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[Enalapril prevents myocardial remodeling in rats with arteriovenous fistula]
L Gonçalves1, F Pacheco, C Santos
1Serviço de Cardiologia dos Hospitais da Universidade de Coimbra.
Insights
Enalapril effectively prevents cardiac myocyte remodelling in rats with arteriovenous fistulas. This study demonstrates enalapril
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cardiac Physiology
Context:
- Cardiac myocyte remodelling is a significant pathological process.
- Arteriovenous fistulas induce volume overload, leading to cardiac changes.
- Understanding preventative strategies is crucial for cardiovascular health.
Purpose:
- To investigate the efficacy of enalapril in mitigating cardiac myocyte remodelling.
- To assess the impact of enalapril on heart structure in a rat model of arteriovenous fistula.
- To evaluate enalapril's role in preventing pathological cardiac hypertrophy.
Summary:
- Rats with arteriovenous fistulas showed increased heart weight and myocyte volume.
- Enalapril treatment prevented these structural changes in the heart.
- Histopathological analysis confirmed enalapril's protective effect against cardiac remodelling.
Impact:
- Enalapril demonstrates potential in preventing adverse cardiac remodelling due to volume overload.
- Findings support enalapril's therapeutic role in conditions mimicking high-output states.
- This research contributes to understanding ACE inhibitor efficacy in cardiac protection.
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.