Remodelação miocárdica na sobrecarga crônica de pressão ou de volume no coração de ratos

Abstract

OBJECTIVETo compare cardiac structural changes in experimental pressure and volume overload models. METHODSThe study analysis included renovascular hypertensive rats (RVH, n=8), normotensive rats with volume overload caused by an aortocaval fi stula (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 signifi cance level of 5%. RESULTSTail 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 signifi cant 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 signifi cant increase in CVF compared to CONT group and ACF group. CONCLUSIONCardiac remodeling patterns following volume or pressure overload are distinct, suggesting that their implications on ventricular dysfunction are not interchangeable.

Treatment with nebivolol combined with physical training promotes improvements in the cardiovascular responses of hypertensive rats

“…Thus, beta-blocker treatment does seem to directly interfere with the amount of connective tissue in the heart, not only by reducing sympathetic activity but also by reducing the release of renin, plasma renin concentration, and thus the expression of cardiac angiotensin II (Varagic et al 2012). The increased myocardial fibrosis observed for the HS group relative to other groups was also observed in other studies that used other models of hypertension (Matsubara et al , 2006Hocher et al 1999;Saam et al 2003). The literature shows that mechanisms involved in cardiac remodeling in hypertensive animals include the stimulation of fibroblasts for collagen synthesis in response to various humoral factors (Challah et al 1995;Nicoletti et al 1996;Hocher et al 1999) and cell necrosis .…”

“…Possible alterations in these components point to myocardial remodeling, which is associated with cardiac dysfunction and can occur in response to mechanical or humoral stimuli (Brilla et al 1996;Weber 2000;Matsubara et al 2006). Our data showed an increase in the percentage of areas containing collagen for the HS animals, which was not reversed by the physical training alone.…”

Proteção miocárdica ao coração hipertrofiado: o eterno desafio

“…By means of signal transduction proteins (Ras, Gaq, Gas) these mediators transmit their signs, activating enzymes (protein kinase C [C-PKC], mitogen-activated protein kinase [MAPK]) which induce the fetal gene expression, constituting the hallmark of pathologic hypertrophy which includes gene alterations involved in the synthesis of contractile proteins, management of intracellular calcium, natriuretic peptides, among others. Concurrently with these changes, there is still fibroblast proliferation and changes in the synthesis of extracelullar matrix which participate in the genesis of remodeling [23] (Table 1).…”

A Redução do Colágeno Tipo I está Associada ao Aumento da Atividade da Metaloproteinase-2 e da Expressão Proteica de Leptina no Miocárdio de Ratos Obesos

“…5 In a stable condition, it contributes to the maintenance of cardiac architecture and function. 6 Several mechanisms act to ensure that the components of matrix degradation by MMP are precisely controlled, including tissue inhibitors of metalloproteinases (TIMP). 7 Cardiac collagen changes in response to neuro-hormonal and mechanical stimuli, 6,8 due to elevated synthesis and decreased degradation or vice versa.…”