title: Cardiac dysfunction in HgCl2-induced nephrotic syndrome.
abstract: The experimental model of HgCl(2) injection is characterized by a systemic autoimmune disease which leads to the development of nephrotic syndrome (NS). NS seems to be accompanied by cardiovascular alterations, since patients with NS present an increased incidence in cardiac disease. The aim of our work was to study the effects of HgCl(2)-induced NS on myocardial function and morphometry. Normotensive Brown-Norway rats were injected with HgCl(2) (1 mg/kg, HgCl(2) group; n = 6, subcutaneous) or the vehicle (control group; n = 6, subcutaneous) on days 0, 2, 4, 7, 9 and 11. The animals were placed in metabolic cages for evaluation of urinary excretion of noradrenaline, sodium, total proteins, albumin and creatinine. Fourteen and 21 days after the first HgCl(2) injection, left ventricle (LV) hemodynamics was evaluated through pressure micromanometers in basal and isovolumetric heartbeats. The heart and gastrocnemius muscle weights and tibial length were also examined. In an additional group of animals cardiac dimensions and ejection fraction were assessed by echocardiography and LV apoptosis and fibrosis were studied. HgCl(2)-injected rats presented proteinuria, albuminuria, hyperlipidemia, anemia, sodium retention and ascites at day 14. These alterations were accompanied by LV hemodynamic changes only in isovolumetric heartbeats. Similarly, on day 21, HgCl(2)-injected rats presented proteinuria, albuminuria, hyperlipidemia, anemia, but no sodium retention or ascites. These animals presented LV systolic and diastolic dysfunction in both basal and isovolumetric heartbeats, as well as cardiac atrophy, LV fibrosis and an increase in myocyte apoptosis. In conclusion, HgCl(2)-induced NS is accompanied by LV dysfunction and can be a promising model for studying the link between NS and cardiac disease.
authors.affiliation: University of Porto, Portugal.
authors.forename: Mónica
authors.initials: M
authors.lastname: Moreira-Rodrigues
authors.forename: Tiago
authors.initials: T
authors.lastname: Henriques-Coelho
authors.forename: Cláudia
authors.initials: C
authors.lastname: Moura
authors.forename: Francisco
authors.initials: F
authors.lastname: Vasques-Nóvoa
authors.forename: Benedita
authors.initials: B
authors.lastname: Sampaio-Maia
authors.forename: Manuel
authors.initials: M
authors.lastname: Pestana
authors.forename: Adelino F
authors.initials: AF
authors.lastname: Leite-Moreira
mesh_terms: D000818:Animals; D017209:Apoptosis; D001284:Atrophy / Q000473:pathology; D001327:Autoimmune Diseases / Q000473:pathology; D005355:Fibrosis; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006331:Heart Diseases / Q000209:etiology; D006439:Hemodynamics; D008297:Male; D008627:Mercuric Chloride / Q000633:toxicity*; D009206:Myocardium / Q000473:pathology; D009404:Nephrotic Syndrome / Q000139:chemically induced* / Q000150:complications; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000737:chemistry; D013997:Time Factors
chemical_list: D008627:Mercuric Chloride; D012964:Sodium; D009638:Norepinephrine