The sequential estimation of plasma catecholamines and whole blood histamine in myocardial infarction

Griffiths, John C.; Leung, F Y

doi:10.1016/0002-8703(71)90262-6

Cited by 55 publications

(18 citation statements)

References 11 publications

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“…Extracellular potassium in the ischemic region is known to be elevated in minutes after coronary occlusion, such an alteration results in a decrease in the membrane potentials (20). These electrophysiological changes, associated with catecholamine release (22,23), may be sufficient to depress the fast responses and induce the slow responses, with a resultant slowing conduction velocity. In this situation, slow channel blockers would be expected to deteriorate further rather than to improve the ischemia-induced conduction delay.…”

Section: Discussionmentioning

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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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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Section: Discussionmentioning

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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“…Besides, total catecholamines decline in the ischemic region to a very low level on the day after coronary occlusion. 24 However, ischemic myocardium still shows markedly depressed action potentials, slow conduction, and a high propensity for reentrant rhythms.…”

Section: Ionic Conductance Abnormalities In Ischemic Myocardiummentioning

confidence: 99%

Reentrant ventricular arrhythmias in the late myocardial infarction period. 7. Effect of verapamil and D-600 and the role of the "slow channel".

El‐Sherif¹,

Lazzara²

1979

Circulation

111

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SUMMARY Reentrant ventricular arrhythmias (RVA) were analyzed in dogs 3-7 days after ligation of the anterior descending coronary artery using averaged "composite" recordings of electrical activity of reentrant pathways (RP) from the epicardial surface of the infarction zone (IZ). Verapamil (V) and D-600 (D) (0.2-0.5 mg/kg i.v.) resulted in slight-to-moderate improvement of conduction in RP with abolition of spontaneous RVA and RVA initiated by premature depolarizations. The effect of V was not blocked by pretreatment with propranolol (0.5 mg/kg i.v.). Using a standard microelectrode technique aad strips of epicardial muscle from the IZ, D (0.5-1 X 10-6 g/ml) slightly improved the upstroke velocity and membrane responses of depressed ischemic cells. In contrast, tetrodotoxin (5 X 10-7 g/ml) further depressed or abolished action potentials of ischemic cells. We conclude: 1) the moderate antiarrhythmic effect of V and D on RVA is the result of improved conduction in RP; 2) this action is partly explained by improvement of a depressed sodium channel and is not related to catecholamine release; 3) slow-response action potentials play no significant role in the genesis of ischemia-related RVA, which probably results from depression of the fast response.IN THE LATE myocardial infarction period (3-7 days after infarction), the propensity for reentrant ventricular arrhythmias is still maintained. In a recently described canine model, reentrant ventricular arrhythmias were remarkably stable, and averaged recordings of the electrical activity of reentrant pathways could be obtained from the epicardial surface of the infarction zone with a specially designed composite electrode.''3 The canine model was used in both in vivo and in vitro experiments to study the mechanism of action of lidocaine4 I and dipherylhydantoin.6 Both drugs owed their antiarrhythmic effect to selective prolongation of refractoriness and depression of conduction in reentrant pathways in ischemic myocardium.In this study, we analyzed the effects of verapamil and its methoxy derivative, D-600, on electrophysiologic properties of ischemic myocardium and on related reentrant ventricular arrhythmias in both in vivo and in vitro experiments. The effect of D-600 on ischemic myocardial cells is also contrasted with that of tetrodotoxin. Both verapamil and D-600 are thought to act by blocking the slow inward current carried by calcium (Ca++)7 9 and possibly by sodium (Na+).1" It has been suggested that slow conduction in depressed cells," including ischemic myocardium,12 that can lead to reentrant ventricular arrhythmias is a property of the slow response action potential. This study provides a direct evaluation of the role that the Material and MethodsIn Vivo ExperimentsAdult mongrel dogs were studied 3-7 days after ligation of the left anterior descending artery just distal to the anterior septal branch. In all dogs, a transmural infarction was evident on gross postmortem examination. Recordings were obtained from the epicardial surface of the infarction zo...

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“…[9][10][11][12][13][14] Patients with acute myocardial infarction frequently exhibit excessive adrenergic activity as evidenced by an elevation of plasma and 24-hour urinary catecholamines. [15][16][17][18][19][20][21][22][23] It was therefore hypothesized that the abbreviated electromechanical systole characteristic of patients with myocardial infarction is a direct reflection of increased sympathetic nervous system activity. The.present investigation was designed to test this hypothesis.…”

Section: Ine Excretionmentioning

confidence: 99%