lidocaine/احتشاء

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Lidocaine reduces canine infarct size and decreases release of a lipid peroxidation product.

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Whether and how lidocaine reduced infarct size in a canine model of ischemia and reperfusion was investigated. Twenty dogs underwent a 90-min left anterior descending artery ligation and 300 min of reperfusion. Infarct size was measured by triphenyl tetrazolium chloride and the region at risk by

Increased alpha-1-acid glycoprotein and lidocaine disposition in myocardial infarction.

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In 15 patients with confirmed myocardial infarction, alpha-1-acid glycoprotein rose significantly from 117 mg/dL at admission to 140 mg/dL at 36 hours (p less than 0.01), but not in 15 age- and sex-matched patients with chest pain only. Twelve patients were given prolonged infusions of lidocaine (2

Prophylactic tocainide or lidocaine in acute myocardial infarction.

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Twenty-nine patients with acute myocardial infarction (AMI) were studied in a randomized double-blind trial of intravenous lidocaine and tocainide, followed by either oral tocainide or placebo without regard to previous therapy, for the prophylaxis of arrhythmias associated with acute infarction. No

Facilitation of reentry by lidocaine in canine myocardial infarction.

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Despite continuing controversies regarding its antiarrhythmic and antifibrillatory efficacy lidocaine is frequently used for the treatment of ventricular arrhythmias occurring in the early phase of acute myocardial infarction (MI). The authors studied the effects of lidocaine in 18 consecutive MI

Lidocaine prophylaxis in acute myocardial infarction.

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Primary ventricular fibrillation (PVF) occurs in approximately 3--10% of uncomplicated acute myocardial infarction (AMI) patients. The major reason for this variability in incidence appears to be population diferences in the time from symptom onset to admission. Other risk factors have not been

Facilitation of reentry by lidocaine in canine myocardial infarction.

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The authors studied the effects of lidocaine in 18 consecutive dogs with myocardial infarction 1 to 4 days after two-stage left anterior descending coronary artery ligation. Electrophysiologic testing was performed in anesthetized dogs after infarction with single-, double-, or triple-programmed

Comparative study of tocainide and lidocaine in patients admitted for suspected acute myocardial infarction.

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The antiarrhythmic effects of tocainide, administered as a bolus injection of 750 mg followed by oral therapy, and conventional lidocaine therapy were evaluated in 40 patients admitted for suspected acute myocardial infarction (AMI) and showing high-grade premature ventricular complexes (PVCs). The

Comparison of antiarrhythmic effects of oral prajmalium bitartrate and intravenous lidocaine in acute myocardial infarction.

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In 35 patients with acute myocardial infarction premature ventricular complexes were quantified from stored continuous electrocardiographic tape recordings using a semiautomated arrhythmia detection system. Seventeen patients, separated at random, received no antiarrhythmic drug and formed the

Ventricular defibrillation in canines with chronic infarction, and effects of lidocaine and procainamide.

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Prior studies in dogs with normal hearts have demonstrated that lidocaine increases but procainamide does not change the energy required for successful defibrillation. Because many postinfarct patients receiving implantable cardioverter defibrillator devices require adjunctive antiarrhythmic

Differences in infarct size with lidocaine as compared with bretylium tosylate in acute myocardial ischemia and reperfusion in pigs.

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The effects of the antiarrhythmic drugs lidocaine and bretylium tosylate on myocardial necrosis were studied in anesthetized pigs subjected to 60-min coronary occlusion followed by 3-h reperfusion. Group A (n = 7) received lidocaine (average dose +/- SD = 1,828 +/- 515 mg) before and during coronary

Lidocaine and the quarternary ammonium compound QX-572 in acute myocardial infarction. A comparative study.

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Patients with suspected or proven acute myocardial infarction complicated by ventricular arrhythmias not corrected by lidocaine therapy (bolus dose 100 mg followed by infusion 2 mg/min) were treated either with an increased dose of lidocaine (bolus dose 50 mg followed by infusion 3 mg/min) or with

A comparative evaluation of the effects of propafenone and lidocaine on early ventricular arrhythmias after acute myocardial infarction.

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A double-blind, placebo-controlled trial comparing the antiarrhythmic effects of lidocaine (given intravenously as a bolus injection of 100 mg followed by an infusion of 2 mg min-1) and propafenone (given as a bolus of 105 mg followed by 300 mg orally every 8 h) was conducted in the first 24 h

[Tetrodotoxin potentiation of the antiarrhythmic action of lidocaine in the late stage of experimental myocardial infarct].

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Lidocaine (4--12 mg/kg) and the specific fast sodium current blocker tetrodotoxin (TTX) (1--6 mg/kg, i. v.) reduced ventricular arrhythmias that occurred 24 h after coronary artery ligation in dogs. Infusion of a mixture of subthreshold doses of lidocaine and TTX decreased ventricular arrhythmias to

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

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The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a

Effects of procainamide and lidocaine on electrically inducible ventricular tachycardia studied with programmed ventricular stimulation in post myocardial infarction.

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The effects of procainamide and lidocaine, representative of class IA and IB antiarrhythmic agents, on electrically inducible ventricular tachycardia (VT) were studied using programmed ventricular stimulation in 47 post myocardial infarction patients at an average of 1.5 months after the onset. The

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