পৃষ্ঠা 1 থেকে 236 ফলাফল
We investigated whether pre-treatment with melatonin, a potent free radical scavenger and antioxidant, would protect against permanent focal cerebral ischemia without reperfusion in a rat middle cerebral artery occlusion (MCAO) model. A single dose of melatonin at 5, 15, or 50 mg/kg or the vehicle
OBJECTIVE
To examine the cytoprotective effect of melatonin or recombinant human growth hormone (hGH) on the early phase of a running myocardial infarction in rats by using the Feulgen staining.
METHODS
Rats were subjected to surgical ligature of the left coronary artery or its sham-operation and
The activation of different physiopathological pathways (neuroinflammation, apoptosis, and oxidation) can lead to secondary brain injury in ischemic stroke, and in animal models the administration of melatonin has reduced that secondary injury. Lower levels of serum melatonin were OBJECTIVE
To test whether melatonin reduces oxidative and inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction.
METHODS
Twenty pigs were randomized to receive a total dosage of 200 mg (0.4 mg/ml) of melatonin, or placebo immediately prior to reperfusion of a
Platelet aggregates appear to have a pathogenic role in the no-reflow phenomenon, which is associated with impaired clinical outcome in patients with ST-segment elevation myocardial infarction (STEMI). Melatonin, a hormone that plays a major role in biological circadian rhythms, is present in human
We evaluated the possible relation between circulating levels of nocturnal melatonin, C-reactive protein, and the development of adverse cardiovascular events in patients with ST-segment elevation myocardial infarction. Patients who had developed adverse events during follow-up had significantly
Objectives Lower serum melatonin levels are found in patients with ischaemic stroke compared with healthy controls. This study aimed to determine whether serum melatonin levels are associated with peroxidation status, antioxidant status, and mortality in patients with ischaemic stroke. Methods
As experimental studies suggest that melatonin is cardioprotective after myocardial infarction (MI), this study sought to investigate the relationships between circulating levels of melatonin and left ventricular (LV) remodelling in patients after acute MI. This prospective study included 161
We examined the time course of changes in the synthesis and levels of endogenous melatonin and in the expression of MT(1) and MT(2) melatonin receptors 1 day, 2 and 4 wk after myocardial infarction (MI) in rats. MI was produced by ligation of the left anterior descending coronary artery.
Myocardial ischemia-reperfusion (I/R) represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. I/R injury is believed to be a consequence of free radical generation in the heart especially during the period of reperfusion. The pineal secretory
Elevated levels of soluble cellular adhesion molecules have been reported in patients with acute coronary syndromes. Likewise, a relation between decreased nocturnal melatonin levels and coronary artery disease has been suggested. The aim of the present study was to investigate the day-night
BACKGROUND
Anxiety and sleep disorders are prevalent problems in patients presenting with ST-segment-elevation myocardial infarction (STEMI). Usually, these problems are managed by benzodiazepines, which-albeit effective-could cause adverse effects and drug interaction.
OBJECTIVE
This study was
BACKGROUND
Pineal and melatonin interactions with the hypothalamo-neurohypophysial system are well documented. In addition, vasopressin and oxytocin secretion are known to be part of the neuroendocrine response to chronic heart failure evoked by myocardial infarction. The present study was
Cyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24
BACKGROUND
Experimental studies have documented the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and limiting cardiac pathophysiology in models of experimental ischemia-reperfusion. Melatonin confers cardioprotection against ischemia-reperfusion