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Introduction Left ventricular hypertrophy and heart failure are crucial problems in nowadays cardiology (Simko et al. 2014). Sex-based differences regarding heart function and outcomes were observed in various cardiovascular pathologies [...], No data are available on heart function in chronic testosterone deficiency and on the effect of estrogen treatment. Eighteen 4-week-old male Lewis rats were randomly divided into 3 groups (n = 6): 1 group of sham-operated rats and 2 groups of castrated rats. Sixty-six weeks after surgery, 1 castrated group received a dose of 17[beta]-estradiol (10 [micro]g/kg per day) and the remaining 2 groups received a placebo subcutaneously for 14 days. Left ventricular (LV) systolic and diastolic functions were measured by transthoracic echocardiography. Castration decreased LV ejection fraction (9%) and fractional shortening (15%) and deteriorated LV diastolic function (94%). 17[beta]3-Estradiol treatment increased LV ejection fraction (15%) and fractional shortening (31%) and improved LV diastolic function (48%). Plasma testosterone concentrations were decreased in both castrated groups. In conclusion, chronic testosterone deficiency induced LV systolic and diastolic dysfunction; these disorders were reversed by short-term treatment with 17[beta]-estradiol. Keywords: chronic testosterone deficiency, 17[beta]3-estradiol, systolic dysfunction, diastolic dysfunction, echocardiography. Aucune donnee n'est accessible quant a la fonction cardiaque en cas de carence prolongee en testosterone ni sur l'effet de l'restrogenotherapie. Nous avons reparti aleatoirement 18 rats Lewis males de 4 semaines dans trois groupes (n = 6): un groupe avec intervention chirurgicale factice (sham) et deux groupes de rats castres. Soixante-six semaines apres l'intervention chirurgicale, l'un des groupes de rats castres a recu une dose de 17[beta]3-estradiol (10 [micro]g/kg par jour) et les deux autres groupes ont recu un placebo, dans les trois cas par voie sous-cutanee pendant 14 jours. Nous avons mesure les fonctions systolique et diastolique du ventricule gauche (VG) a l'aide de l'echocardiographie transthoracique. La castration a entraine une diminution de la fraction d'ejection du VG (9%) avec un raccourcissement fractionnel (15%) et une deterioration de la fonction diastolique du VG (94%). L'administration de 17[beta]3-estradiol a entraine une augmentation de la fraction d'ejection du VG (15%) avec un raccourcissement fractionnel (31%) et une amelioration de la fonction diastolique du VG (48%). Les concentrations plasmatiques de testosterone s'abaissaient dans les deux groupes de rats castres. En conclusion, la carence prolongee en testosterone entrainait un dysfonctionnement systolique et diastolique du ventricule gauche; ces troubles s'inversaient avec l'administration de 17[beta]3-estradiol a court terme. [Traduit par la Redaction] Mots-cles : carence prolongee en testosterone, 17[beta]3-estradiol, dysfonctionnement systolique, dysfonctionnement diastolique, echocardiographie.

This study investigated whether ivabradine, a selective If current inhibitor reducing heart rate (HR), is able to improve survival and prevent left ventricular (LV) remodeling in isoproterenol‐induced heart damage. Wistar rats were treated for 6 weeks: controls (n = 10), ivabradine (10 mg/kg/day orally; n = 10), isoproterenol (5 mg/kg/day intraperitoneally; n = 40), and isoproterenol plus ivabradine (n = 40). Isoproterenol increased mortality, induced hypertrophy of both ventricles and LV fibrotic rebuilding, and reduced systolic blood pressure (SBP). Ivabradine significantly increased survival rate (by 120%) and prolonged average survival time (by 20%). Furthermore, ivabradine reduced LV weight and hydroxyproline content in soluble and insoluble collagen fraction, reduced HR and attenuated SBP decline. We conclude that ivabradine improved survival in isoproterenol‐damaged hearts. [ABSTRACT FROM AUTHOR]

The arrhythmogenic potential of β1-adrenoceptor autoantibodies (β1-AA), as well as antiarrhythmic properties of omega-3 in heart diseases, have been reported while underlying mechanisms are poorly understood. We aimed to test our hypothesis that omega-3 (eicosapentaenoic acid-EPA, docosahexaenoic acid-DHA) may inhibit matrix metalloproteinase (MMP-2) activity to prevent cleavage of β1-AR and formation of β1-AA resulting in attenuation of pro-arrhythmic connexin-43 (Cx43) and protein kinase C (PKC) signaling in the diseased heart. We have demonstrated that the appearance and increase of β1-AA in blood serum of male and female 12-month-old spontaneously hypertensive rats (SHR) was associated with an increase of inducible ventricular fibrillation (VF) comparing to normotensive controls. In contrast, supplementation of hypertensive rats with omega-3 for two months suppressed β1-AA levels and reduced incidence of VF. Suppression of β1-AA was accompanied by a decrease of elevated myocardial MMP-2 activity, preservation of cardiac cell membrane integrity and Cx43 topology. Moreover, omega-3 abrogated decline in expression of total Cx43 as well as its phosphorylated forms at serine 368 along with PKC-ε, while decreased pro-fibrotic PKC-δ levels in hypertensive rat heart regardless the sex. The implication of MMP-2 in the action of omega-3 was also demonstrated in cultured cardiomyocytes in which desensitization of β1-AR due to permanent activation of β1-AR with isoproterenol was prevented by MMP-2 inhibitor or EPA. Collectively, these data support the notion that omega-3 via suppression of β1-AA mechanistically controlled by MMP-2 may attenuate abnormal of Cx43 and PKC-ε signaling; thus, abolish arrhythmia substrate and protect rats with an advanced stage of hypertension from malignant arrhythmias. [ABSTRACT FROM AUTHOR]

This study investigated the effect of lisinopril (angiotensin-converting enzyme inhibitor) on potential behavioural alterations in spontaneously hypertensive rats (SHR). Three groups of 15-17-week-old rats were investigated for 2 weeks: Wistar control group, SHR group and SHR+lisinopril group. Systolic blood pressure (SBP) was normal in Wistar rats, SHR expressed hypertension and lisinopril normalized the SBP. We observed increased time spent in and increased frequency of entries to the central area of the open field in SHR, while lisinopril induced a trend to reduce the time spent in the central area of the open field and reduced the frequency of entries there. There was a positive correlation between SBP and reduced anxiety-like behaviour in normotensive rats; no correlations in the SHR or SHR+lisinopril groups were observed. We conclude that lisinopril normalized the increase in SBP and partly reversed the alterations of anxiety-like behaviour in SHR. [ABSTRACT FROM AUTHOR]