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Research Article Free access | 10.1172/JCI105657

Ventricular Arrhythmias and K+ Transfer during Myocardial Ischemia and Intervention with Procaine Amide, Insulin, or Glucose Solution

Timothy J. Regan, Maureen A. Harman, Patrick H. Lehan, William M. Burke, and Henry A. Oldewurtel

Department of Medicine, the New Jersey College of Medicine, the Thomas J. White Cardiopulmonary Institute, Jersey City, New Jersey

Department of Medicine, B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

‡

This work was done during the tenure of an Established Investigatorship of the American Heart Association.

Address requests for reprints to Dr. Timothy J. Regan, Department of Medicine, New Jersey College of Medicine, 24 Baldwin Avenue, Jersey City, N. J. 07304.

*

Received for publication 20 September 1966 and in revised form 1 June 1967.

Supported in part by U.S. Public Health Service grants HE 06376 and HE 5510, and grants from the American and New Jersey Heart Associations.

Presented in part at the meeting of the American Society for Clinical Investigation, 1 May 1965.

Find articles by Regan, T. in: PubMed | Google Scholar

Department of Medicine, the New Jersey College of Medicine, the Thomas J. White Cardiopulmonary Institute, Jersey City, New Jersey

Department of Medicine, B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

‡

This work was done during the tenure of an Established Investigatorship of the American Heart Association.

Address requests for reprints to Dr. Timothy J. Regan, Department of Medicine, New Jersey College of Medicine, 24 Baldwin Avenue, Jersey City, N. J. 07304.

*

Received for publication 20 September 1966 and in revised form 1 June 1967.

Supported in part by U.S. Public Health Service grants HE 06376 and HE 5510, and grants from the American and New Jersey Heart Associations.

Presented in part at the meeting of the American Society for Clinical Investigation, 1 May 1965.

Find articles by Harman, M. in: PubMed | Google Scholar

Department of Medicine, the New Jersey College of Medicine, the Thomas J. White Cardiopulmonary Institute, Jersey City, New Jersey

Department of Medicine, B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

‡

This work was done during the tenure of an Established Investigatorship of the American Heart Association.

Address requests for reprints to Dr. Timothy J. Regan, Department of Medicine, New Jersey College of Medicine, 24 Baldwin Avenue, Jersey City, N. J. 07304.

*

Received for publication 20 September 1966 and in revised form 1 June 1967.

Supported in part by U.S. Public Health Service grants HE 06376 and HE 5510, and grants from the American and New Jersey Heart Associations.

Presented in part at the meeting of the American Society for Clinical Investigation, 1 May 1965.

Find articles by Lehan, P. in: PubMed | Google Scholar

Department of Medicine, the New Jersey College of Medicine, the Thomas J. White Cardiopulmonary Institute, Jersey City, New Jersey

Department of Medicine, B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

‡

This work was done during the tenure of an Established Investigatorship of the American Heart Association.

Address requests for reprints to Dr. Timothy J. Regan, Department of Medicine, New Jersey College of Medicine, 24 Baldwin Avenue, Jersey City, N. J. 07304.

*

Received for publication 20 September 1966 and in revised form 1 June 1967.

Supported in part by U.S. Public Health Service grants HE 06376 and HE 5510, and grants from the American and New Jersey Heart Associations.

Presented in part at the meeting of the American Society for Clinical Investigation, 1 May 1965.

Find articles by Burke, W. in: PubMed | Google Scholar

Department of Medicine, the New Jersey College of Medicine, the Thomas J. White Cardiopulmonary Institute, Jersey City, New Jersey

Department of Medicine, B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

‡

This work was done during the tenure of an Established Investigatorship of the American Heart Association.

Address requests for reprints to Dr. Timothy J. Regan, Department of Medicine, New Jersey College of Medicine, 24 Baldwin Avenue, Jersey City, N. J. 07304.

*

Received for publication 20 September 1966 and in revised form 1 June 1967.

Supported in part by U.S. Public Health Service grants HE 06376 and HE 5510, and grants from the American and New Jersey Heart Associations.

Presented in part at the meeting of the American Society for Clinical Investigation, 1 May 1965.

Find articles by Oldewurtel, H. in: PubMed | Google Scholar

Published October 1, 1967 - More info

Published in Volume 46, Issue 10 on October 1, 1967
J Clin Invest. 1967;46(10):1657–1668. https://doi.org/10.1172/JCI105657.
© 1967 The American Society for Clinical Investigation
Published October 1, 1967 - Version history
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Abstract

To assess the relation of ventricular arrhythmias to myocardial K+ movement during ischemia, we placed an electrode catheter in the left anterior descending coronary artery for thrombus production in intact anesthetized dogs. 85Kr injections distal to the thrombus permitted serial coronary blood flow measurements. Animals of Group I with a moderate flow reduction exhibited no arrhythmia or myocardial egress of K+. In Group II, marked flow reduction was accompanied by an injury potential and loss of K+ from the ischemic site, before and during ventricular tachycardia.

Therapeutic interventions were performed in animals having the same degree of ischemia as Group II. Systemic procaine amide in Group III interrupted the tachycardia and egress of K+, despite persistent ischemia. Group IV did not respond to intracoronary insulin with K+ uptake, as did normal dogs, and progressed to fibrillation. During the production of hyperglycemia in Group V, myocardial loss of K+ ceased with maintenance of sinus rhythm. Hemodynamic factors did not appear to have a major role in the genesis of the arrhythmia.

Since intracoronary infusion of K+ in normal dogs similarly altered repolarization and produced fibrillation, it would appear that during ischemia egress of K+ before development of the arrhythmia indicates a major role of the ion in pathogenesis. This view is supported by the myocardial loss of K+ and arrhythmia induced in normal dogs by strophanthidin and by the fact that pharmacologic regulation of K+ loss is associated with correction of the arrhythmia, despite persistence of low blood flow.

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