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antiadrenergic/isquemia

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The effect of adenosine receptor blockade and adrenergic blockade on myocardial stunning [left anterior descending coronary artery (LAD) occluded for 10 min and reperfused for 180 min] was studied in 38 open-chest cats. A control group (Control) was compared with two other groups in which adenosine
Melatonin has potent cardioprotective properties. These actions have been attributed to its free radical scavenging and anti-oxidant actions, but may also be receptor mediated. Melatonin also exerts powerful anti-adrenergic actions based on its effects on contractility of isolated papillary muscles.

The role of catecholamines in ischemia.

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In myocardial ischemia, sympathetic activity of the heart is closely connected with the progression of cell injury and the incidence of malignant arrhythmias. Adrenergic stimulation of the ischemic myocardium is due to increased local norepinephrine concentrations in the heart, whereas the plasma

Cardiac sympathetic activity in myocardial ischemia: release and effects of noradrenaline.

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Sympathetic overactivity in myocardial ischemia is closely associated with the progression of myocyte injury and the incidence of malignant arrhythmias. Adrenergic stimulation of the ischemic myocardium is predominantly due to increased local noradrenaline concentrations in the heart, whereas plasma
OBJECTIVE The postulate that ischemic preconditioning caused an attenuation in ischemia induced increases in tissue cAMP, and that this may pertain to the mechanism of ischemic preconditioning, was investigated in the isolated rat heart. A significant reduction in tissue cAMP in preconditioned
BACKGROUND Vasoconstriction occurs after percutaneous transluminal coronary angioplasty (PTCA) along the dilated vessel. The vasomotor changes, initiated by the mechanical stretch of the stenotic region, are thought to be due to various mechanisms but whether the sympathetic nervous system plays a
Sympathetic hyperactivity plays a major role in the genesis of malignant arrhythmias during acute myocardial ischemia. An experimental model in which life-threatening arrhythmias are specifically and consistently induced by the interaction between acute myocardial ischemia and left stellate ganglion

Beneficial effects of a new carbacyclin derivative, ZK 36 374, in acute myocardial ischemia.

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The potential therapeutic value of the chemically stable carbacyclin analog ZK 36 374 was studied in acute myocardial ischemia (MI). In anesthetized cats, the left anterior descending coronary artery was ligated and 30 min later an i.v. infusion of ZK 36 374 (0.18 microgram/kg X min) on vehicle was
The value of K+ channel blockade in preventing lethal arrhythmias, and specifically those triggered by acute myocardial ischemia and sympathetic hyperactivity, remains unproven. To address this issue, we tested the antifibrillatory effect of d-sotalol, and Ikr blocker, d,l-sotalol, its racemic

[The effects of Carvedilol, a beta-blocker, in experimental ischemia-reperfusion kidney injury].

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Carvedilol is a recently introduced drug with multiple action with a non-selective beta-antiadrenergic and selective alpha1-antiadrenergic action used for treatment of mild to medium severe hypertension. The authors investigated in their experiments the protective effect of carvedilol under
Moxonidine has been shown to be antiarrhythmic during ischaemia in vivo. This study aimed to investigate its electrophysiological effects in isolated working rabbit hearts in vitro. Monophasic action potential duration, effective refractory period and conduction delay were measured at three

Cardioprotective effect of melatonin against ischaemia/reperfusion damage.

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Melatonin (N-acetyl-5-methoxytryptamine) has been shown by several workers to protect the heart against ischaemia/reperfusion damage. Melatonin, both in the picomolar and micromolar range, significantly reduces infarct size and improves functional recovery during reperfusion. This may be due to its

[Antianginal and antiadrenergic therapy in acute coronary syndrome].

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In recent years cardiology has opened new chapters in the treatment of acute coronary syndrome (ACS). The acute therapeutic procedures include antianginal, anticoagulant and revascularization therapy. Optimal therapeutic procedure in ACS has two objectives: 1) quick removal of the factors causing

Antiadrenergic effects of adenosine on His-Purkinje automaticity. Evidence for accentuated antagonism.

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The effects of adenosine on the human His-Purkinje system (HPS) were studied in nine patients with complete atrioventricular (AV) block. Adenosine had minimal effect on the control HPS cycle length, but in the presence of isoproterenol increased it from 906 +/- 183 to 1,449 +/- 350 ms, P less than
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