SANTANA, V. L.; http://lattes.cnpq.br/4655427049694076; SANTANA, Vanessa Lira de.
Resumo:
This thesis consists of three chapters that address the mitral valve disease
(MVD) in dogs under the aspects of cardiac function, renal and its therapy. Two of the
chapters are presented as scientific article and as a case report. In the first chapter aimed
to correlate the concentrations of cardiac biomarker N-terminal prohormone of B-type
natriuretic peptide (NT-proBNP) and hormone aldosterone in dogs with mitral valve
disease (MVD) to the findings of echodopplercardiograms, x-rays and serum
biochemical tests. It also estimated the components of biological variability of NTproBNP.
There was a reduction in mean aldosterone and a small positive correlation
with aldosterone serum Na+ in GMVDA and negative correlation of NT-proBNP with
Na+ serum in GMVDT. Serum average concentrations of NT-proBNP of MVD groups
were above the average of the GC, but there was no significant difference; the amounts
resulting from r-IoI was 2.66 and RCV 47.3%. The ratio of left atrial diameter - aorta
(LA/Ao) showed up increased comparing T0 the GMVDA to GMVDT; the DC of
GMVDT had significant difference when compared to the CG; animals Class B2 and C,
when spread over the treatment time, had the shortening fraction values (FS) and
ejection fraction (EF) of T0-GMVDA and GMVDT above the GC. These findings
demonstrated that treatment employed in dogs with MVD this study stabilized NTproBNP
values even after one year of treatment and the use of ACE inhibitors
determined reduction in aldosterone concentrations and consequent reduction in blood
pressure and congestive heart failure. The second chapter proposed to evaluate the
glomerular filtration rate (GFR), fractional excretion of electrolytes and Cystatin C in
dogs with MVD before and during treatment with ACE inhibitors (enalapril and
benazepril) associated with furosemide. There was a significant reduction of serum
aldosterone between the times of GMVD and groups; P/U C, creatinine, urea, Cystatin
C were normal before and no change after treatment; GFR remained normal, but with
reduction throughout treatment. There was an increase of mean EF Na+, K+ and Cl- both
in relation to the reference value on the GC indicating tubular injury. However, EF
Ca+2i and EF P been increased, indicating a reduction in tubular reabsorption both before and during treatment. Given the results can be concluded that the MVD caused
reduction in GFR and tubular damage, but the diuretic action of furosemide in tubular
reabsorption did not compromise the homeostasis of electrolytes. The third chapter
described the renal repercussion on a dog with MVD treated with furosemide,
pimobendan and benazepril and concluded that the MVD caused tubular injury and
proteinuria persisted and worsened after the initiation of treatment with furosemide and
benazepril. Thus, it was verified the presence of cardiorenal syndrome that should be
monitored in order to adapt the treatment to minimize early renal lesions.