title: Controlled postcardioplegia reperfusion: mechanism for attenuation of reperfusion injury.
abstract: OBJECTIVE
  Controlled reperfusion and secondary cardioplegia are used to minimize reperfusion injury. The mechanisms for their benefit are incompletely defined and may include attenuation of myocyte sodium uptake.
  
  
  METHODS
  Pigs had 1 hour of cardioplegic arrest followed by reperfusion with blood (control) or warm cardioplegic solution followed by blood (test). Reperfusion injury in the control and test groups was quantified by measuring changes of intramyocyte ion content with atomic absorption spectrometry and by analyzing electrophysiologic recovery from recordings of reperfusion arrhythmias.
  
  
  RESULTS
  Control animals had an increase in intramyocyte sodium content at 5 minutes after initiating reperfusion (+20.2 micromol/g dry weight, P <.04), whereas the test group had an insignificant decrease (-14.0 micromol/g dry weight, P =.33). The first rhythm after initiating reperfusion was more often ventricular fibrillation in the control group (100% vs 50%, P <.02), and the control group required more defibrillations to establish a nonfibrillating rhythm (4.5 +/- 1.2 vs 1.1 +/- 0.3, P <.03).
  
  
  CONCLUSIONS
  Controlled reperfusion eliminated the increase in intramyocyte sodium that was observed in the control group at 5 minutes after cardioplegic arrest. This improvement in myocyte ion homeostasis during postcardioplegia reperfusion was associated with fewer reperfusion arrhythmias. These data support the hypothesis that attenuation of myocyte sodium gain during postischemic reperfusion is a mechanism by which controlled reperfusion and secondary cardioplegia are beneficial.
authors.affiliation: Department of Surgery, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. wholman@holman.cvsr.uab.edu
authors.forename: W L
authors.initials: WL
authors.lastname: Holman
authors.forename: J L
authors.initials: JL
authors.lastname: Skinner
authors.forename: C R
authors.initials: CR
authors.lastname: Killingsworth
authors.forename: J M
authors.initials: JM
authors.lastname: Rogers
authors.forename: S
authors.initials: S
authors.lastname: Melnick
authors.forename: R E
authors.initials: RE
authors.lastname: Ideker
authors.forename: S B
authors.initials: SB
authors.lastname: Digerness
mesh_terms: D000818:Animals; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006324:Heart Arrest, Induced / Q000379:methods; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000628:therapy*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D013552:Swine
chemical_list: D002314:Cardioplegic Solutions