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Comparison of the effects of intrapericardial and intravenous aldosterone infusions on left ventricular fibrosis in rats
Author(s) -
MinnaardHuiban Monica,
Hermans J.J. Rob,
Essen Helma,
Bitsch Nicole,
Smits Jos F.M.
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.09.012
Subject(s) - aldosterone , medicine , fibrosis , cardiac fibrosis , heart failure , cardiology , saline , endocrinology
Background: Aldosterone plays a detrimental role in the pathology of chronic heart failure. An important mechanism resides in its ability to evoke extensive fibrosis in the heart. However, the locations of the aldosterone interaction sites responsible for triggering cardiac fibrosis are puzzling. Extra‐cardiac aldosterone actions are known to contribute to cardiac fibrosis but whether local cardiac aldosterone actions are involved is unclear. Aims: This study aimed to investigate whether local aldosterone actions contribute to cardiac fibrosis in vivo . Methods: Saline treated male Wistar rats were intravenously (systemically) or intrapericardially (locally) infused for 8 weeks with 75 or 750 ng/h aldosterone to monitor end point left ventricular epicardial collagen levels (histology). Results: Perivascular fibrosis was observed only at high dose aldosterone infusions and was not different for the administration routes. Regarding interstitial fibrosis however, clear differences between the administration routes were seen. Intrapericardial aldosterone infusions increased interstitial collagen levels 1.72× ( P <0.05) at low dose, but –surprisingly– had no significant effect at high dose. In contrast, intravenous aldosterone had no significant effect at low dose but increased interstitial collagen 1.72× ( P <0.05) at high dose. Conclusion: Our data suggest that local cardiac aldosterone actions contribute to the development of left ventricular interstitial fibrosis.