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Recurrent ST Elevation Myocardial Infarction from Norepinephrine-induced Coronary Vasospasm.

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Myocardial infarction with no obstructive coronary atherosclerosis (MINOCA) is a distinct clinical syndrome characterized by evidence of myocardial infarction with normal or near-normal coronary arteries on angiography (stenosis severity < 50%). Coronary artery spasm, as seen in "variant

Life changes and urinary norepinephrine in myocardial infarction.

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The relationship between norepinephrine and stress caused by life changes was assessed using urinary norepinephrine levels and responses to a 57-item stress questionnaire interview obtained from 21 post-myocardial infarction and 27 healthy control male and female subjects. High correlations between

Cognitive Deficits Following a Post-Myocardial Infarct in the Rat Are Blocked by the Serotonin-Norepinephrine Reuptake Inhibitor Desvenlafaxine.

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Myocardial infarction (MI) in animal models induces cognitive deficits as well as the activation of caspase in the limbic system; both can be blocked by 2 weeks of treatment following MI using tricyclic antidepressants or selective serotonin uptake blockers. Here we used three different treatment

Inhibition of nonexocytotic norepinephrine release by desipramine reduces myocardial infarction size.

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During myocardial ischemia, a substantial accumulation of norepinephrine occurs in the ischemic zone due to a local nonexocytotic release of norepinephrine. Norepinephrine release is driven by the neuronal monoamine transporter (NET), which reverses its usual transmembrane transport direction. We

Action potentials of cardiac muscle in healing infarcts: response to norepinephrine and caffeine.

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Previous studies have shown that the muscle fibers that survive on the epicardial surface of a 5- or 14-day-old infarct in canine hearts have reduced or absent plateau phase during repolarization. Since the absence of a plateau phase could be related to a decrease in the slow inward current, we

Norepinephrine turnover in the heart and blood vessels of rats subjected to bilateral renal infarction.

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The total norepinephrine (NE) content, the uptake of [3H]NE, the turnover rate and the synthesis rate of the neurotransmitter at the heart and blood vessels have been studied during the development of hypertension in rats subjected to bilateral renal infarction. Normal and sham-operated rats were

[Effects of acute beta-adrenoceptor blockage (metoprolol i.v.) on plasma norepinephrine concentration and hemodynamics in postmyocardial infarction patients].

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The effect of acute beta-adrenoceptor blockage (Metoprolol) (M), 0.1 mg/kg i.v.) on left ventricular performance has been investigated at rest and during exercise in 15 patients with 2--3 months old transmural myocardial infarctions. Coronary venous and arterial norepinephrine (NE) concentrations

Regional reduction in ventricular norepinephrine after healing of experimental myocardial infarction in cats.

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Regional ventricular norepinephrine and myosin heavy chain concentrations were measured in two models of healed left ventricular myocardial infarction in cats. One model was characterized by a well-defined dense transmural scar (discrete myocardial infarction), while the other demonstrated a pattern

Metabolism of norepinephrine in noninfarcted heart muscle after experimental myocardial infarction.

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A marked, reversible decline in cardiac norepinephrine (NE) stores was noted after experimental myocardial infarction. Uptake and accumulation of tracer dose of dl-[7-14C]norepinephrine appeared to be unchanged as well as the rate of degradation. Despite marked variations in pool size the

Prognostic value of plasma atrial natriuretic factor, norepinephrine and epinephrine in acute myocardial infarction.

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Neurohumoral activation in acute myocardial infarction (AMI) may reflect the degree of hemodynamic compromise, contribute to the progression of heart failure and augment to the risk of serious ventricular arrhythmias. Consequently, assessment of neurohumoral variables may provide an index of

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

Studies of the interrelationship between plasma norepinephrine, plasma renin activity and acute myocardial infarction in dogs.

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Serial determinations of plasma norepinephrine and renin activity were made in dogs following acute ligation of the left anterior descending coronary artery. Increases in both substances closely paralleled increases in creatine phosphokinase activity, heart rate and the incidence of ventricular

Ischemic postconditioning and size of myocardial infarction during inhibition of norepinephrine reuptake.

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We studied the effect of inhibition of norepinephrine reuptake during the reperfusion period on the size of infarction zone after focal myocardial ischemia and under conditions of ischemic postconditioning. In groups 1 and 2, 30-min occlusion of the left coronary artery followed by 120-min

Norepinephrine response to exercise of rats with a chronic myocardial infarction.

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Plasma and tissue norepinephrine (NE) concentrations were determined at rest and after 45 min of swimming in rats with a surgically induced myocardial infarction (MI) and in rats having undergone a sham operation (SHAM). The MI rats had moderate-sized infarcts and demonstrated decreases in maximal

Pre-ischemic depletion of brain norepinephrine decreases infarct size in normothermic rats exposed to transient focal cerebral ischemia.

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This study examined the importance of brain norepinephrine concentration on outcome from a focal ischemic insult. Fasted temperature-controlled male Wistar rats pretreated with DSP-4, (N-(chloroethyl)-N-ethyl-2-bromobenzylamine), to selectively deplete brain norepinephrine, were subjected to

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