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Effect of reserpine upon the haemodynamic course of recovery following experimental myocardial infarction.
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Acute haemodynamic consequences of coronary artery ligation were evaluated in twenty-four anaesthetized open-chest dogs, nine of which were pretreated with reserpine. The following parameters were measured before, and at 15-min intervals following ligation for at least five hours : ECG, mean
[Myocardial infarction caused by reserpine treatment].
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Reserpine therapy and shock in myocardial infarction.
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[Slowing down of the heart over a long period by reserpine . (Remote results in a series of cases of irreducible chronic cardiac insufficiency following myocardial infarct)].
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[Is the prevention of myocardial infarct using reserpine also possible in man?].
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Impaired beta-adrenergic stimulation in the uninvolved ventricle post-acute myocardial infarction: reversible defect due to excessive circulating catecholamine-induced decline in number and affinity of beta-receptors.
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Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to isoproterenol was tested in the isolated perfused heart preparation. Adenylate cyclase activity, phosphodiesterase activity, and beta-receptor binding characteristics were determined in a
Endothelin B-receptors and sympathetic activation: impact on ventricular arrhythmogenesis during acute myocardial infarction.
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OBJECTIVE
We investigated the role of endothelin-B receptors on sympathetic activation originating from the adrenal gland or from the myocardium and its impact on arrhythmogenesis during acute myocardial infarction.
METHODS
We studied two groups of rats (n=120, 284±2 g), namely wild-type and
Pharmacological interventions and myocardial infarct size in rat.
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Infarction was produced in male albino rats by left coronary artery ligation and infarct size was measured using NBT staining. Imidazole significantly decreased the myocardial infarct. The effect did not appear to be mediated through the thromboxane synthetase inhibitory property of imidazole
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
Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease?
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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur
[Effects of sympathetic block on post-infarction cardiac hypertrophy and their impact on myocardial contractility].
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OBJECTIVE
To investigate the effects of chronic subcutaneous administration of reserpine (Res) or propranolol (Prop) on the postinfarction myocardial hypertrophy and the effects of Prop treatment on myocardial contractility in rats.
METHODS
Male albino rats (3-month-old) were submitted to left
Ischemic preconditioning fails to limit infarct size in reserpinized rabbit myocardium. Implication of norepinephrine release in the preconditioning effect.
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BACKGROUND
Infarct size reduction by ischemic preconditioning is believed to be mediated by adenosine; however, whether adenosine is the factor responsible for the initiation of this protection remains unknown. It is possible that during preconditioning, adenosine stimulates receptors on presynaptic
[Changes in metallothionein content of the heart and liver during acute myocardial infarction in rats].
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Metallothionein (MT) is an important endogenous anti-injury substance involved in the defensive system. In myocardial infarction model produced by left coronary artery occlusion in-rat, the content of left ventricular myocardial MT was significantly increased to a maximum on 4th day by 6-fold
CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis.
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CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long-chain fatty acids (FA). Previously, we found that the spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene that results in reduced transport of long-chain FA into
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
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