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Simvastatin, atorvastatin, and pravastatin are equally effective in improving the hemodynamic status of type 1 diabetic rats (1051.14)
Author(s) -
Quidgley Jose,
Cruz Nildris,
Melendez George,
Crespo Maria
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1051.14
Subject(s) - pravastatin , medicine , simvastatin , atorvastatin , ejection fraction , cardiac function curve , oxidative stress , cardiology , fibrosis , statin , endocrinology , stroke volume , endothelial dysfunction , pharmacology , cholesterol , heart failure
Statins improve cardiovascular (CV) status of diabetic patients. The underlying mechanisms remain unclear. We compared the effects of a four‐week administration of 10 mg/kg/day atorvastatin (AV), simvastatin (SV), and pravastatin (PV) on the CV function of (STZ)‐diabetic rats. Echocardiographic parameters, endothelial function, cholesterol levels, perivascular fibrosis and oxidative stress markers were evaluated. Cholesterol levels (mg/dl) were higher in STZ (249±16) than in CT (156±7) (n=10, P<0.05), and were not modified with this statin dose. AV and SV improved ejection fraction, stroke volume and cardiac output index (n=10, P<0.05), while PV only improved ejection fraction and stroke volume. Vascular relaxation was improved by all statins, and abolished by 1 mM LNAME, suggesting a NO‐dependent mechanism. In addition, all statins significantly reduced perivascular fibrosis (µm/100g BW) from 10.59±0.40 in untreated STZ to 9.0±0.3 (AV), 8.8±0.4 (SV), and 9.0±0.4 (PV), and levels of the oxidative stress markers MDA and 4‐HAE. The cholesterol‐independent hemodynamic benefits observed with all statins may be secondary to reductions of oxidative stress. The latter, by improving endothelial function, will reduce vascular tone and remodeling, decrease cardiac workload and improve systolic performance. Grant Funding Source : Supported by MBRS‐RISE R25‐GM061838.