title: Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia.
abstract: BACKGROUND
  Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.
  
  
  RESULTS
  After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
  
  
  CONCLUSIONS
  The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Surgery, Carlyle Fraser Heart Center-Cardiothoracic Research Laboratory, Crawford Long Hospital of Emory University School of Medicine, Atlanta, GA 30365-2225, USA.
authors.forename: V H
authors.initials: VH
authors.lastname: Thourani
authors.forename: R S
authors.initials: RS
authors.lastname: Ronson
authors.forename: D G
authors.initials: DG
authors.lastname: Van Wylen
authors.forename: S T
authors.initials: ST
authors.lastname: Shearer
authors.forename: S L
authors.initials: SL
authors.lastname: Katzmark
authors.forename: Z Q
authors.initials: ZQ
authors.lastname: Zhao
authors.forename: D C
authors.initials: DC
authors.lastname: Han
authors.forename: R A
authors.initials: RA
authors.lastname: Guyton
authors.forename: J
authors.initials: J
authors.lastname: Vinten-Johansen
mesh_terms: D000241:Adenosine / Q000008:administration & dosage*; D000700:Analgesics / Q000008:administration & dosage*; D000818:Animals; D001794:Blood Pressure; D002315:Cardiopulmonary Bypass; D004285:Dogs; D006324:Heart Arrest, Induced / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D018047:Receptors, Purinergic P1
chemical_list: D000700:Analgesics; D018047:Receptors, Purinergic P1; D000241:Adenosine