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Effect of catecholamine depletion on myocardial infarct size in dogs: role of catecholamines in ischemic preconditioning.
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OBJECTIVE
Cardioprotective adaptation to brief periods of ischemia and reperfusion is termed ischemic preconditioning (PC). Limitation of infarct size by preconditioning is associated with marked slowing of ischemic metabolism. The cause of metabolic slowing has not been determined but may involve
Altered norepinephrine content and ventricular function in p75NTR-/- mice after myocardial infarction.
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Cardiac sympathetic neurons stimulate heart rate and the force of contraction through release of norepinephrine. Nerve growth factor modulates sympathetic transmission through activation of TrkA and p75NTR. Nerve growth factor plays an important role in post-infarct sympathetic remodeling. We used
Spontaneous atrial fibrillation initiated by tyramine in canine atria with increased sympathetic nerve sprouting.
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BACKGROUND
Chronic left ventricular myocardial infarction (LVMI) promotes atrial and pulmonary veins (PV) sympathetic nerve sprouting.
OBJECTIVE
To test the hypothesis that sympathetic stimulation with tyramine initiates atrial fibrillation (AF) by early after depolarization (EAD)-mediated triggered
Metabolic pathways involved in Xin-Ke-Shu protecting against myocardial infarction in rats using ultra high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry.
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Xin-Ke-Shu (XKS) is a patent drug used for coronary heart diseases in China. This study evaluated the protective effect of XKS against isoproterenol (ISO)-induced myocardial infarction (MI). For its underlying mechanism in rats with MI, a metabonomic approach was developed using ultra
Studies of the fate of tyramine in dogs: the effect of monoamine oxidase inhibition, portafemoral shunt and coronary artery ligation on the kinetics of tyramine.
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Radioimmunoassay of tyramine (T) was used to investigate the kinetics of T in plasma of three groups of dogs (control, pretreated with monoamine oxidase inhibitor and those with portafemoral shunt). Furthermore, the influence of coronary artery ligation on the T content of the heart was studied.
Ischemic preconditioning fails to limit infarct size in reserpinized rabbit myocardium. Implication of norepinephrine release in the preconditioning effect.
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BACKGROUND
Infarct size reduction by ischemic preconditioning is believed to be mediated by adenosine; however, whether adenosine is the factor responsible for the initiation of this protection remains unknown. It is possible that during preconditioning, adenosine stimulates receptors on presynaptic
Infarction-induced cytokines cause local depletion of tyrosine hydroxylase in cardiac sympathetic nerves.
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Myocardial infarction causes a heterogeneity of noradrenergic transmission that contributes to the development of ventricular arrhythmias and sudden cardiac death. Ischaemia-induced alterations in sympathetic transmission include regional variations in cardiac noradrenaline (NA) and in tyrosine
A possible role of noradrenaline in the development of myocardial infarction: an experimental study in the isolated rat heart.
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Isolated rat hearts were perfused with buffer containing noradrenaline 10(-7) to 10(-4) M. A dose-dependent depletion of glycogen and ATP were seen together with a leakage of ASAT and creatine phosphokinase (CK). The damage induced by noradrenaline could be prevented by addition of a beta-blocker
Myocardial Injury from Tranylcypromine-Induced Hypertensive Crisis Secondary to Excessive Tyramine Intake.
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Monoamine oxidase inhibitors (MAOIs) are known to cause hypertensive crisis when combined with intake of tyramine, classically found in cheese. We present a case of MAOI-induced hypertensive crisis leading to significant troponin release after soft cheese intake. A 51-year-old lady presented with
The effect of tyramine infusion and exercise on blood flow, coagulation and clot microstructure in healthy individuals.
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The long term benefits of exercise on the cardiovascular status of a patient have been proven, however, their benefit/risk relationship with exercise intensity is unclear. Furthermore, many thromboembolic diseases such as myocardial infarction and ischaemic stroke are associated with profound
Effective stimulation of cardiac contractility and myocardial metabolism by impromidine and dimaprit--two new H2-agonistic compounds--in the surviving, catecholamine-insensitive myocardium after coronary occlusion.
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Left ventricular infarctions were produced in guinea pigs, and the contractile response to beta-adrenergic and H2-histaminergic stimulation was tested in isolated perfused heart preparations. Adenylate cyclase activity and binding characteristics of sarcolemmal beta 1-, H2-, and muscarinic
Defibrotide, an antithrombotic substance that preserves postsynaptic alpha- and beta-adrenergic function in post acute infarcted rabbit hearts.
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Defibrotide, a simple strand polydeoxyribonucleotide of mammalian origin with a molecular weight of 20,000 daltons, given intravenously to the rabbit before and after production of left ventricular infarction, prevents the alteration of the contractile response to postsynaptic adrenergic stimulation
Adrenergic activation confers cardioprotection mediated by adenosine, but is not required for ischemic preconditioning.
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BACKGROUND
The aim of this study was to determine whether (1) adrenergic activation is cardioprotective, (2) adrenergic cardioprotection occurs via adenosine receptor activation, and (3) ischemic preconditioning requires alpha-adrenergic activation.
METHODS
Anesthetised open chest rabbits underwent
Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit.
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The role of catecholamines in ischemic preconditioning is unclear. Accordingly, the effects of tyramine-induced norepinephrine release and alpha 1-receptor blockade were examined. Ischemic preconditioning with a 5-minute coronary occlusion 10 minutes before a 30-minute ischemic interval resulted in
Effect of acute intravenous cocaine administration on endothelium-dependent vasodepressor responses to acetylcholine.
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BACKGROUND
Cardiovascular events commonly associated with acute and chronic cocaine abuse include coronary vasospasm, arrhythmias, myocardial infarction, and sudden death. It has been suggested that cocaine causes endothelial dysfunction and vasoconstriction by inhibiting local production of nitric
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