norepinephrine/infarction

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

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

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

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

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

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

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 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

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

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

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

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

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

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

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