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Increased Ventricular Vulnerability in a Chronic Ethanol Model Despite Reduced Electrophysiologic Responses to Catecholamines
Author(s) -
Patel Ravindra,
McArdle Joseph J.,
Regan Timothy J.
Publication year - 1991
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1991.tb00601.x
Subject(s) - medicine , catecholamine , ventricular fibrillation , repolarization , basal (medicine) , cardiology , anesthesia , norepinephrine , epinephrine , endocrinology , electrophysiology , dopamine , insulin
An increased incidence of sudden death has been reported in chronic alcoholism. To assess electrical vulnerability of the heart, action potential responses, and the role of the sympathetic system, a well‐nourished canine model has been studied intact under chloralose anesthesia after 1 year of ethanol consumption at 36% of caloric intake. Two alcoholic groups were compared with controls (Group 1). In Group 2 myocardial vulnerability was assessed after chronic EtOH and superimposed acute administration. In Group 3 basal vulnerability was related to circulating norepinephrine and release of neurohormone from the myocardium. Subsequently the responsiveness to catecholamine infusion was determined. To assess vulnerability an electrode catheter was placed in the right ventricular apex. The basal ventricular fibrillation threshold (VFT) was reduced to 27 ± 3 ma in Group 2 versus 43 ± 1.0 in Group 1. Acute infusion of ethanol in Group 2 further reduced the threshold. Group 3 had a reduced basal VFT. Baseline arterial plasma levels of norepinephrine were 8‐fold higher and coronary venous levels 13 times higher in the alcoholic group than in Group 1. However, VFT was not responsive to infused epinephrine, compared with Group 1 controls. In vitro study of superfused ventricular tissue from Group 3 revealed that basal action potential amplitude, overshoot, and resting potential were comparable with normals. Basal repolarization time (90%) was 198 ± 12 msec in Group 3 versus 215 ± 6 msec in Group 1 ( p < 0.05). After acute EtOH, repolarization time was shortened to 170 ± 8.6 in Group 1 at 90 mg% ethanol ( p < 0.002), with minimal further change up to 280 mg%. There was no significant change in Group 3. Isoproterenol (10 ‐8 to 10 ‐8 ) shortened repolarization time maximally to 74% of basal in Group 1, and 85% of basal in Group 3 ( p < 0.01). Thus, despite reduced in vivo and in vitro electrophysiologic responses to exogenous catecholamines in this chronic ethanol model, an increase of circulating NE appeared to promote increased ventricular vulnerability.