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Beneficial effects of folic acid supplementation on left ventricular volume overload
Author(s) -
Rezk Bashir M,
Lord Kevin C,
Reed Ryan E,
Hutchinson Kirk R,
Espinoza Carmen,
McIlwain Elizabeth,
ElKak Abd ElAziz A,
Varner Kurt J,
Lucchesi Pamela A
Publication year - 2008
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.22.1_supplement.970.28
Subject(s) - oxidative stress , apoptosis , volume overload , medicine , tunel assay , endocrinology , ventricular remodeling , pressure overload , chemistry , muscle hypertrophy , heart failure , biochemistry , cardiac hypertrophy
Cardiovascular disease is the major cause of worldwide morbidity and mortality. This is the first study to investigate the cardioprotective effects of folic acid (FA) on left ventricular remodeling in response to acute volume overload generated by aorto‐caval fistula (ACF) Adult male Sprague‐Dawley rats were subjected to ACF for 72 hr ± pretreatment with folic acid (30 mg/kg/day) along with sham operated controls. Echocardiography and in vivo pressure volume loops indicated left ventricular (LV) dilation in ACF vs. sham that was associated with oxidative stress (decreased GSH/GSSG ratio), extracellular matrix (ECM) degradation and apoptosis. Interestingly, TUNEL‐positive cells resided only in the microvascular component of the ACF LV. Endothelial cell apoptosis lead to decreased LV capillary density, whereas ECM degradation in response to ACF was associated with mast cell degranulation and increased MT1‐MMP expression compared to sham. Folic acid supplementation remarkably reversed LV dilation, prevented apoptosis, decreased oxidative stress, and increased both VEGF isoform expression and capillary density despite continued volume overload induced by ACF. The prominent cardioprotective effects of FA may be due to its potent antioxidant and proangiogenic activities.