Drugs online research references
Vnitr Lek. 1998 Jun;44(6):336-41.
[The effect of ramipril on metabolic, renal and cardiac function in hypertension and type II diabetes mellitus]
[Article in Czech]
Vitovec J, Spinar J.
II. interni klinika FN U sv. Anny LF MU, Brno.
OBJECTIVE: To assess the effect of ramipril on indicators of glucose metabolism, incl. insulin resistance, on renal function with microalbuminuria, changes of some echocardiographic signs of hypertrophy and compliance of the left ventricle in patients with hypertension and type II diabetes mellitus. MATERIAL AND METHODS: The authors examined 32 patients with hypertension grade I and II and with diabetes type II, who had ramipril, 2.5-10 mg/day, for a period of six months. The examination before and after long-term treatment comprised basic biochemical sampling incl. concentrations of immunoreactive insulin, C-peptide and glycated haemoglobin and also complete functional examination of the kidneys, incl. microalbuminuria. Echocardiographic examination was focused on assessment of signs of hypertrophy and compliance of the left ventricle. Treatment of diabetes was not changed in the course of 6 months. RESULTS: In addition to the anticipated drop of blood pressure a declining trend of insulin resistance was recorded, there was a significant decline of microalbuminuria and a rise of natriuresis, the left ventricle mass declined and its compliance improved. CONCLUSION: Ramipril one of the inhibitors of angiotensin converting enzyme is an effective and useful medication for type II diabetics suffering from hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9820056&dopt=Abstract
Eur J Clin Pharmacol. 1996;49 Suppl 1:S29-33.
Mega-trials: is meta-analysis an alternative?
Lubsen J.
SOCAR Research SA, Givrins, Switzerland.
Large scale placebo-controlled trials with clinical end-points are not possible when other compounds with proven efficacy are already available. Hence, the question arises whether the available experience from placebo-controlled phase III trials can be analysed jointly to assess whether an effect on clinical end-points exists. This question was answered for the new ACE inhibitor ramipril, with which five exercise capacity trials were done in similar patients with heart failure. Meta-analysis showed that ramipril reduced the occurrence of the combined event death or hospitalisation by 32% (P = 0.05), based on the customary 'intention-to-treat' comparison for large scale trials. From this analysis, the lesson has been learnt that a drug development programme must be carefully planned to allow for this type of meta-analysis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8834929&dopt=Abstract
Circulation. 1999 Sep 21;100(12):1291-7.
Nitric oxide modulates mitochondrial respiration in failing human heart.
Loke KE, Laycock SK, Mital S, Wolin MS, Bernstein R, Oz M, Addonizio L, Kaley G, Hintze TH.
Department of Physiology, New York Medical College, Valhalla, NY, USA.
Background-Our objective for this study was to investigate whether nitric oxide (NO) modulates tissue respiration in the failing human myocardium. Methods and Results-Left ventricular free wall and right ventricular tissue samples were taken from 14 failing explanted human hearts at the time of transplantation. Tissue oxygen consumption was measured with a Clark-type oxygen electrode in an airtight stirred bath containing Krebs solution buffered with HEPES at 37 degrees C (pH 7.4). Rate of decrease in oxygen concentration was expressed as a percentage of the baseline, and results of the highest dose are indicated. Bradykinin (10(-4) mol/L, -21+/-5%), amlodipine (10(-5) mol/L, -14+/-5%), the ACE inhibitor ramiprilat (10(-4) mol/L, -21+/-2%), and the neutral endopeptidase inhibitor thiorphan (10(-4) mol/L, -16+/-5%) all caused concentration-dependent decreases in tissue oxygen consumption. Responses to bradykinin (-2+/-6%), amlodipine (-2+/-4%), ramiprilat (-5+/-6%), and thiorphan (-4+/-7%) were significantly attenuated after NO synthase blockade with N-nitro-L-arginine methyl ester (10(-4) mol/L; all P<0.05). NO-releasing compounds S-nitroso-N-acetyl-penicillamine (10(-4) mol/L, -34+/-5%) and nitroglycerin (10(-4) mol/L, -21+/-5%), also decreased tissue oxygen consumption in a concentration-dependent manner. However, the reduction in tissue oxygen consumption in response to S-nitroso-N-acetyl-penicillamine (-35+/-7%) or nitroglycerin (-16+/-5%) was not significantly affected by N-nitro-L-arginine methyl ester. Conclusions-These results indicate that the modulation of oxygen consumption by both endogenous and exogenous NO is preserved in the failing human myocardium and that the inhibition of kinin degradation plays an important role in the regulation of mitochondrial respiration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10491373&dopt=Abstract
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