title: Coronary autoregulation protects against harmful effects of commonly used cardioplegia delivery pressure.
abstract: OBJECTIVE
  Hearts or parts of hearts are often ischemic prior to infusion of the cardioplegic solution and have a more or less dilated coronary bed. We made an investigation whether coronary dilation just prior to induction of cardiac arrest by aortic clamping and infusion of crystalloid cardioplegic solution would influence cardioprotection.
  
  
  METHODS
  Isolated buffer-perfused rat hearts (100 cm H2O pressure (= 73.5 mmHg), 37 degrees C) were used. After a stabilization period the perfusion of 8 rats (group 1) was stopped and the hearts arrested with 5 ml CS (100 cm H2O, 12 degrees C). Equal amounts of cardioplegic solution were then delivered every 20 minutes for the entire 3 1/2 hour hypothermic ischemic period. Following ischemia the hearts were reperfused for 60 minutes. In group 2 (n = 8) 1 ml 10(-2) mmol Papaverine was given into the aortic root just prior to the first cardioplegic solution infusion in order to induce coronary vasodilation. The procedure was identical in the two groups during ischemia and reperfusion.
  
  
  RESULTS
  During the ischemic period coronary resistance increased in group 2. During reperfusion group 2 had lower coronary flow (P = 0.001), left ventricle developed pressure (P = 0.002) and a higher creatine kinase release (P = 0.003) than group 1 hearts. Group 2 also had a lower adenosine-triphosphate (6.51 +/- 0.40 mumol.g-1 and 14.03 +/- 0.59 mumol.g-1, respectively, P = 0.011), creatine phosphate (24.70 +/- 1.02 mumol.g-1 and 36.50 +/- 1.31 mumol.g-1, respectively, P = 0.020) and a larger fall in dry/wet-weight ratio (1.7 +/- 0.4 and 0.8 +/- 0.5, respectively, P = 0.043).
  
  
  CONCLUSIONS
  Vasodilation (i.e. ischemia) just prior to infusion of crystalloid cardioplegic solution may impair myocardial protection even when the cardioplegic solution is delivered at a relatively low and presumably safe pressure.
authors.affiliation: Department of Surgery, University of Tromsø, Regionsykehuset i Tromsø, Norway.
authors.forename: O
authors.initials: O
authors.lastname: Irtun
authors.forename: D G
authors.initials: DG
authors.lastname: Sørlie
mesh_terms: D000818:Animals; D002314:Cardioplegic Solutions / Q000008:administration & dosage*; D003326:Coronary Circulation / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology; D006706:Homeostasis / Q000502:physiology*; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D002314:Cardioplegic Solutions