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noradrenaline/infarci
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Abnormal vasoconstrictor responses to angiotensin II and noradrenaline in isolated small arteries from patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
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OBJECTIVE
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterized by ultrastructural abnormalities in small cerebral and systemic vessels. We assessed vasomotor function in systemic small arteries in CADASIL.
METHODS
We studied 10 CADASIL
Noradrenaline protects in vivo rat heart against infarction and ventricular arrhythmias via nitric oxide and reactive oxygen species.
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BACKGROUND
Our previous study showed that pretreatment with noradrenaline via opening of the mitochondrial ATP-sensitive potassium channel protects myocardium against ischemia/reperfusion injuries. We have hypothesized that production of nitric oxide (NO) and generation of reactive oxygen species
Plasma adrenaline and noradrenaline in patients with acute myocardial infarction. Relationship to ventricular arrhythmias of varying severity.
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Plasma adrenaline (A) and noradrenaline concentrations (NA) were determined in 41 patients admitted to the coronary care unit (CCU). Eleven with suspected acute myocardial infarction (AMI), subsequently excluded as a diagnosis, had significantly elevated A and NA compared with 20 normal resting
Lower plasma noradrenaline and blood viscosity on carvedilol vs atenolol in men with recent myocardial infarction.
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The Carvedilol Acute Myocardial Infarction Study (CAMIS) investigates cardiac remodeling in patients (n = 250) randomized to carvedilol vs atenolol and treated for 12 months after acute myocardial infarction. In a sub-study, we compared sympathetic, hemorrheological and vascular effects in small but
Noradrenaline-induced increases in calcium and tension in skeletal muscle conductance and resistance arteries from rats with post-infarction heart failure.
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We tested the hypothesis that arterial reactivity to noradrenaline is augmented in congestive heart failure (CHF), which could contribute to the deleterious changes in peripheral vascular resistance and compliance in this condition. From male Wistar rats with post-infarction CHF and sham-operated
[Noradrenaline and adrenaline content in different areas of the heart in patients dying of myocardial infarct].
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Noradrenaline and adrenalin levels in different sections of the heart of persons deceased of myocardial infarction were measured, this being paralleled by determining the content of the said amines in the adrenal glands. It is shown that the noradrenaline level in the myocardium was down by
Regulation of tissue noradrenaline in the rat myocardial infarction model of chronic heart failure.
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OBJECTIVE
The aim was to evaluate mechanisms regulating tissue noradrenaline in congestive heart failure.
METHODS
Tissue noradrenaline was measured in the conscious post myocardial infarction rat model of congestive heart failure and in sham operated rats (1) under control conditions, (2) 6 h after
Influence of dobutamine and dopamine on hemodynamics and plasma concentrations of noradrenaline and renin in patients with low cardiac output following acute myocardial infarction.
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The comparative hemodynamic effects of dobutamine and dopamine were studied in 6 patients with low cardiac output resulting from acute myocardial infarction. Plasma levels of noradrenaline and renin were measured before and during a 5 microgram/kg/min infusion of each of the drugs. Dobutamine had a
Plasma adrenaline and noradrenaline concentrations and dopamine-beta-hydroxylase activity in myocardial infarction with and without cardiogenic shock.
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In patients with myocardial infarction, with or without cardiogenic shock, plasma noradrenaline and adrenaline concentrations are increased. However, plasma noradrenaline concentrations are considerably higher in patients with cardiogenic shock when compared with those with uncomplicated myocardial
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
The metabolic role of endogenous catecholamines in acute myocardial infarction: effects of reserpinization and of infused noradrenaline.
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A significant decrease of the noradrenaline content of the ischemic as well as non-ischemic parts of the myocardium was found in rats after ligation of the left coronary artery. The eventual role of released noradrenaline in the anaerobic metabolism of the heart was investigated. A highly
[Effect of heparin and xylocaine on the excretion of adrenaline and noradrenaline in patients with myocardial infarct].
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Influence of dobutamine and dopamine on hemodynamics and plasma concentrations of noradrenaline and renin in patients with low cardiac output following acute myocardial infarction.
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[Plasma ANP, noradrenaline concentrations at rest and during standardized exercise test in post-infarct patients in comparison with simultaneous 99m Tc radionuclide ventriculography parameters with reference to their diagnostic value].
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[The status of the sympathico-adrenal system in the acute stage of cerebral infarct (based on data of adrenaline and noradrenaline excretion)].
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