Captopril–furosemide survival study in experimental heart failure

Abstract

The strategy of diuretic drug administration remains to be defined in heart failure as experimental and clinical evidence have clearly established the benefit of neurohormonal blockade. The impact of addition of diuretic treatment to angiotensin-converting enzyme inhibition on survival remains to be demonstrated. The objectives of the study were to evaluate cardiovascular and renal effects of addition of diuretic treatment to captopril (2 g/L, in drinking water), on survival, on the experimental model of heart failure. Rats were followed for 10 months after coronary ligation. Echocardiographic, hemodynamic, morphometry and renal function investigations were then performed on surviving rats. Survival (from 34 to 61%), diuresis and natriuresis were significantly improved compared to control group only in animals treated with a combination of captopril + furosemide. In treated group: cardiac dimensions were reduced with left ventricular fractional shortening significantly increased in combination group (from 22.4 to 28%); captopril + furosemide animals had highest heart rate and lowest systolic and diastolic blood pressures; body and heart weight were reduced, but kidney weight was significantly increased with furosemide (1.7 g in control vs. 2 g in capto + furo); plasma renin activity and angiotensin 1 were greatly increased, and moderately stimulated in control. In conclusion, this combination of drugs significantly improved cardiac remodeling and survival of animals, increased diuresis and natriuresis despite stimulation of plasma renin activity and kidney hypertrophy.

Furosemide induces mortality in a rat model of chronic heart failure

“…A retrospective analysis of a possible coherency between the diuretic effect and the mortality in the furosemide treated animals showed that animals subjected to a larger diuretic effect tended to show a poorer survival rate. Moreover, the furosemide dose in our study (10 mg/kg/d) was not high compared to those in previous experimental studies, ranging from 4 mg [24] to 30 mg [12,32], 40 mg, 80 mg [20] and 100 mg/(kg day) [12]. Since the incidence of volume depletion under furosemide treatment was previously reported to be dose dependent [33] the adequate dose which was used in our study did not elicit an especially large diuresis.…”

Transient tricuspid valve regurgitation following surgical treatment of cor triatriatum dexter in a dog

“…It could be hypothesised that pharmacotherapy and cardiac remodelling over the course of several months accounted for the decrease in TR and eventual complete resolution of clinical signs. Several drugs including association of angiotensin‐converting enzyme (ACE) inhibitor and loop diuretics, as used in this study, have been proven to help in cardiac remodelling in experimental model of heart failure in rats (Mougenot and others 2005). It could therefore be hypothesised that chronic use of the combination of furosemide (loop diuretic) and benazepril (ACE inhibitor) may have elicited some cardiac remodelling, buffering the effect of atrial dilatation and ventricular eccentric hypertrophy observed in the natural course of tricuspid regurgitation.…”