Cardiac dysfunction in HgCl2-induced nephrotic syndrome.
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.
Moreira-Rodrigues
Mónica
M
University of Porto, Portugal.
Henriques-Coelho
Tiago
T
Moura
Cláudia
C
Vasques-Nóvoa
Francisco
F
Sampaio-Maia
Benedita
B
Pestana
Manuel
M
Leite-Moreira
Adelino F
AF
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
D008627:Mercuric Chloride; D012964:Sodium; D009638:Norepinephrine