BACKGROUND: Female sex hormones may have protective effects against arrhythmias, including reperfusion arrhythmias (RAs), but the mechanisms are still not completely known. METHODS AND RESULTS: Serial changes in rat hearts (rhythm, apoptosis and the its infuencing factors; cardiac vinculin mRNA expression and connexin43 (Cx43) dephosphorylation) were examined during periods of ischemia-reperfusion with and without estrogen treatment. After reperfusion, although the incidence of arrhythmias became higher in both the vehicle-group and estrogen-group, compared with the ischemia period, estrogen prevented reperfusion-induced upregulation of the incidence of arrhythmias, especially ventricular premature beats (VPB) and ventricular tachycardia (VT). The duration of VT and fibrillation, and the number of VPB and VT, were all significantly decreased in the estrogen-group. The expression of cardiac vinculin mRNA decreased significantly in the vehicle-group but not in the estrogen-group. Cx43 dephosphorylation and myocyte apoptosis increased in both groups, but the values for the estrogen-group were all markedly lower than those for the vehicle-group. A selective estrogen receptor (ER) beta agonist prevented reperfusion-induced upregulation of the incidence of both VPB and VT significantly; a selective ERalpha agonist had no significant influence. CONCLUSIONS: Estrogen can protect the heart against RAs, at least in part, mediated through gap junctions. Upregulation of ERbeta but not ERalpha mediated most of the estrogen-induced cardioprotection against RA.
BACKGROUND: Female sex hormones may have protective effects against arrhythmias, including reperfusion arrhythmias (RAs), but the mechanisms are still not completely known. METHODS AND RESULTS: Serial changes in rat hearts (rhythm, apoptosis and the its infuencing factors; cardiac vinculin mRNA expression and connexin43 (Cx43) dephosphorylation) were examined during periods of ischemia-reperfusion with and without estrogen treatment. After reperfusion, although the incidence of arrhythmias became higher in both the vehicle-group and estrogen-group, compared with the ischemia period, estrogen prevented reperfusion-induced upregulation of the incidence of arrhythmias, especially ventricular premature beats (VPB) and ventricular tachycardia (VT). The duration of VT and fibrillation, and the number of VPB and VT, were all significantly decreased in the estrogen-group. The expression of cardiac vinculin mRNA decreased significantly in the vehicle-group but not in the estrogen-group. Cx43 dephosphorylation and myocyte apoptosis increased in both groups, but the values for the estrogen-group were all markedly lower than those for the vehicle-group. A selective estrogen receptor (ER) beta agonist prevented reperfusion-induced upregulation of the incidence of both VPB and VT significantly; a selective ERalpha agonist had no significant influence. CONCLUSIONS: Estrogen can protect the heart against RAs, at least in part, mediated through gap junctions. Upregulation of ERbeta but not ERalpha mediated most of the estrogen-induced cardioprotection against RA.
Authors: Ariane A Sickinghe; Suzanne J A Korporaal; Hester M den Ruijter; Elise L Kessler Journal: Front Endocrinol (Lausanne) Date: 2019-07-03 Impact factor: 5.555
Authors: S Q Savergnini; A M Reis; R A S Santos; P E B Santos; A J Ferreira; A P Almeida Journal: Braz J Med Biol Res Date: 2012-10-30 Impact factor: 2.590