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Basic Res Cardiol. 1991;86 Suppl 1:157-63.
Cardiac remodelling and myocardial contractility in patients with congestive heart failure treated with furosemide and enalapril.

Baur LH, Schipperheyn JJ, Bann J, van der Laarse A, van der Wall EE, van Dijk AD, Buis B, Manger Cats V, Bruschke AV.

Department of Cardiology, University Hospital Leiden, The Netherlands.

Eleven patients with congestive heart failure class II-IV (NYHA) caused by ischemic heart disease were studied before and three months after adding enalapril to their treatment with furosemide. After an infarction the heart dilates gradually, mainly as a result of slippage of myocardial fiber bundles. It is known that the addition of an ACE-inhibitor to the medical treatment unloads the heart and gradually, within a period of 3 months, reduces heart size. Objectives of this study were to demonstrate remodelling by recording diastolic pressure-volume relations before and after treatment. The study addresses the question of whether regression of dilation, induced by the ACE-inhibitor treatment, improves the oxygen supply-demand ratio and, as a result, the contractility of the heart muscle. Treatment resulted in a reduction of vascular resistance (1479 to 1182 dyn.s.cm-5, p less than 0.05) and of the left ventricular end-diastolic (130 to 108 ml per m2 body surface area, p less than 0.05) and end-systolic (102 to 81 ml per m2 body surface area, p less than 0.01) volume index. The slope of the end-systolic pressure-volume relation, measured using vena cava occlusion and beat-to-beat recording of pressure and volume loops, remained unchanged. Indices of oxygen-supply demand ratio such as a drop of ejection fraction during exercise and parameters of active diastolic relaxation also did not change. Addition of an ACE-inhibitor induces regression of ventricular dilation, but no indications were found that it improves the condition of the cardiac muscle.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1827982&dopt=Abstract




Hypertension. 1997 Jan;29(1 Pt 1):91-7.
Neonatal angiotensin-converting enzyme inhibition in the rat induces persistent abnormalities in renal function and histology.

Guron G, Adams MA, Sundelin B, Friberg P.

Department of Physiology, Institute of Physiology and Pharmacology, Goteborg, Sweden.

Recently, we reported that neonatal blockade of the renin-angiotensin system in the rat produces irreversible abnormalities in renal histology associated with increased diuresis. In the present study, we assessed the long-term consequences of neonatal angiotensin-converting enzyme inhibition on renal function. Rats were injected with 10 mg.kg-1.d-1 enalapril or vehicle from day 3 to day 24 after birth. Urine concentrating ability, renal function, and renal histology were assessed in 16-week-old rats. There was a twofold increase in diuresis and water intake in enalapril-treated rats throughout the study course. Urine osmolality after 24 hours of water deprivation was 1008 +/- 108 and 2549 +/- 48 mOsm.kg-1 (P < .05) in enalapril- and vehicle-treated rats, respectively. Glomerular filtration rate (0.54 +/- 0.03 versus 0.75 +/- 0.06 mL.min-1x100 g body wt-1, P < .05) and effective renal plasma flow (1.76 +/- 0.09 versus 2.19 +/- 0.14 mL.min-1x100 g body wt-1, P < .05) were reduced in neonatally enalapril-treated versus control rats. Absolute and fractional urinary sodium excretion values were elevated (P < .05) in enalapril-treated rats. Semiquantitative assessment of renal histology demonstrated statistically significant degrees of papillary atrophy, interstitial fibrosis and inflammation, tubular atrophy and dilatation, and focal glomerulosclerosis in neonatally enalapril-treated rats. In conclusion, neonatal angiotensin-converting enzyme inhibition in the rat produces irreversible alterations in renal function and morphology, demonstrating the importance of an intact renin-angiotensin system neonatally for normal renal development.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9039086&dopt=Abstract




Rev Port Cardiol. 1994 May;13(5):417-22, 381.
[Enalapril prevents myocardial remodeling in rats with arteriovenous fistula]

[Article in Portuguese]

Goncalves L, Pacheco F, Santos C, Cabrita S, Beja M, Providencia LA.

Servico de Cardiologia dos Hospitais da Universidade de Coimbra.

AIM OF THE STUDY: To evaluate the efficacy of enalapril in preventing cardiac myocyte remodelling in rats with arteriovenous fistulas. EXPERIMENTAL DESIGN: We distributed thirty males Wistar rats in 3 groups: group A (control), group B (fistula) and group C (fistula + enalapril). An end to side fistula between the femoral artery and vein was produced in the right thighs of rats from groups B and C. Oral enalapril (0.07 mg/kg/day) was given to rats from group C. After 8 weeks the rats were sacrificed and their heart removed for pathologic study. RESULTS: Body weight evolution was similar in all groups. Heart weight increased in group B (1.78 +/- 0.2 g) when compared to group A (1.55 +/- 0.11 g), (p < 0.02), and was similar (p = n.s.) in groups A and C (1.58 +/- 0.13 g). Heart weight/Body weight ratio was also increased in group B (4.4 +/- 0.55 mg/g) when compared to group A (3.6 +/- 0.5 mg/g), (p < 0.01), but was similar in groups A and C (3.66 +/- 0.4 mg/g) (p = n.s.). An increase in wall thickness was detected in group B in the right ventricle (p < 0.03), septum (p < 0.01) and left ventricle (p < 0.01) when compared to groups A and C. Myocytes cytoplasm volume fraction was increased in group B, when compared with group A, in all segments studied (right ventricle p = 0.011, septum p = 0.025, and left ventricle p = 0.031). Groups A and C were similar. CONCLUSION: Enalapril prevents the structural remodelling of cardiac myocytes in this model of volume overload induced by an arteriovenous fistula.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7917387&dopt=Abstract












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