salicylates has been researched along with Ventricular-Fibrillation* in 2 studies
2 other study(ies) available for salicylates and Ventricular-Fibrillation
Article | Year |
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Reduction of postischaemic ventricular dysfunction and arrhythmias by trapping hydroxyl radicals with salicylic acid.
Recent studies have suggested the ability of salicylic acid (SA) to trap the hydroxyl radicals (.OH) generated in reperfused ischaemic myocardium. This study was designed to examine the effect of SA on reperfusion-induced arrhythmias and postischaemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with SA for 10 min. Hearts were then made ischaemic for 30 min, followed by 30 min of reperfusion. The left-ventricular contractile functions, including left-ventricular developed pressure (LVDP) and its first derivative (LV dp/dt), and creatine kinase (CK) release, were determined before and after ischaemia. Epicardial electrocardiograms (ECG) were also employed to analyse the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP and LV dp/dt, and reduced CK release, as compared to the control group (p < 0.05). The incidence of VT and VF during reperfusion was also significantly reduced by SA (p < 0.05). Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces ventricular dysfunction and attenuates ventricular arrhythmias by trapping OH radicals upon reperfusion in isolated rat hearts. Topics: Animals; Anti-Arrhythmia Agents; Creatine Kinase; Electrocardiography; Free Radical Scavengers; Hydroxyl Radical; In Vitro Techniques; Male; Myocardial Ischemia; Rats; Rats, Sprague-Dawley; Salicylates; Salicylic Acid; Tachycardia, Ventricular; Thiobarbituric Acid Reactive Substances; Ventricular Fibrillation; Ventricular Function, Left; Ventricular Pressure | 1993 |
Acute poisoning with dextropropoxyphene. Clinical symptoms and plasma concentrations.
Out of 14 cases of poisoning assumed to be due to dextropropoxyphene-containing drugs, propoxyphene and its main metabolite norpropoxyphene could be demonstrated in 11. The concentrations of the drugs were determined shortly after admission and then after 2, 4, 6 and 10 hours (in four cases also after 16 hours). The highest plasma concentration of propoxyphene, 0.74 mug/ml, was found in one case of fatal poisoning. Another patient with a plasma concentration of 0.51 mug/ml showed signs of severe respiratory depression but survived after respirator therapy. In the patients with lower plasma concentrations the poisoning had a benign course. In most cases the plasma concentration of norpropoxyphene exceeded that of propoxyphene even in the first blood sample. Topics: Acidosis; Acute Disease; Adolescent; Adult; Arrhythmia, Sinus; Aspirin; Barbiturates; Dextropropoxyphene; Drug Combinations; Ethanol; Female; Humans; Male; Middle Aged; Respiration Disorders; Salicylates; Time Factors; Ventricular Fibrillation | 1976 |