title: Simultaneous endocardial and epicardial monophasic action potential recordings during brief periods of coronary artery ligation in the dog: influence of adrenaline, beta blockade and alpha blockade.
abstract: Local differences in the time course of recovery of excitability during the early phase of myocardial ischaemia are important in the genesis of arrhythmias. Catecholamines are known to encourage the formation of arrhythmias and adrenergic blockade is a recognised therapeutic regime. The purpose of this study was to compare the effect of short periods of coronary artery ligation on endocardial and epicardial repolarisation time, to assess any disparity between the two surfaces, and investigate the influence of catecholamines and adrenergic blockade. Simultaneous left ventricular endocardial and epicardial monophasic action potentials (MAPs) were recorded during short periods of left anterior descending coronary artery (LAD) ligation in 9 open chested dogs. Recordings were made during two 90 s periods of LAD ligation. Two further ligations were made during infusion of adrenaline (1 microgram.kg-1.min-1). Subsequently ligations were made after beta blockade with propranolol (0.25 mg.kg-1) and then in the presence of a combination of alpha blockade (phentolamine, 0.15 mg.kg-1) and beta blockade. MAP duration was measured at 90% repolarisation. LAD ligation produced a marked shortening of MAP duration epicardially with only minimal shortening endocardially, which resulted in a highly significant difference between the repolarisation times on the two surfaces. The disparity between surfaces tended to be augmented by adrenaline and was significantly minimised by either beta blockade alone or in combination with alpha blockade. Our results show rapid development of substantial regional differences in repolarisation time between endocardium and epicardium in response to "ischaemia".(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Cardiology, Middlesex Hospital, Medical School, London.
authors.forename: P
authors.initials: P
authors.lastname: Taggart
authors.forename: P M
authors.initials: PM
authors.lastname: Sutton
authors.forename: D W
authors.initials: DW
authors.lastname: Spear
authors.forename: H F
authors.initials: HF
authors.lastname: Drake
authors.forename: R H
authors.initials: RH
authors.lastname: Swanton
authors.forename: R W
authors.initials: RW
authors.lastname: Emanuel
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D001794:Blood Pressure; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D003331:Coronary Vessels; D004285:Dogs; D004699:Endocardium / Q000503:physiopathology*; D004837:Epinephrine / Q000494:pharmacology*; D005260:Female; D008026:Ligation; D008297:Male; D010496:Pericardium / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D004837:Epinephrine