Affiliation:
1. Cardiovascular Section, Department of Medicine, Hahnemann Medical College and Hospital Philadelphia, Pennsylvania
Abstract
The effects of quinidine and its interactions with potassium (K) on atrio-ventricular (A-V) conduction were studied in isolated, perfused rabbit hearts, utilizing microelectrode techniques. Quinidine gluconate (10 mg/liter) was added to perfusion fluid containing either normal [K
+
] (4.5 mEq/liter), low [K
+
] (1.5 mEq/liter), or high [K
+
] (7.5 mEq/liter). The following observations were made: (A) The marked prolongation of A-V conduction time produced by quinidine was antagonized by low K
+
and enhanced by high K
+
concentration. (B) Quinidine or high K
+
concentration prolonged the A-V interval by slowing intra-atrial and His-Purkinje-ventricular conduction. (C) Low K
+
concentration depressed conduction in the N region of the A-V node. (D) Lowering K
+
concentration in the presence of quinidine shortened the A-V interval by enhancing His-Purkinje-ventricular conduction. (E) Quinidine and high K
+
concentration increased the action potential amplitude in the nodal and the node-His regions of the A-V node while low K
+
concentration showed opposite effects. Hence, different regions of the A-V conducting system were selectively influenced by these agents. A-V conduction in the presence of low K
+
and quinidine depends upon the net results of their antagonism within individual fiber types. The importance of these interrelationships in pharmacologic approach to A-V conduction disturbances is stressed.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
54 articles.
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