[Myocardial remodeling in chronic pressure or volume overload in the rat heart].
OBJECTIVE
To compare cardiac structural changes in experimental pressure and volume overload models.


METHODS
The study analysis included renovascular hypertensive rats (RVH, n = 8), normotensive rats with volume overload caused by an aortocaval fistula (ACF, n = 10) and control rats (CONT, n = 8). After four weeks, tail cuff blood pressure (SBP) was recorded. Rats were killed, the hearts were excised and the right and left ventricles (RV&LV) were weighed (RVW&LVW). Using histological sections, myocyte cross sectional areas (MA). LV wall thickness (LVWT) LV cavity diameter (LVD), normalized LVWT (LVWT/LVD) and collagen volume fraction (CVF) were measured. The comparisons were made using the ANOVA and Tukey test for a significance level of 5%.


RESULTS
Tail cuff blood pressure (mmHg) was higher in the RVH group (RVH = 187 +/- 22; CONT = 125 +/- 10; ACF = 122 +/- 6, p < 0.05). LV hypertrophy was observed in the RVH and ACF groups. The ACF group presented a significant increase in size of LVD, compared to CONT and RVH. The absolute and normalized ventricular wall thickness were similar among the groups. The RVH group presented a significant increase in CVF compared to CONT group and ACF group.


CONCLUSIONS
Cardiac remodeling patterns following volume or pressure overload are distinct, suggesting that their implications on ventricular dysfunction are not interchangeable.
Matsubara
Luiz Shiguero
LS
Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Unesp, Botucatu, SP. lsmatsu@cardiol.br
Narikawa
Silvia
S
Ferreira
Ana Lucia dos Anjos
AL
Paiva
Sergio Alberto Rupp de
SA
Zornoff
Leonardo Mamede
LM
Matsubara
Beatriz Bojikian
BB
D000818:Animals; D001164:Arteriovenous Fistula / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D002306:Cardiac Volume / Q000502:physiology*; D004195:Disease Models, Animal; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D018754:Ventricular Dysfunction / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology*