Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In anesthetized dogs, the cumulative intravenous administration of 1.0-40.0 mg/kg sulphinpyrazone failed to alter the ventricular excitation threshold, ventricular refractory period and ventricular fibrillation threshold determined during nonobstructed coronary blood flow. Sulphinpyrazone, however, did attenuate the reduction in the ventricular fibrillation threshold occurring during transient myocardial ischemia. G25671, the sulfide metabolite of sulphinpyrazone, failed to alter ventricular refractoriness and 'nonischemic' ventricular fibrillation thresholds, and was minimally effective in reducing the decrease in 'ischemic' fibrillation thresholds when administered in cumulative intravenous doses of 5.0-20.0 mg/kg. In conscious dogs in the subacute phase of anterior myocardial infarction, the administration of a cumulative 10.0-40.0 mg/kg sulphinpyrazone failed to alter the mode of induction, rate or morphology of ventricular tachyarrhythmias initiated by programmed ventricular stimulation. These data suggest that neither sulphinpyrazone nor its sulfide metabolite possess primary electrophysiologic properties which might contribute directly to significant antiarrhythmic or antifibrillatory activity.
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PMID:Electrophysiologic and antiarrhythmic actions of sulphinpyrazone and its sulfide metabolite G25671. 310 7

We examined if inhibition of endogenous prostaglandin (PG) synthesis reduced the severity of ventricular arrhythmia and the incidence of ventricular fibrillation (VF) following occlusion of the left anterior descending coronary artery (LAD) in anesthetized cats. We also determined whether the PGs were interacting in a facilitory manner with the sympathetic nervous system to produce arrhythmia and VF after LAD occlusion. Sulfinpyrazone, an inhibitor of cyclo-oxygenase enzyme, or vehicle was administered intravenously to cats 1 h before LAD occlusion. Sulfinpyrazone completely (p less than 0.001) inhibited the release of 6-keto-PGF1 alpha into the great cardiac vein following LAD occlusion. Sulfinpyrazone (100 mg/kg) significantly (p less than 0.001) reduced the amount of ventricular arrhythmia and the incidence of VF (p less than 0.05) in the 1st h after LAD occlusion. In addition to 6-keto-PGF1 alpha sulfinpyrazone also (p less than 0.001) inhibited the increase in plasma norepinephrine from the heart due to sympathetic nervous system stimulation following LAD occlusion. Since sulfinpyrazone was ineffective in increasing the dose of digoxin required to produce arrhythmia and death, sulfinpyrazone apparently did not depress cardiac excitability. Finally, the extent of infarction resulting from LAD occlusion was not different in sulfinpyrazone-treated animals compared with control. These data indicate that sulfinpyrazone, by inhibiting endogenous PG synthesis in the heart following LAD occlusion, may prevent a facilitory interaction between PGs and the sympathetic nervous system that contributes, in part, to the development of ventricular arrhythmia and VF normally associated with this event.
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PMID:Effect of sulfinpyrazone on ventricular arrhythmia, prostaglandin synthesis, and catecholamine release following coronary artery occlusion in the cat. 618 74

The effects of sulfinpyrazone were studied in 33 chloralose-anesthetized dogs. Ventricular fibrillation thresholds, mid diastolic thresholds and duration of the effective refractory period were determined in the normal heart after intravenous administration of sulfinpyrazone, 30 mg/kg body weight. The drug significantly raised the ventricular fibrillation threshold by 24 percent and the mid diastolic threshold by 36 percent and prolonged the effective refractory period by seven percent. The influence of sulfinpyrazone during acute myocardial ischemia was evaluated before and during a 10 minute occlusion of the left anterior descending coronary artery and after abrupt release of the occlusion. Although the drug afforded significant protection during coronary occlusion, it had no effect on the ventricular fibrillation threshold after reperfusion. Because potent cardiocardiac reflexes are elicited during ischemia, the influence of sulfinpyrazone on the ventricular fibrillation threshold was studied during norepinephrine infusion. Sulfinpyrazone attenuated the reduction of the ventricular fibrillation threshold during sympathetic humoral stimulation. Its effect was additive to beta adrenergic blockade with practolol and membrane stabilization with lidocaine. This investigation suggests that sulfinpyrazone exerts significant effects on ventricular vulnerability of both the normal and the ischemic myocardium. Further studies are needed to elucidate its precise mechanism of action.
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PMID:Effects of sulfinpyrazone on ventricular vulnerability in the normal and the ischemic heart. 710 58

Clinical and experimental studies indicate that ventricular arrhythmias, mainly ventricular fibrillation, are responsible for sudden cardiac death. A recent double-blind multicenter trial ("Anturane Reinfarction Trial") showed that the incidence of sudden cardiac death was reduced in Sulfinpyrazone-treated patients after acute myocardial infarction compared with the placebo group, although the rate of reinfarctions was not diminished. We investigated the efficacy of Sulfinpyrazone on the reduction and prevention of ventricular arrhythmias and primary ventricular fibrillation, utilizing a standardized experimental canine preparation. At normal therapeutic and at high cumulative doses of the drug, a reduction in ventricular arrhythmias within the first 24 hours after coronary occlusion could not be observed. Sulfinpyrazone failed also to alter the ventricular vulnerability to fibrillation in the very early myocardial infarction period. Furthermore, haemodynamics, contractility and oxygen consumption of the heart were not changed. These experimental findings show that the reduction in sudden cardiac deaths in Sulfinpyrazone-treated patients cannot be attributed to antiarrhythmic effects of the drug. Further research is needed to delineate the mechanism of action of Sulfinpyrazone as reported by the Anturane Reinfarction Trial Research Group.
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PMID:[Effects of sulfinpyrazone on early ventricular fibrillation and 2d-phase arrhythmias in acute myocardial infarction (author's transl)]. 746 58