Drugs online research references
Biol Pharm Bull. 1995 Oct;18(10):1454-5.
Determination and properties of acetyl conjugate of N-desisopropylpropranolol, AcNDP.
Noda A, Ono Y, Wu X, Kudo K, Jitsufuchi N, Eto S, Noda H.
Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
1-Acetamino-3-(1-naphthyloxy)-2-propanol (AcNDP) detected in human urine was formed as a metabolite of propranolol (PL) via 1-amino-3-(L-naphthyloxy)-2-propanol (N-desisopropylpropranolol, NDP). The excreted amount of AcNDP was determined by GC-MS using an isotope dilution method. More than 40% of total AcNDP in 24 h urine was detected 10 h after the oral administration of PL to two volunteers, and the total amounts during 24 h urine were at least 1.9-3.9% of the PL dose. As AcNDP is an intermediate metabolite of PL, its urinary amount cannot be determined exactly. Incidentally, AcNDP was chemically stable and was not formed from NDP when acetyl CoA was added to the inactivated hepatocyte system. Thus, the acetylation of NDP, an aliphatic primary amine, was confirmed to be catalyzed by N-acetyltransferase, and interestingly, the acetyl conjugation was inhibited not by sulfamethazine but by p-amino benzoic acid.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8593456&dopt=Abstract
Am J Cardiol. 1977 May 26;39(6):816-20.
Cardiac Death in the first 6 months after myocardial infarction: potential for mortality reduction in the early posthospital period.
Moss AJ, DeCamilla J, Davis H.
In a prospective postmyocardial infarction study of 759 patients aged less than 66 years, 42 posthospital cardiac deaths (42 of 759; 6 percent) occurred during a 6 month follow-up period. The average age of those who died was 53.5 +/- 8.8 (+/- standard error) years, and postmortem examination was obtainedon 36 percent. Almost 60 percent of the 6 month posthospital mortality occurred within 2 months after hospital discharge. Fifty-five percent of the cardiac deaths occurred either outside th ehospital or within hospital emergency departments, and 62 percent of the deaths were sudden (within 12 hours) or unwitnessed. The suspected mechanism of cardiac death was a primary arrhythmia in 62 percent, and a definite or probable myocardial infarction was diagnosed in only 41 percent. Use of digitalis and diuretic and antiarrhythmic agents was significantly (P is less than 0.025) greater in this group during the week before death than in a comparison survivor group; no difference in use of propranolol or tranquilizers was noted between the two groups. Fifty percent of the group that died had two or more of the following factors: death outside the hospital, sudden death, primary arrhythmic death. These findings indicate that a considerable potential exists for reducing cardiac death in the early posthospital phase of myocardial infarction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=860693&dopt=Abstract
Toxicol Appl Pharmacol. 1996 Mar;137(1):1-7.
The effects of extracellular ions on beta-blocker cardiotoxicity.
Kerns W 2nd, Ransom M, Tomaszewski C, Kline J, Raymond R.
Department of Emergency Medicine, Division of Toxicology, Carolinas Medical Center, Charlotte, North Carolina 28232-2861, USA.
The mechanism of beta-blocker induced cardiotoxicity is poorly understood. One possible explanation is that beta-blockers induce ion dyshomeostasis, resulting in cardiac hyperpolarization. The intent of this study was to determine if modifying extracellular ions would reverse cardiotoxicity from two beta-blockers: propranolol (PROP) and atenolol (ATEN). Two treatments were studied: low extracellular K+ and high extracellular Na+. Isolated rat hearts were perfused on a Langendorff apparatus with Krebs-Henseleit- Bicarbonate buffer (KHB) solution. Toxicity (Tox) was induced by perfusing hearts for 30 min with KHB + PROP [5 microgram/ml] or KHB + ATEN [2.5 mg/ml]. Subsequently, hearts were perfused with KHB containing either PROP or ATEN, but modified by lowering K+ [2.3 mM] or raising Na+ [160 mM] for a 30-min treatment (Tx) period. Hearts were paced near the end of treatment. Cardiodynamics were monitored via a balloon-tipped catheter in the left ventricle. The first derivative of LV pressure (dP/dt) with respect to time served as our index of myocardial performance. Tx groups were as follows: (1) KHB only, (2) PROP only, (3) PROP + K, (4) PROP + Na, (5) ATEN only, (6) ATEN 4 K, and (7) ATEN + Na. PROP induced negative chronotropic effects and rendered the hearts refractory to pacing. ATEN demonstrated similar chronotropic toxicity plus decreased myocardial contractility. Tx with low extracellular K+ and high extracellular Na+ increased HR and restored the ability to pace, thereby reversing toxicity. These data suggest that beta-blocker toxicity is mediated via hyperpolarization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8607134&dopt=Abstract
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