title: Exercise unmasks autonomic dysfunction in swine with a recent myocardial infarction.
abstract: OBJECTIVE
  Severe congestive heart failure is associated with autonomic imbalance consisting of an increased sympathetic and decreased parasympathetic activity. In the present study, we investigated the influence of alterations in autonomic balance on cardiovascular function in 11 swine with left ventricular (LV) dysfunction produced by a 2- to 3-week-old myocardial infarction (MI).
  
  
  METHODS
  Swine underwent permanent occlusion of the left circumflex coronary artery resulting in MI of the lateral LV wall. Autonomic activity was studied 2-3 weeks later using blockers of muscarinic (atropine), alpha-adrenergic (phentolamine) and beta-adrenergic (propranolol) receptors.
  
  
  RESULTS
  Under resting conditions, parasympathetic and sympathetic control of the heart and coronary circulation were similar in MI and normal swine. In contrast, during exercise of MI compared to normal swine, (i) there was a more pronounced gradual inhibition of parasympathetic control of heart rate with increasing exercise intensity; (ii) circulating catecholamines increased excessively, resulting in an increased beta-adrenergic influence on heart rate, while (iii) the beta-adrenergic influence on global left ventricular contractility was decreased, reflecting a blunted left ventricular beta-adrenergic responsiveness. Furthermore, (iv) an alpha-adrenergic vasoconstrictor influence was absent in the anterior LV wall of both MI and normal swine, while (v) the beta-adrenergic vasodilator influence in the coronary circulation was not different between normal and MI swine, which, in conjunction with the elevated catecholamine levels during exercise, suggests a diminished beta-adrenergic responsiveness of coronary resistance vessels within remote non-infarcted myocardium in MI swine.
  
  
  CONCLUSIONS
  Swine with a recent MI display autonomic dysfunction, which is characterized by a more pronounced inhibition of parasympathetic influence and an exaggerated increase in sympathetic drive during exercise, as well as reduced myocardial and coronary vascular beta-adrenergic responsiveness.
authors.affiliation: Experimental Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands. d.duncker@erasmusmc.nl
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Duncker
authors.forename: David B
authors.initials: DB
authors.lastname: Haitsma
authors.forename: David A
authors.initials: DA
authors.lastname: Liem
authors.forename: Pieter D
authors.initials: PD
authors.lastname: Verdouw
authors.forename: Daphne
authors.initials: D
authors.lastname: Merkus
mesh_terms: D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D004195:Disease Models, Animal; D005080:Exercise Test / Q000379:methods; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D010101:Oxygen Consumption / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D011976:Receptors, Muscarinic / Q000502:physiology; D013552:Swine; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology
chemical_list: D011943:Receptors, Adrenergic, beta; D011976:Receptors, Muscarinic; D001285:Atropine; D011433:Propranolol