Hamida Aboalgasm1, Morea Petersen1, Asfree Gwanyanya2. 1. Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. 2. Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. Email: asfree.gwanyanya@uct.ac.za.
Abstract
OBJECTIVE: Chronic diabetes mellitus is associated with detrimental cardiovascular complications and electrolyte imbalances such as hypomagnesaemia. We investigated the effect of magnesium (Mg2+) on cardiac function and the possible role of histological and electrical alterations in chronic, streptozotocin-induced diabetic rats. METHODS: Wistar rats were treated once intraperitoneally with streptozotocin or citrate, and then daily with MgSO4 or saline for four weeks. Cardiac contractile and electrocardiographic parameters were measured on Langendorff-perfused hearts. Other hearts were histologically stained or immunoblotted for the mitochondrial ATP synthase (ATP5A). RESULTS: In diabetic hearts, Mg2+ prevented a diabetes-induced decrease in left ventricular developed pressure and improved contractility indices, as well as attenuated the reduction in heart rate and prolongation of QT interval, but not the QT interval corrected for heart rate (QTc). Histologically, there were neither differences in cardiomyocyte width nor interstitial collagen. The expression of ATP5A was not different among the treatment groups. CONCLUSIONS: Mg2+ supplementation improved cardiac contractile activity in chronic diabetic hearts via mechanisms unrelated to electrocardiographic or histologically detectable myocardial alterations.
OBJECTIVE: Chronic diabetes mellitus is associated with detrimental cardiovascular complications and electrolyte imbalances such as hypomagnesaemia. We investigated the effect of magnesium (Mg2+) on cardiac function and the possible role of histological and electrical alterations in chronic, streptozotocin-induced diabetic rats. METHODS: Wistar rats were treated once intraperitoneally with streptozotocin or citrate, and then daily with MgSO4 or saline for four weeks. Cardiac contractile and electrocardiographic parameters were measured on Langendorff-perfused hearts. Other hearts were histologically stained or immunoblotted for the mitochondrial ATP synthase (ATP5A). RESULTS: In diabetic hearts, Mg2+ prevented a diabetes-induced decrease in left ventricular developed pressure and improved contractility indices, as well as attenuated the reduction in heart rate and prolongation of QT interval, but not the QT interval corrected for heart rate (QTc). Histologically, there were neither differences in cardiomyocyte width nor interstitial collagen. The expression of ATP5A was not different among the treatment groups. CONCLUSIONS: Mg2+ supplementation improved cardiac contractile activity in chronic diabetic hearts via mechanisms unrelated to electrocardiographic or histologically detectable myocardial alterations.