Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-dose intravenous nitroglycerin infusion can be safely administered during acute myocardial infarction to unload the left ventricle and salvage ischemic myocardium and left ventricular geometry and function. In an experimental conscious dog model, low-dose infusion titrated to decrease mean blood pressure by 10% over the first 6 hours after coronary artery ligation resulted in 51% decrease in infarct size, 54% decrease in preload, and more than 50% increase in collateral blood flow. The same benefits were seen when methoxamine was given to counteract that 10% decrease in blood pressure. Similar short-term nitroglycerin infusion also limited remodeling in the dog model. More important, no myocardial salvage was seen with excessive nitroglycerin-induced hypotension to levels less than 80 mm Hg. Clinically, prolonged low-dose nitroglycerin infusion was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients with acute infarction: 154 received nitroglycerin and 156 received placebo. Nitroglycerin was titrated to reduce mean blood pressure by 10% in normotensive patients and up to 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not to less than 80 mm Hg. Nitroglycerin produced several benefits compared with placebo: (1) smaller creatine kinase infarct size; (2) less regional left ventricular dysfunction, better global ejection fraction, and less infarct expansion and thinning; (3) better clinical functional status and hemodynamics; (4) fewer inhospital complications such as acute left ventricular failure and dilation due to marked infarct expansion, left ventricular thrombus, cardiogenic shock, and infarct extension; and (5) fewer deaths up to 1 year in patients with anterior Q-wave infarction.
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PMID:Intravenous nitroglycerin unloading in acute myocardial infarction. 183 97

A strain of Agrobacterium sp. S-1231 was isolated from one of the soil samples taken from Beijing area. In 4 days' cultivation it was found to produce extracellular polysaccharide and about 24 grams per liter of sugar-containing substrate. At the same concentrations, the polymer produced higher viscosity than that of xanthan gum (Kelzan). The viscosities of 0.2%, 0.5% and 1.0% solutions of this polymer were found to be 840, 5200 and 15000 cp respectively, measured with a Brookfield LVF viscosimeter at 6 rpm. Besides its pseudoplastic rheological properties and the excellent stability towards pH, it had unusual compatibility with high levels of salts and provided shear thinning properties similar to that in fresh water. Moreover, it is also compatible with cationic dyes without precipitation. Unlike other microbial polysaccharides, the viscosities of this polymer remained constant at different temperatures under 65 degrees C, but it decreased sharply in a narrow range of temperatures between 70-75 degrees C.
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PMID:Rheological properties of the extracellular polysaccharide from Agrobacterium sp.S-1231. 212 92

Evidence of acute infarct expansion and the frequency of the acute infarct expansion syndrome (acute infarct dilatation and thinning associated with hypotension and left ventricular failure but no evidence of new necrosis) occurring at two days or more after a first acute Q-wave myocardial infarction were studied using serial two-dimensional echocardiography in 221 consecutive patients (100 anterior, 121 inferior). Patients with symptomatic pericarditis were treated with indomethacin (group 1, n = 73) or ibuprofen (group 2, n = 49) and those without symptomatic pericarditis received neither drug (group 3, n = 99). The overall frequency of the acute infarct expansion syndrome was 13% and 69% of these were among the pericarditis groups. The syndrome was significantly more frequent in group 1 (22%) than group 2 (8%) (P less than 0.05) or group 3 (9%) (P less than 0.025). Serial echocardiograms revealed more expansion with greater percentage increase in the infarct containing segment length in group 1 than group 2 or group 3 (18% versus 9% versus 9%, P less than 0.005). However, the decreases in infarct segment thickness were similar in groups 1 (24%) and 2 (25%) but greater (P less than 0.001) than in group 3 (7%). Despite similar infarct size and infarct thinning in groups 1 and 2, the degree of infarct expansion was greater and the infarct expansion syndrome more frequent in group 1. However, when allowance was made for the potential protective effect of prior use of intravenous nitroglycerin and concomitant use of nifedipine, indomethacin and ibuprofen had similar effects on expansion. Thus, indomethacin or ibuprofen should be used with caution after Q-wave infarction so as to avoid further expansion. The fact that short term use of other drugs might modify infarct remodelling should be considered in studies attempting to assess efficacy of one particular drug.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarct expansion during indomethacin or ibuprofen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling. 256 3

The hypothesis that nitrates might effectively limit left ventricular remodeling and improve function after acute myocardial infarction has been tested in experimental and clinical models, with special attention to the pathophysiologic evolution of remodeling. In 1 clinical study, before the thrombolytic era, the effects of low-dose intravenous nitroglycerin infusion for the first 48 hours during acute myocardial infarction was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients (154 nitroglycerin; 156 placebo). Nitroglycerin proved to be safe and produced several benefits compared with placebo: (1) smaller infarct size; (2) less left ventricular dysfunction; (3) less infarct expansion and thinning; (4) better functional status; (5) fewer in-hospital complications such as left ventricular failure, left ventricular thrombus, cardiogenic shock, and infarct extension; and (6) fewer deaths up to 1 year. Two subsequent clinical studies in the thrombolytic era, with low-dose intravenous nitroglycerin infusion during infarction over the first 48 hours followed by buccal nitrate (eccentric dose regimen) or placebo during healing over 6 weeks postinfarction, indicated that prolonged nitrate therapy effectively limited left ventricular remodeling and improved function further compared with placebo.
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PMID:Effects of nitrate therapy on ventricular remodeling and function. 827 53