Drugs online research references
Cardiology. 1994;85 Suppl 1:7-12.
Use and abuse of clinical trials. Is the timing of treatment critical?
Tognoni G.
Laboratory of Clinical Pharmacology, Mario Negri Institute, Milan, Italy.
The timing of treatment for any condition is dependent on the underlying pathophysiology. One of the issues to consider is whether decreasing the time to intervention can be translated into recognisable benefits. Key data have been generated over the last 10 years which are relevant to the treatment of acute myocardial infarction (MI), including results of the large-scale 'mega-trials' in broad population groups. The therapeutic interventions which will be considered here are beta blockers, aspirin, thrombolytics and angiotensin-converting enzyme (ACE) inhibitors. Of these, aspirin seems to be the least time-dependent, provided it is administered within 12-24 h of symptom onset. Mortality benefits associated with beta blocker therapy increase as the time of administration from symptom onset is reduced and the extent to which thrombolytic therapy is beneficial is also clearly time dependent. The results from GISSI-3 and ISIS-4, which recruited a broader patient population than in previous trials, were concordant, showing a significant improvement in survival after five to six weeks' treatment. The message from GISSI-3 was that administration of ACE inhibitors within 24 h of symptom onset will improve survival and left ventricular function provided patients are hemodynamically stable, are not hypotensive and have no renal dysfunction; 76 lives were saved (representing an 11% risk reduction in mortality) after six weeks' lisinopril treatment, 54 of which were saved in the first five days.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7743538&dopt=Abstract
Biochem Biophys Res Commun. 1992 Apr 15;184(1):306-9.
The functional role of tyrosine-200 in human testis angiotensin-converting enzyme.
Chen YN, Ehlers MR, Riordan JF.
Center for Biochemical and Biophysical Sciences and Medicine, Harvard Medical School, Boston, MA 02115.
The active site of angiotensin-converting enzyme (ACE) has been shown by chemical modification to contain a critical tyrosine residue, identified as Tyr-200 in human testis ACE (hTACE). We have expressed a mutant hTACE containing a Tyr-200 to Phe mutation. The mutant exhibits a marked decrease in kcat: 15-fold and 7-fold for the hydrolysis of furanacryloyl-Phe-Gly-Gly and angiotensin I, respectively, whereas its Km increases by only 1.6- and 2.2-fold, respectively. We conclude that Tyr-200 is not required for substrate binding. Instead, the effect on kcat together with a 100-fold decrease in affinity for the ACE inhibitor lisinopril indicates that Tyr-200 may participate in catalysis by stabilizing the transition state complex. Thus, Tyr-200 in hTACE has a role analogous to that of Tyr-198 in carboxypeptidase A.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1314588&dopt=Abstract
J Hypertens Suppl. 1988 Dec;6(4):S145-7.
Modulation of left ventricular hypertrophy by dietary salt and inhibition of angiotensin converting enzyme.
Fernandez D, Bolli P, Snedden W, Vasdev S, Fernandez PG.
Department of Medicine, Memorial University Medical School, St John's Newfoundland, Canada.
The interactions of blood pressure, salt intake and angiotensin converting enzyme (ACE) inhibition were investigated in the Dahl salt-sensitive (DS) and salt-resistant (DR) strains of rats. Eight-week-old DS and DR (40 of each) were separately randomized to receive a low- (0.4% NaCl) or a high- (8% NaCl) salt diet for 3 weeks. Thereafter the rats were further separated randomly to receive the ACE inhibitor lisinopril (3-8 mg/kg per day) or no drug treatment for 11 weeks. In untreated DS rats blood pressure rose, paralleled by a higher left ventricular mass (ratio left ventricular weight/body weight) irrespective of salt intake. Lisinopril lowered blood pressure to normotensive levels in all groups except DS rats on a high-salt diet, despite doses of up to 100 mg/kg per day, although there was a significant fall in blood pressure. Lisinopril reduced left ventricular mass significantly on the low- but not on the high-salt diet. Plasma renin activity increased on lisinopril treatment in all groups except DS rats on the high-salt diet. Regression of an increased left ventricular mass by ACE inhibition seemed to be impaired by a high salt intake, even when blood pressure was lowered. Therefore, although for regression of left ventricular hypertrophy, reduction of afterload was the leading factor, this might be adversely affected by a high salt intake.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2853724&dopt=Abstract
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