Key result
Testosterone deficiency induced by castration attenuated adverse late cardiac remodeling after myocardial infarction in rats by reducing myocyte hypertrophy and preserving contraction force.
Why the study?
Testosterone is associated with an increased risk of coronary heart disease, prompting evaluation of cardiac remodeling after myocardial infarction in rats with testosterone deficiency.
Does testosterone deficiency reduce adverse late cardiac remodeling after acute myocardial infarction in rats?
Does testosterone deficiency reduce adverse late cardiac remodeling after acute myocardial infarction in rats?
p-value: p=<0.05
In a rat model of myocardial infarction, testosterone deficiency induced by castration attenuated adverse cardiac remodeling and preserved myocardial contractility.
Warrants caution on testosterone therapy post-MI; leaves open translation of rat remodeling effects to humans.
Testosterone is associated with an increased risk of coronary heart disease. This study evaluated cardiac remodeling 60 days after myocardial infarction (MI) in rats with testosterone deficiency. One week after castration, the animals underwent myocardial infarction. Rats were divided into four groups: orchidectomized (OCT); orchidectomized and infarcted (OCT+MI), MI and control (Sham). The myocyte cross-sectional area and the papillary muscle contractility were evaluated 8 weeks after MI. The coronary bed was perfused with Biodur E20 resin to evaluate the neovascularization after MI. Data were expressed as mean ± SEM followed by ANOVA. Castration reduced myocyte hypertrophy when compared to Sham and myocardial infarction alone as well as preserved the contraction force and activation time after myocardial infarction. After beta-adrenergic stimulation, activation and relaxation kinetics were less impaired in the OCT+MI group than in the MI group. Contraction force was preserved in the OCT+MI group after beta-adrenergic stimulation. Multiple scanning electronic microscope images were obtained to characterize changes in the coronary arteries. Capillary density index was increased in the MI and OCT+MI groups compared with control. The MI and OCT+MI groups were characterized by irregular vessel arrangements with distorted shape, abrupt changes in vessel direction, as well as abrupt changes in diameter after bifurcations when compared to Sham and OCT. The results indicated that testosterone deficiency attenuates adverse cardiac remodeling after MI. Novel findings in this study were that testosterone deficiency in rats, induced by castration, changes the later remodeling after MI, when compared with non castrated rats. The absence of this androgenous hormone seems to be benefic against pathological hypertrophy.
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Corrêa et al. (2019) studied Myocardial infarction (n=200). Orchidectomy (Testosterone deficiency) vs. Myocardial infarction without orchidectomy was evaluated on Myocyte cross-sectional area and papillary muscle contractility (p=<0.05). Testosterone deficiency induced by castration attenuated adverse late cardiac remodeling after myocardial infarction in rats by reducing myocyte hypertrophy and preserving contraction force.
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