Drugs online research references
Cor Vasa. 1991;33(5):384-96.
The effect of metoprolol on left ventricular systolic and diastolic function in essential hypertension.
Hradec J, Kral J, Petrasek J.
IIIrd Medical Department, 1st Faculty of Medicine, Charles University, Prague, Czechoslovakia.
Using ultrasound techniques, parameters of left ventricular systolic and diastolic function were assessed in 23 patients with degree I-II essential hypertension treated with metoprolol. Metoprolol administration was followed by increases in ejection fraction (p less than 0.01) and stroke volume (p less than 0.05), a decrease in heart rate (p less than 0.01) while cardiac output remained unchanged. Left ventricular filling was abnormal in 12 patients (52.2%). After metoprolol, the ratio of early diastolic to late diastolic transmitral velocity (E/A) rose; the increase indirectly correlated both with the baseline value of E/A (r = -0.59, p less than 0.01), and the change in heart rate (t = -0.65, p less than 0.01). Improved left ventricular diastolic filling was significant only in patients showing abnormal baseline diastolic function, and may be due to the decrease in heart rate rather than a direct effect exerted by metoprolol on the myocardium.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1839784&dopt=Abstract
Biochem Pharmacol. 1986 Aug 15;35(16):2757-61.
Metoprolol oxidation by rat liver microsomes. Inhibition by debrisoquine and other drugs.
Lennard MS, Crewe HK, Tucker GT, Woods HF.
The oxidative metabolism of metoprolol has been shown to display genetic polymorphism of the debrisoquine-type. The use of in vitro inhibition studies has been proposed as a means of defining whether one or more forms of cytochrome P-450 are involved in the monogenically-controlled metabolism of two substrates. We have, therefore, tested the ability of debrisoquine and other substrates to inhibit the oxidation of metoprolol by rat liver microsomes. Debrisoquine and guanoxan were potent competitive inhibitors of the alpha-hydroxylation and O-desmethylation of metoprolol as well as its metabolism by all routes (measured by substrate disappearance). Cimetidine and ranitidine, drugs which are known to impair the clearance of metoprolol in man, showed an inhibitory action comparable to that of debrisoquine in rat liver microsomes. Antipyrine, a compound whose metabolism is not impaired in poor metabolisers of debrisoquine, was found to be only a weak inhibitor of the metabolism of metoprolol. These findings suggest that the oxidation of metoprolol is linked closely to that of debrisoquine, cimetidine and ranitidine but not to that of antipyrine in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2943287&dopt=Abstract
J Diabet Complications. 1987 Apr-Jun;1(2):45-52.
Antihypertensive treatment: long-term reversal of progression of albuminuria in incipient diabetic nephropathy. A longitudinal study of renal function.
Christensen CK, Mogensen CE.
Second University Clinic of Internal Medicine, Kommunehospitalet, Aarhus C, Denmark.
This study was undertaken to clarify whether antihypertensive treatment has any effect on the rate of progression of kidney disease in patients with incipient diabetic nephropathy. Six insulin-dependent diabetic men with incipient nephropathy (urinary albumin excretion above 15 micrograms/min and total protein excretion below 0.5 g/24 h) were first given metoprolol (200 mg daily) with the subsequent addition of hydroflumethiazide. At the start of antihypertensive treatment, mean patient age was 32 +/- 4.2 years (SD) and mean duration of diabetes was 18 +/- 1.2 years. The patients were followed with repeated measurements of urinary albumin excretion for a mean of 5.4 +/- 3.1 years prior to, and for 4.7 +/- 1.3 years (SD) during treatment. Mean arterial blood pressure declined significantly during treatment, e.g., the values at 6 months before initiation of treatment being compared with values during the last 6 months of treatment fell from 107 mmHg +/- 7.6 to 93 +/- 3.8 (2p = 1.5%). Albumin excretion decreased from 131.0 micrograms/min X/divided by 2.9 (geometric mean X/divided by tolerance factor) to 41.7 micrograms/min X/divided by 2.9 (2p = 1.2%). Albumin clearance in per cent of glomerular filtration rate decreased from a mean of 0.0030 +/- 0.0019% (SD) to 0.0011 +/- 0.0010% (2p = 4.6%). The mean yearly increase in urinary albumin excretion before treatment was 18.0 +/- 17.0% (mean +/- SD); during treatment urinary albumin excretion decreased 19 +/- 10% per year (2p = 0.7%). No changes were seen in renal plasma flow (516 +/- 31.0 ml/min to 520 +/- 66 ml/min (n = 5)).(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2969901&dopt=Abstract
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