Testosterone deficiency prevents left ventricular contractility dysfunction after myocardial infarction

Júnior, Rogério Faustino Ribeiro; Ronconi, Karoline Sousa; Jesus, Itamar Couto Guedes de; Almeida, Paulo Henrique Ribeiro Fernandes; Forechi, Ludimila; Vassallo, Dalton Valentim; Guatimosim, Sílvia; Stefanon, Ivanita; Fernandes, Aurélia Araújo

doi:10.1016/j.mce.2017.06.011

Cited by 20 publications

(11 citation statements)

References 34 publications

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“…Combined with clinical and previous studies, VA has the effect of stimulating androgen secretion (Zang et al, 2016). Androgen has been shown to improve cardiac function, which may be related to altering the key proteins involved in Ca 2+ handling (Ribeiro et al, 2018;Barske et al, 2019). Besides, we found that there was no significant positive correlation between the dose and efficacy of VA, which was an interesting result.…”

Section: Discussionsupporting

confidence: 57%

Velvet Antler Ameliorates Cardiac Function by Restoring Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats With Heart Failure After Myocardial Infarction

Shi

Zhao

et al. 2021

Front. Pharmacol.

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Objective: Velvet antler (VA; cornu cervi pantotrichum), a well-known traditional Chinese medicine, has been shown to exert cardioprotective effects. The purpose of this study was to investigate the effect of VA on heart failure (HF) caused by ischemia-reperfusion, and explore its possible mechanism from the regulation of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 2 alpha (SERCA2a).Methods: A rat model of HF was established by ligating the left anterior descending coronary artery of male Sprague–Dawley rats (n = 88). One week after surgery, VA (200, 400, or 800 mg/[kg day−1]) or enalapril (1 mg/[kg day−1]) was administered daily for the next 4 weeks. Heart function was detected by echocardiography and histopathological analysis. The serum BNP level was measured by ELISA, and the expression of SERCA2a, PLB, PLB-Ser16, and PKA was determined by western blotting. SERCA2a and PLB mRNA levels were determined by real-time quantitative PCR.Results: Compared with the sham group, cardiac function in the HF group, including the serum BNP level, heart mass index, myocardial collagen deposition, and left ventricular ejection fraction, was markedly reduced; however, these changes could be reversed by VA treatment. In addition, VA (200 mg/[kg·d−1]) inhibited the decrease of SERCA2a and PLB mRNA levels and SERCA2a, PLB, PLB-Ser16, and PKA protein expression and restored the activity of SERCA2a and PKA. Enalapril affected only PLB protein expression.Conclusion: VA can improve myocardial fibrosis and ventricular remodeling in rats, thereby helping to restore cardiac function. The underlying mechanism may be related to the upregulation of the expression and activation of PKA and PLB and the restoration of the expression and activity of SERCA2a.

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Section: Discussionsupporting

confidence: 57%

Velvet Antler Ameliorates Cardiac Function by Restoring Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats With Heart Failure After Myocardial Infarction

Shi

Zhao

et al. 2021

Front. Pharmacol.

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“…Thus, it is possible to suggest that testosterone deficiency contributes to improved contractile response after MI. It is known that the cell changes induced by testosterone deficiency prevent impaired contractility caused by MI and increased transient calcium 8 weeks after the onset of the event [10]. This same study found an increase in SERCA expression in the left ventricle of testosterone-deficient infarcted animals, as well as increased SERCA / phospholamban ratio and phospholamban phosphorylation.…”

Section: Discussionmentioning

confidence: 55%

“…The corrosion casts were subsequently analyzed by scanning electron microscopy (SEM). Orchidectomy was performed according to previously described methods [10]. Briefly, the animals were anesthetized intramuscularly with ketamine (50 mg/kg) and xylazine (10 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

Testosterone deficiency reduces the effects of late cardiac remodeling after acute myocardial infarction in rats

et al. 2019

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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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“…Consistent with human data, plasma testosterone levels were lower in DCM+S mice than in DCM-S mice, irrespective of diet ( Figure 6 A), but transcripts for cardiac LV androgen receptor were not significantly altered (1.06-fold, not significant) by sexual interactions. Although a causal effect of endogenous and exogenous testosterone on heart function is controversial and not fully understood [ 33 , 34 , 35 ], some animal and clinical studies suggest that testosterone may negatively affect cardiac contractile function [ 36 , 37 , 38 , 39 , 40 , 41 , 42 ] and cause salt and water retention, contributing to risk of edema [ 33 ].…”

Section: Resultsmentioning

confidence: 99%

In Experimental Dilated Cardiomyopathy Heart Failure and Survival Are Adversely Affected by a Lack of Sexual Interactions

Tripathi

Sullivan

Fan

et al. 2020

IJMS

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Nearly one in three people in the U.S. will develop heart failure (HF), characterized by fluid retention (edema) in the lungs and elsewhere. This leads to difficult breathing, deterioration of physical capacity, restriction of normal activities and death. There is little data about the safety and effects of sexual interactions in patients with HF. We tested whether a lack of sexual interactions affected pathophysiological outcomes in a pre-clinical mouse model of dilated cardiomyopathy that recapitulates the progressive stages of human HF. Male mice were randomly given access to, or deprived from, sexual interactions with female mice, which were confirmed by videography and generation of offspring. Cohousing with access to sexual interactions markedly prolonged survival, while cohousing without access to sexual activity did not. Sexual interactions improved systolic function, reduced HF-associated edema, altered transcription of heart contractile protein genes and decreased plasma testosterone levels. To determine whether testosterone levels contributed to survival, testosterone levels were experimentally reduced. Reduction of testosterone levels significantly prolonged survival. Taken together, in mice with dilated cardiomyopathy, sexual activity altered cardiac contractile gene transcription, improved systolic function, reduced edema and prolonged survival which may be in part due to lower testosterone levels.

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Testosterone deficiency prevents left ventricular contractility dysfunction after myocardial infarction

Cited by 20 publications

References 34 publications

Velvet Antler Ameliorates Cardiac Function by Restoring Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats With Heart Failure After Myocardial Infarction

Velvet Antler Ameliorates Cardiac Function by Restoring Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats With Heart Failure After Myocardial Infarction

Testosterone deficiency reduces the effects of late cardiac remodeling after acute myocardial infarction in rats

In Experimental Dilated Cardiomyopathy Heart Failure and Survival Are Adversely Affected by a Lack of Sexual Interactions

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