In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction.

Kupersmith, Joel; Antman, Elliott M.; Hoffman, Brian F.

doi:10.1161/01.res.36.1.84

Cited by 120 publications

(30 citation statements)

References 33 publications

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“…Continuous electrical activities recorded within the ischemic region and which were associated with ventricular extrasystoles, provide supporting evidence for this concept (3,4). Although precise infor mation relating to the localization of the delay and the existence of re-entry is not available, The effects of various antiarrhythmic agents such as lidocaine (8,9), procainamide (8), aprindine (10), propranolol (8,11) and verapamil (10,12) on the ischemia-induced conduction delay have been studied in canine experimental models of acute myocardial infarction.…”

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confidence: 99%

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Effects of Polyamines on Ethylmorphine N-Demethylation in Rat Liver Microsomes

Nakaya

Hattori

Kanno

1980

Japanese Journal of Pharmacology

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Abstract-Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 or 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3--2.3 msec, p<0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 1.9 msec (p<0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.74-4.9 msec (p<0.05) and 8.4-4--1.8 msec (p<0.001), respec tively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.Electrophysiological studies on the ischemic myocardium have shown that ventricular arrhythmias of the early phase are due to the re-entrant mechanism (1, 2). Delayed activation The effects of various antiarrhythmic agents such as lidocaine (8, 9), procainamide (8),

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confidence: 99%

“…Drugs possessing a fast channel blocking property have been shown to increase the ischemia induced conduction delay (8)(9)(10). Verapamil has been found to reduce the conduction delay in ischemic myocardium (10).…”

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confidence: 99%

Effects of Polyamines on Ethylmorphine N-Demethylation in Rat Liver Microsomes

Nakaya

Hattori

Kanno

1980

Japanese Journal of Pharmacology

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“…A natural extension of these experiments has been study of the effects of antiarrhythmic agents on the models, including characterization of cellular electrophysiological effects of these drugs. Most of the studies to date have focused on drug effects on acutely ischemic or early healing tissue (Brennan and Wit, 1973;Sasyniuk and Kus, 1973;Hondeghem et al, 1974;Sasyniuk et al, 1974;Kupersmith et al, 1975;Kus et al, 1975;El-Sherif et al, 391 1977; Allen et al, 1978;Brennan et al, 1978;Cardinal and Sasyniuk, 1978;El-Sherif and Lazzara, 1978;Lazzara et al, 1978;Wang et al, 1979;Guse et al, 1980). Our data in the present study demonstrate different effects of a membrane-active antiarrhythmic agent (procainamide) on acutely injured ventricular muscle cells compared to cells which have survived prior ischemic injury and overlie the scar of a healed myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological effects or procainamide in acute and healed experimental ischemic injury of cat myocardium.

Myerburg¹,

Bassett

Epstein

et al. 1982

Circulation Research

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SUMMARY. We studied the effects of a membrane-active antiarrhythmic agent, procainamide (PA), on cellular electrophysiological consequences of ischemic injury to cat ventricular muscle. The left ventricles of 90-to 120-minute acute myocardial infarctions (AMI) (n = 14), and 2-to 4-month healed myocardial infarctions (HMI) (n = 17), were studied by microelectrode techniques in isolated tissue bath. Control action potential duration at 90% repolarization (APD90) recorded from ventricular muscle cells in AMI areas were short (114 ± 4 msec) compared to recordings from cells in normal areas (136 ± 6 msec) (P < 0.001). In contrast, APD90 of cells surviving ischemia in HMI preparations were longer than normals (159 ± 5 vs. 140 ± 5 msec, P < 0.001). After 60 minutes of exposure to PA, the APD90 of all cells was prolonged, but the absolute and relative magnitudes of prolongation were greater in AMI cells (mean = +40 msec, +35%), than in HMI cells (mean = +19 msec, +13%), P < 0.001. The prolongation of APD90 of normal cells was intermediate. Local refractory period changes paralleled APD90 changes. In seven additional HMI preparations, sustained ventricular activity was induced by premature stimulation. APD90 of HMI cells prolonged less than APD90 of normal cells during exposure to PA in these preparations, and decreased differences of APD90 between normal and HMI cells was associated with loss of inducibility of sustained ventricular activity. The effect of tetrodotoxin (TTX) was compared to the effect of PA in four HMI preparations to determine whether impaired delivery of test substances caused only an apparent decreased responsiveness to PA in HMI zones. TTX caused nearly identical prolongations of conduction times in HMI zones and normal zones, whereas PA caused different effects on APD90 in the two zones. In conclusion, PA alters the time course of repolarization of AMI cells more than that of HMI cells, decreasing the dispersion of repolarization in a given AMI or HMI preparation. The decreased dispersion correlated with loss of ability to induce sustained ventricular activity. Finally, the decreased responsiveness of HMI cells to PA does not appear to be due to impaired delivery to cell membranes, but, rather, appears to be a membrane difference persisting in cells which have survived ischemic injury. (Circ Res 50: 386-393, 1982) IN STUDIES of experimental myocardial infarction in cats, we have observed that the cellular electrophysiological abnormalities resulting from acute ischemic injury (90-120 minutes) differ from those which persist long-term (2-4 months) after healing from acute injury (Myerburg et al., 1978; Myerburg et al., in press). Transmembrane action potentials recorded from endocardial cells overlying acute myocardial infarction areas had variable decreases in resting membrane potential, upstroke amplitude, and dV/dt m ax, and shortened action potential durations. In contrast, the majority of surviving endocardial ventricular muscle cells overlying healed myocardial infarction scars were charac...

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“…In all experiments in which a 2 mg/kg lidocaine bolus was injected, the effect of the drug was seen within 30 sec of the injection, reached maximum within 1-2 min, persisted for 4-8 min, and almost completely disappeared within [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] min.…”

Section: Effect Of Lidocaine On Re-entrant Ventricular Tachycardiasmentioning

confidence: 99%

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

El‐Sherif¹,

Scherlag²,

Lazzara³

et al. 1977

Circulation

114

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SUMMARY 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 therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected.

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In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction.

Cited by 120 publications

References 33 publications

Effects of Polyamines on Ethylmorphine N-Demethylation in Rat Liver Microsomes

Effects of Polyamines on Ethylmorphine N-Demethylation in Rat Liver Microsomes

Electrophysiological effects or procainamide in acute and healed experimental ischemic injury of cat myocardium.

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

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