03) at comparable maximal workload and at unchanged double product. There was a correlation (positive) of changes in flow with changes in coronary lumen diameter (r = 0.65, p less than 0.01), with ST segment response to exercise (r = 0.83, p less than 0.001), and with (inverse) norepinephrine plasma concentration (r = -0.70, p less than 0.01); no correlation was found between ST segment response and changes in arterial lumen diameter. In a few cases nifedipine did not improve or even worsened the response to exercise; in them coronary flow was unchanged or reduced and norepinephrine plasma levels were modestly or greatly increased, respectively. After 4-week treatment with nifedipine (10-20 mg 4 times daily), the effort ST segment shift was further diminished to 4.4 +/- 3.5 mm (p less than 0.03) despite a slightly increased double product. Plasma norepinephrine values, as compared to those following acute nifedipine, were reduced by 40% in patients with further improvement and unchanged in patients whose exercise performance did not vary.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2093432&dopt=Abstract
Pharmacology. 1990;40(3):137-49.
Comparative anti-ischemic effects of dihydropyridine calcium antagonists in isolated perfused rat hearts: relationship of cardiodepression and cardioprotection.
Grover GJ, Dzwonczyk S, Sleph PG.
Department of Pharmacology, Squibb Institute for Medical Research, Princeton, N.J.
A comparison was made of the anti-ischemic effects of dihydropyridine calcium antagonists in isolated globally ischemic rat hearts. Pretreatment with amlodipine, nifedipine, nitredipine, or nisoldipine reduced reperfusion enzyme (lactate dehydrogenase) release and contracture after 25 min of global ischemia and 30 min of reperfusion. Increasing concentrations of all compounds resulted in proportionally smaller reductions in the severity of ischemia, with larger decreases in nonischemic tissue contractility occurring. Reperfusion function was significantly improved at 30 min with nifedipine only; however, at 60 min reperfusion function was significantly improved for all except nisoldipine. Washout data from nonischemic hearts (rate of disappearance of cardiodepressant effects) showed that the dihydropyridines washed out in the following order (fastest to slowest): nifedipine greater than nitrendipine greater than nisoldipine greater than amlodipine. Thus, these dihydropyridines are anti-ischemic, though at higher concentrations cardiodepressant effects increase disproportionately. Differences in washout also effect the ability of these compounds to improve reperfusion function.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2333320&dopt=Abstract
tu-bs.de
The title compounds 5 were received from the saponification of ethyl 3-aminobenzo[b]furan-2-carboxylate (3) followed by reaction with acetylenedicarboxylic diesters. The esters 5 reacted with alkyl iodides to give mixtures of the 4-alkoxypyridines 8 and the N-alkylpyridones 9. Alkaline hydrolysis of the esters 5, 8 and 9 yielded the carboxylic acids 6, 11 and 12. The carboxylic acid 6 could be decarboxylated to afford the annulated pyridone 7. The tetrazoles 21 and 22 were synthesized starting from the esters 8 and 9. At first, reduction afforded carbinoles, subsequent selective oxidation yielded the aldehydes 15 and 16, which were converted into aldoximes. Dehydration of the aldoximes formed nitriles, which added hydrazoic acid. The carbaldehydes 15 and 16 reacted in the Hantzsch-Synthesis with beta-aminocrotonic acid esters to form the 1,4-dihydropyridines (DHP) 23 and 24, which could be dehydrogenated to obtain the pyridines 25 and 26. The unsymmetrical pyridine compound 27b was isolated as a by-product using 15b in the DHP-synthesis. The DHP 23 and 24 were more stable against oxidation than the reference drug nifedipine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10989836&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||