Drugs online research references
J Pharm Biomed Anal. 1996 May;14(7):773-81.
Time-resolved fluoroimmunoassay for the determination of lisinopril and enalaprilat in human serum.
Yuan AS, Gilbert JD.
Department of Drug Metabolism, Merck Research Laboratories, West Point, PA 19486, USA.
A solid-phase immunoassay with detection based on time-resolved fluorescence (TR-FIA) has been developed for the determination of lisinopril and enalaprilat in human serum. The immunogen was prepared by coupling lisinopril to bovine serum albumin through a two-step reaction with difluorodinitrobenzene. An antiserum specific to both lisinopril and enalaprilat was used. The assay is based on the competitive immunoassay principle in which the drug competes with biotin-labeled drug for a limited quantity of primary antibody bound via sheep anti-rabbit globulin to the wells of microtitration strips. At the end of the first incubation, the unbound biotin-labeled drug is washed away. In the second step, europium-labeled streptavidin (specific to biotin) reacts with the biotin already bound to the solid-phase antibody. After a washing step, the addition of an enhancement solution dissociates the europium ions from the labeled streptavidin into solution. The fluorescence from each sample is inversely proportional to the concentration of the drug in the sample. The assay demonstrates good accuracy, reproducibility and specificity at serum concentrations down to 0.5 ng ml-1. However, the useful concentration range of TR-FIA is much narrower than that obtained by double antibody radioimmunoassay (RIA).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8809701&dopt=Abstract
word match zestril online literature
Biochem Mol Med. 1996 Feb;57(1):19-24.
Protein synthesis during regression of left ventricular hypertrophy with lisinopril in abdominal aortic constriction model of hypertension.
Siddiq T, Richardson PJ, Trotter SE, Preedy VR.
Department of Internal Medicine, University of Texas Medical Branch at Galveston, Texas, 77550, USA.
The use of lisinopril was assessed in inducing regression of established left ventricular hypertrophy. Left ventricular hypertrophy was achieved by aortic constriction in the rat. Lisinopril was administered in drinking water (5 mg/kg body weight/day) to aortic constricted rats starting from Day 30 for a period of further 30 days. At the end of 60 days the rates of protein synthesis were measured using the flooding dose technique. Lisinopril reduced the mixed protein contents of the regressed left ventricle from 223 +/- 7 mg to 175 +/- 10 mg/left ventricle in the aortic constricted rats; P < 0.01, all data are means +/- SEM, n = 5-8. The regression of left ventricular mass occurred along with simultaneous decrease in the rate of protein synthesis (i.e., 6.56 +/- 0.33 in aortic constricted rats versus 4.40 +/- 0.44%/day, in lisinopril treated left ventricles, P < 0.05). However, the expanded cardiocyte fiber thickness remained unchanged despite lisinopril treatment (i.e., 20.4 +/- 0.7 in aortic constricted rats versus 19.5 +/- 0.6 microm in regressed left ventricles, P > 0.05). The results indicate that regression of pressure overloaded hypertrophy with lisinopril primarily occurs by a decrease in protein synthesis in the connective tissue components of the left ventricle, although cytoskeletal components may be unaffected.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8812722&dopt=Abstract
word match zestril online literature
Thromb Res. 1996 Jul 15;83(2):143-52.
The ACE-inhibitor lisinopril affects plasma insulin levels but not fibrinolytic parameters.
Zehetgruber M, Beckmann R, Gabriel H, Christ G, Binder BR, Huber K.
Department of Cardiology, University of Vienna, Austria.
There is evidence that ACE-inhibitors exert beneficial effects on endogenous fibrinolysis in patients with previous myocardial infarction. It is still unknown if this effect is restricted to this patient group only and by which mechanisms ACE-inhibitors exhibit the profibrinolytic effects. One possible explanation might be the positive influence of ACE-inhibitors on insulin metabolism by decreasing plasma insulin which in turn could decrease PAI-1, a major regulator of the fibrinolytic system. Therefore the present study examines the relationship between insulin and PAI-1 plasma levels during intravenous glucose tolerance tests before and after administration with the ACE-inhibitor lisinopril in 12 male obese patients with angiographically proven coronary artery disease and borderline hypertension. After a 4-weeks wash-out period glucose tolerance tests were performed before and after lisinopril-treatment (10mgs/d) for 12 weeks. After the treatment period, fasting plasma insulin level decreased from 15.6 +/- 2.1 to 11 +/- 1.8 uU/ml, p < or = 0.01. Stimulated levels of insulin during glucose tolerance test also significantly decreased by lisinopril (peak insulin from 57 +/- 10 to 41.2 +/- 7.3 uU/ml, p < or = 0.02). Basal plasma tissue plasminogen activator antigen, PAI-1 total antigen and PAI-1 "active" antigen were unaffected by therapy (8.4 +/- 0.5 vs 8.6 +/- 0.5 ng/ml, 118 +/- 20 vs 124 +/- 16 ng/ml and 21 +/- 7 vs 30 +/- 7 ng/ml, respectively). Our data confirm a beneficial effect of lisinopril on plasma levels of insulin but failed to demonstrate any profibrinolytic effect in this study population, thus questioning the postulated mechanism of influencing endogenous fibrinolysis by changes of plasma insulin.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8837313&dopt=Abstract
word match zestril online literature
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Antibiotics and prescription medications online literature ||