title: Coronary vascular regulation during postcardioplegia reperfusion.
abstract: BACKGROUND
  This study extends previous investigations of global and regional myocardial blood flow during early postcardioplegia reperfusion. The hypothesis tested is that coronary vascular regulation becomes abnormal within 3 minutes after the start of postcardioplegia reperfusion.
  
  
  METHODS
  Pigs (n = 40) were supported by cardiopulmonary bypass and 38 degrees C blood cardioplegic solution was infused. A control preischemic microsphere injection (No. 1) was given in asystolic hearts. Groups 1 to 3 had 1 hour of hypothermic cardioplegic arrest. Group 4 (control group) had 1 hour of perfusion without cardioplegia. A blood cardioplegic solution at 38 degrees C and 70 mm Hg pressure was infused to maintain asystole during the initial 7 to 10 minutes of reperfusion in all groups. Left ventricular intracavitary pressures were set at 0, 10, 20, or 0 mm Hg in groups 1, 2, 3, and 4 (n = 10 pigs per group), respectively, during the initial 7 minutes of reperfusion. The ventricle was then decompressed. At 30 seconds, 3 minutes, and 6 minutes after reperfusion, microsphere injections 2, 3, and 4 were given in asystolic hearts. Microsphere injection No. 5 was given 10 minutes after reperfusion in beating vented hearts.
  
  
  RESULTS
  (1) Left ventricular distention during the initial 7 minutes of reperfusion after hypothermic cardioplegic arrest attenuates postischemic hyperemia. (2) Left ventricular intracavitary pressure of 20 mm Hg during reperfusion causes a decrease in endocardial blood flow relative to epicardial blood flow at 6 minutes after reperfusion. (3) Global myocardial blood flow during postcardioplegia reperfusion falls significantly below preischemic control values despite the return of electromechanical activity.
  
  
  CONCLUSIONS
  Coronary vascular regulation (i.e., coronary resistance and metabolic flow recruitment) becomes abnormal within 3 minutes after the start of reperfusion after hypothermic blood cardioplegic arrest.
authors.affiliation: Division of Cardiothoracic Surgery, University of Alabama at Birmingham 35294-0007, USA.
authors.forename: E R
authors.initials: ER
authors.lastname: Ferguson
authors.forename: R D
authors.initials: RD
authors.lastname: Spruell
authors.forename: W V
authors.initials: WV
authors.lastname: Vicente
authors.forename: C P
authors.initials: CP
authors.lastname: Murrah
authors.forename: W L
authors.initials: WL
authors.lastname: Holman
mesh_terms: D000818:Animals; D001769:Blood; D002314:Cardioplegic Solutions; D003326:Coronary Circulation; D006324:Heart Arrest, Induced; D007036:Hypothermia, Induced; D007773:Lactates / Q000378:metabolism; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D013552:Swine; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D002314:Cardioplegic Solutions; D007773:Lactates