Drugs online research references
Life Sci. 2000 Aug 11;67(12):1409-21.
Poor regression of myocardial hypertrophy following concomitant chronic alcohol ingestion and angiotensin converting enzyme (ACE) inhibition.
Patel VB, Sandhu G, Dunn MJ, Mantle D, Rodrigues LM, Griffiths JR, Wassif W, Richardson PJ, Preedy VR.
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
In the following study we examined the combined effect of chronic alcohol administration and anti-hypertensive drug treatment in spontaneously hypertensive rats (SHR). SHR were fed alcohol for six weeks while taking the angiotensin converting enzyme (ACE) inhibitor lisinopril. After six weeks, protein synthesis rates, contractile protein levels and protease activities were examined in control; alcohol; control+lisinopril; alcohol+lisinopril groups. Lisinopril treatment significantly reduced left ventricular mass, protein content and contractile proteins in control rats, but these effects were not as pronounced in alcohol+lisinopril rats. Protein synthesis rates in both mixed and myofibrillar fractions were not significantly different in any of the 4 groups. The enzyme activities of the proteases cathepsin D and dipeptidyl aminopepetidase I increased in control+lisinopril rats, however, this effect was not evident in alcohol+lisinopril rats. Contractile proteins identified by one-dimensional electrophoresis showed that lisinopril treatment reduced all contractile proteins in control rats. However, in alcohol+ lisinopril rats, myosin heavy chain was higher than in control+lisinopril rats. In summary, alcohol ingestion impairs the regression of the hypertrophic myocardium in SHR on ACE-inhibitor treatment, which was reflected by altered protein metabolism. This study suggests that successful anti-hypertensive treatment may not be achieved if alcohol misuse is evident.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10983838&dopt=Abstract
Am J Forensic Med Pathol. 2000 Sep;21(3):287-99.
Commonly encountered prescription medications in medical-legal death investigation: a guide for death investigators and medical examiners.
Heninger MM.
Fulton County Medical Examiner's Office, Atlanta, Georgia 30312, USA.
The most common prescription medications encountered and recorded in the normal course of a death investigation by a medical examiner's office in a moderate-sized jurisdiction in an urban city are tallied, based on data collected from 2233 deaths reported in 1998. Medication history was available for 775 of these deaths and is reviewed in this study. The 25 most common medications are each briefly discussed, particularly adverse effects and possible toxicity of concern in the investigation of death. Medications to treat cardiovascular disease are by far the most commonly encountered. The 10 most common medications regardless of category were furosemide, digoxin, nitroglycerin, potassium, lisinopril, warfarin, albuterol, nifedipine, codeine, and amlodipine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10990295&dopt=Abstract
grape.med.tottori-u.ac.jp
It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11004022&dopt=Abstract
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