title: Myocardial protection against global ischemia with Krebs-Henseleit buffer-based cardioplegic solution.
abstract: BACKGROUND
  The Krebs-Henseleit buffer is the best perfusion solution for isolated mammalian hearts. We hypothesized that a Krebs-Henseleit buffer-based cardioplegic solution might provide better myocardial protection than well-known crystalloid cardioplegic solutions because of its optimal electrolyte and glucose levels, presence of buffer systems, and mild hyperosmolarity.
  
  
  METHODS
  Isolated Langendorff-perfused rat hearts were subjected to either global ischemia without cardioplegia (controls) or cardioplegic arrest for either 60 or 180 min, followed by 120 min of reperfusion. The modified Krebs-Henseleit buffer-based cardioplegic solution (mKHB) and St. Thomas' Hospital solution No. 2 (STH2) were studied. During global ischemia, the temperatures of the heart and the cardioplegic solutions were maintained at either 37°C (60 min of ischemia) or 22°C (moderate hypothermia, 180 min of ischemia). Hemodynamic parameters were registered throughout the experiments. The infarct size was determined through histochemical examination.
  
  
  RESULTS
  Cardioplegia with the mKHB solution at moderate hypothermia resulted in a minimal infarct size (5 ± 3%) compared to that in the controls and STH2 solution (35 ± 7% and 19 ± 9%, respectively; P < 0.001, for both groups vs. the mKHB group). In contrast to the control and STH2-treated hearts, no ischemic contracture was registered in the mKHB group during the 180-min global ischemia. At normothermia, the infarct sizes were 4 ± 3%, 72 ± 6%, and 70 ± 12% in the mKHB, controls, and STH2 groups, respectively (P < 0.0001). In addition, cardioplegia with mKHB at normothermia prevented ischemic contracture and improved the postischemic functional recovery of the left ventricle (P < 0.001, vs. STH2).
  
  
  CONCLUSIONS
  The data suggest that the Krebs-Henseleit buffer-based cardioplegic might be superior to the standard crystalloid solution (STH2).
authors.affiliation: Institute of Experimental Medicine, V, A, Almazov Federal Heart, Blood and Endocrinology Centre, Saint Petersburg, Russia.
authors.forename: Sarkis M
authors.initials: SM
authors.lastname: Minasian
authors.forename: Michael M
authors.initials: MM
authors.lastname: Galagudza
authors.forename: Yuri V
authors.initials: YV
authors.lastname: Dmitriev
authors.forename: Dmitry I
authors.initials: DI
authors.lastname: Kurapeev
authors.forename: Timur D
authors.initials: TD
authors.lastname: Vlasov
mesh_terms: D000818:Animals; D002314:Cardioplegic Solutions / Q000737:chemistry / Q000494:pharmacology*; D002316:Cardiotonic Agents / Q000737:chemistry / Q000494:pharmacology*; D005947:Glucose / Q000737:chemistry / Q000494:pharmacology; D006323:Heart Arrest; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric; D014325:Tromethamine / Q000737:chemistry / Q000494:pharmacology; D014693:Ventricular Fibrillation; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D002314:Cardioplegic Solutions; D002316:Cardiotonic Agents; C074097:Krebs-Henseleit solution; D014325:Tromethamine; D005947:Glucose
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