Cardiac alterations induced by moderate zinc deficiency during fetal life and growth

Abstract

AimTo evaluate the cardiac function, morphology and nitric oxide synthase (NOS) activity at 81 days of life in response to fetal and postnatal growth moderate zinc deficiency. Female Wistar rats received from the beginning of pregnancy up to weaning low (L:8 ppm) or control (C:30 ppm) zinc diet. After weaning, male offspring of each group of mothers fed low (l) or control (c) zinc diet during 60 days (Cc, Ll, Lc). We determined systolic blood pressure (SBP) by indirect tail‐cuff technique, cardiac NOS activity (pmol 14C L‐citrulline/g.tissue. min), myocytes diameter (MD, μm) and TGF‐β (% total area) by immunohistochemistry in heart. Left ventricular (LV) function was assessed by echocardiography, studying diastolic (d) and systolic (s) LV wall (LVW, mm), septum (LVS, mm) and ejection fraction (EF %).Statisticst‐test. Cc Ll SBP (mmHg) 122±2 141±5* dLVS 2.3±0.1 1.8±0.1* sLVS 3.3±0.1 2.7±0.03* dLVW 2.7±0.2 2.1±0.1* sLVW 3.5±0.3 2.6±0.1* EF% 79±7 66±4* NOS 204±6 164±10* TGF‐β 40.2±1.5 49.9±1.5* Major MD 31.8±0.6 26.5±0.8* Minor MD 18.2±0.3 14.1±0.5* Values are means±SEM; p<0.05 vs Cc; n=8 rats/group. Adequate zinc diet in low offpring after weaning (Lc) was unable to avoid alterations induced during fetal life. Zinc restriction during fetal life and growth may program heart diseases in adult life. Supported by: UBA‐Conicet.