Cardiovascular research
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Cardiovascular research · Aug 2005
Role of mitochondrial re-energization and Ca2+ influx in reperfusion injury of metabolically inhibited cardiac myocytes.
We used isolated myocytes to investigate the role of mitochondrial re-energization and Ca2+ influx during reperfusion on hypercontracture, loss of Ca2+ homeostasis and contractile function. ⋯ Reperfusion-induced hypercontracture, and loss of Ca2+ homeostasis and contractile function are initiated following mitochondrial re-energization. The hypercontracture requires the production of oxidative ATP but not Ca2+ influx during reperfusion. Loss of Ca2+ homeostasis and contractile function are linked to Ca2+ influx during reperfusion, probably via opening of mitochondrial permeability transition pores.
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Cardiovascular research · Mar 2005
Adenosine produces nitric oxide and prevents mitochondrial oxidant damage in rat cardiomyocytes.
To examine if adenosine prevents oxidant-induced mitochondrial dysfunction by producing nitric oxide (NO) in cardiomyocytes. ⋯ Adenosine protects mitochondria from oxidant damage through a pathway involving A(2) receptors, eNOS, NO, PI3-kinase/Akt, and Src tyrosine kinase.
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Cardiovascular research · Feb 2005
Tranilast attenuates cardiac matrix deposition in experimental diabetes: role of transforming growth factor-beta.
The pathological accumulation of extracellular matrix is a characteristic feature of diabetic cardiomyopathy that is directly related to a loss of function. Tranilast (n-[3,4-anthranilic acid), used for the treatment of fibrotic skin diseases, has also been shown to inhibit transforming growth factor-beta (TGF-beta)-induced matrix production in kidney epithelial cells. ⋯ These findings indicate that tranilast has antifibrotic actions in the Ren-2 model of experimental diabetic cardiac disease by mechanisms that might attributable to reduced TGF-beta activity.
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Cardiovascular research · Dec 2004
Nitric oxide contributes to oxygen demand-supply balance in hypoperfused right ventricle.
The present study examined the role of nitric oxide (NO) in oxygen demand-supply balance in hypoperfused canine right ventricular myocardium. ⋯ During right coronary hypoperfusion, right ventricular function is well maintained, but myocardial oxygen consumption falls, reflecting an increase in oxygen utilization efficiency. NO contributes to this adaptation to hypoperfusion by restraining myocardial oxygen consumption, and by promoting coronary vasodilation with less severe reduction in myocardial PO(2). NO has an important role in right ventricular oxygen demand-supply balance when right coronary perfusion pressure is reduced.
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Cardiovascular research · Nov 2004
Case ReportsA novel SCN5A mutation manifests as a malignant form of long QT syndrome with perinatal onset of tachycardia/bradycardia.
Congenital long QT syndrome (LQTS) with in utero onset of the rhythm disturbances is associated with a poor prognosis. In this study we investigated a newborn patient with fetal bradycardia, 2:1 atrioventricular block and ventricular tachycardia soon after birth. ⋯ These findings suggest that the Na(v)1.5/V1763M channel dysfunction and possible neighboring mutants contribute to a persistent inward current due to altered inactivation kinetics and clinically congenital LQTS with perinatal onset of arrhythmias that responded to lidocaine and mexiletine.