title: Effect of cardioplegia infusion pressure on coronary artery endothelium and cardiac mechanical function.
abstract: OBJECTIVE
  Monitoring of cardioplegia infusion pressure may be important, particularly in immature hearts and in hearts without coronary artery disease. We have investigated the effects of infusion pressure on the preservation of the isolated rat heart.
  
  
  METHODS
  Hearts (five in each group) were subjected to a single (20 ml) infusion of St. Thomas' Hospital cardioplegic solution at pressures of 60, 120, 180 and 240 cmH2O (44-176 mmHg), followed by 30 min of hypothermic (20 degrees C) ischemia.
  
  
  RESULTS
  Mean recovery of cardiac output (expressed as a percentage of its preischemic value) decreased with increasing infusion pressure: 96.1 +/- 0.6%, 87.3 +/- 2.1% (P < 0.05 vs. 60 cmH2O), 79.3 +/- 2.8% (P < 0.05 vs. 120 cmH2O), 72.0 +/- 3.0% (not significant vs. 180 cmH2O), respectively. Endothelial function, as assessed by pre- and post-ischemic ability to secrete NO in response to 5-hydroxytryptamine, remained relatively normal after infusion at 60 cmH2O, but changed from vasodilation to vasoconstriction after infusion at 240 cmH2O. Electron microscopy revealed mild endothelial damage after infusion at 240 cmH2O, which was greatly exacerbated by reperfusion and was accompanied by regions of myocyte damage compatible with reperfusion of unprotected myocardium. The relationship between cardioplegia infusion pressure and infusion time was not linear and implied that infusion pressures greater than 120 cmH2O caused vascular smooth muscle constriction.
  
  
  CONCLUSIONS
  These results suggest that even mildly raised cardioplegia infusion pressures may be detrimental to cardiac preservation and the effects are possibly mediated through endothelial damage and pressure-induced coronary vasoconstriction.
authors.affiliation: Department of Cardiothoracic Surgery, National Heart and Lung Institute, Harefield Hospital, Middlesex, UK.
authors.forename: O
authors.initials: O
authors.lastname: Katayama
authors.forename: M
authors.initials: M
authors.lastname: Amrani
authors.forename: S
authors.initials: S
authors.lastname: Ledingham
authors.forename: J
authors.initials: J
authors.lastname: Jayakumar
authors.forename: R T
authors.initials: RT
authors.lastname: Smolenski
authors.forename: N
authors.initials: N
authors.lastname: Severs
authors.forename: S
authors.initials: S
authors.lastname: Rothery
authors.forename: M H
authors.initials: MH
authors.lastname: Yacoub
mesh_terms: D000818:Animals; D001469:Barotrauma / Q000473:pathology*; D001639:Bicarbonates / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003331:Coronary Vessels / Q000293:injuries* / Q000473:pathology; D004730:Endothelium, Vascular / Q000293:injuries* / Q000473:pathology; D006874:Hydrostatic Pressure; D008274:Magnesium / Q000494:pharmacology; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D012965:Sodium Chloride / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology
chemical_list: D001639:Bicarbonates; D002314:Cardioplegic Solutions; C041711:St. Thomas' Hospital cardioplegic solution; D012965:Sodium Chloride; D011189:Potassium Chloride; D008274:Magnesium; D002122:Calcium Chloride