INTRODUCTION: The unsystematic use of anabolic steroids, synthetic analogs of testosterone, implies enhanced cardiovascular risk and cardiac hypertrophy. Thus, increased right ventricular mass corrected by the body weight (e.g.right ventricular hypertrophy -RVH) could raise the risk for development of pulmonary arterial hypertension (PAH). OBJECTIVES: to examine the effects of long-term chronic treatment with nandrolone decanoate on the RVH and its relationship with PAH in rats. METHODS: 16 three-month Wistar male rats were treated with nandrolone decanoate (6.0 mg/kg-1 body weight; DECA, n=8) or control vehicle (CONT, n=8). The drug and vehicle were administered by a single injection in the femoral muscle once a week for 4 weeks. After the treatment, rats were anesthetized with chloral hydrate (4.0mL/kg-1, ip), and catheterized in the femoral artery. Twenty-four hours later, mean arterial pressure (MAP) and heart ratio were measured. The heart, kidneys and liver were removed, weighed and the rates of hypertrophy (RH) were measured, which were calculated by the ratio of the weight of the organs by the body weight (mg.g-1). RESULTS: DECA treatment increased body weight (338 ± 6g; p <0.01) vs. CONT (315 ± 5g). This treatment had no effect on the MAP (CONT, 110±4mmHg, DECA, 113 ± 4mmHg). However, the bradycardia of animals treated with DECA (321 ± 13bpm, p<0.01) was significantly lower than that of CONT (368 ±11bpm). RH increased (p <0.01) the cardiac ventricles and the kidneys, but not in the liver. The correlation between the RVH and MAP in DECA showed positive and higher Pearson's coefficient (r² = 0.4013) vs CONT (r² = 0.0003). CONCLUSIONS: It was concluded that chronic nandrolone decanoate treatment induced bradycardia and RVH, which suggests increased risk for PAH.
anabolic steroids; blood pressure; ventricular hypertrophy; pulmonary arterial hypertension
