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antiadrenergic/infarction
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 28 rezultatus
Hemodynamic and antiadrenergic effects of dronedarone and amiodarone in animals with a healed myocardial infarction.
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Prisijungti Registracija
The hemodynamic and antiadrenergic effects of dronedarone, a noniodinated compound structurally related to amiodarone, were compared with those of amiodarone after prolonged oral administration, both at rest and during sympathetic stimulation in conscious dogs with a healed myocardial infarction.
Antifibrillatory efficacy of ersentilide, a novel beta-adrenergic and Ikr blocker, in conscious dogs with a healed myocardial infarction.
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OBJECTIVE
IKr blockade is ineffective in preventing ventricular fibrillation elicited by the interaction between acute myocardial ischemia and elevated sympathetic activity. This depends in part on the fact that adrenergic activation offsets more than 50% of the action potential prolonging effect of
Opposing effects on infarction of delta and kappa opioid receptor activation in the isolated rat heart: implications for ischemic preconditioning.
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Delta-opioid receptors are known to participate in the protection found following ischemic preconditioning (IPC), but the role of kappa-receptors in IPC is currently controversial. Langendorff-perfused rat hearts received 35 min regional ischemia and 2 h reperfusion. PC (2 cycles 5 min global
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
Carvedilol versus metoprolol in the acute phase of myocardial infarction:.
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Beta-adrenergic blockers provide significant cardioprotection during acute ischemia and reperfusion. To further explore the effects of additional alpha-1-adrenoceptor blockade on autonomic modulation in acute myocardial infarction (AMI), carvedilol was compared with metoprolol in the setting of
Acute electrophysiologic effects and antiarrhythmic/antifibrillatory activity of intravenous amiodarone in a chronic feline infarction model.
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In animal studies, amiodarone has substantial and immediate antiarrhythmic/antifibrillatory action during acute myocardial ischemia. The magnitude of this effect is discordant with the minor degree of prolongation of ventricular action potential duration (APD) and refractoriness which occurs
Activated partial thromboplastin time correlates with methoxyhydroxyphenylglycol in acute myocardial infarction patients: therapeutic implications for patients at cardiovascular risk.
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OBJECTIVE
Acute myocardial infarction (AMI) is associated with increased coagulation which in the presence of unstable atheroma or endothelial damage leads to occlusive coronary vessel thrombosis. AMI is usually characterized by increased levels of catecholamines. It is possible there may be a link
Melatonin receptor-mediated protection against myocardial ischaemia/reperfusion injury: role of its anti-adrenergic actions.
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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.
Mortality reduction by antiadrenergic modulation of arrhythmogenic substrate: significance of combining beta blockers and amiodarone.
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Over the last 3 decades, there have been numerous experimental and clinical studies that utilized beta blockers for acute as well as chronic myocardial syndromes, especially in the setting of myocardial infarction in which the focus has been on mortality reduction. The results of these studies
[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
The cardioprotective effect of rosmarinic acid on acute myocardial infarction and genes involved in Ca2+ homeostasis.
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Acute myocardial infarction (AMI) is a common cause of hospitalisation and high mortality due to lethal arrhythmias. Sarcoplasmic reticulum Ca2+ ATPase (SERCA2) and ryanodine receptor (RyR2) regulate the cytosolic Ca2+ ion concentration. Rosmarinic acid (RA) is one of the most common caffeic esters
Phosphodiesterase 2 Protects Against Catecholamine-Induced Arrhythmia and Preserves Contractile Function After Myocardial Infarction.
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BACKGROUND
Phosphodiesterase 2 is a dual substrate esterase, which has the unique property to be stimulated by cGMP, but primarily hydrolyzes cAMP. Myocardial phosphodiesterase 2 is upregulated in human heart failure, but its role in the heart is unknown.
OBJECTIVE
To explore the role of
Carvedilol protects against lethal reperfusion injury through antiadrenergic mechanisms.
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We examined the effect of carvedilol as compared with that of a combination of propranolol and doxazosin on lethal reperfusion injury in 21 feline hearts subjected to 40-min regional ischemia and 180-min reperfusion. A control group (n = 7) was compared with one group given carvedilol, a
Antiadrenergic cardiovascular adverse effects of high-dose amiodarone loading regimen.
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A 55-year-old patient with inferior wall infarction was treated effectively for ventricular tachycardia with high-dose oral amiodarone loading regimen (5 g within 16 hours). Serial pharmacokinetic studies demonstrated a rapid temporary increase in amiodarone plasma concentration to a maximum of 3.40
Ventricular arrhythmias: antiadrenergic therapy for the patient with coronary artery disease.
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Patients who have had a recent myocardial infarction (MI) are at high risk of ventricular arrhythmias that often cause sudden cardiac death. It is believed that sympathetic overactivity in the peri-infarction period may alter the electrophysiology and structure of the myocardium, thus placing these
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