title: New HTK-N46B cardioplegia provides superior protection during ischemia/reperfusion in failing hearts.
abstract: OBJECTIVE
  The aim of this paper was to improve operative outcome during open-heart surgery in patients with failing hearts, the composition of cardioplegic solutions has to be further optimized. HTK-N46b, a novel cardioplegic solution, has been developed for efficient protection of the energy state of myocytes as well as endothelial cells. Aim of this study is the evaluation of HTK-N46b in comparison to its precursor Custodiol® (HTK) in failing rat hearts undergoing ischemia/reperfusion.
  
  
  METHODS
  In male Sprague Dawley rats myocardial infarction (MI) was induced by LAD ligation. Six weeks after MI cardiac function was determined by transthoracic echocardiography. Sixteen animals with hearts showing a fractional shortening <25% were randomly assigned to two groups, HTK (N.=8) and HTK-N46b (N.=8). After excision hearts were evaluated in an erythrocyte-perfused isolated working heart model. Cold ischemia (4°C) for 60 minutes was followed by 45 minutes of reperfusion. Cardiac arrest was induced either with HTK or HTK-N46b at the beginning of ischemia.
  
  
  RESULTS
  At similar preischemic fractional shortening (HTK-N46b: 14.41±1.83% vs. HTK: 14.91±1.92%; NS) postischemic recovery of stroke volume and stroke work were significantly improved in the HTK-N46b rat hearts compared to HTK. Concerning recovery of coronary flow there was no difference between groups. At the end of reperfusion the HTK-N46b protected group revealed higher levels of ATP (HTK-N46b: 22.01±0.89 nmol/mg protein vs. HTK: 16.83±1.72 nmol/mg protein; P<0.05) and energy charge (HTK-N46b: 0.82±0.02 vs. HTK: 0.74±0.02; P<0.05).
  
  
  CONCLUSIONS
  HTK-N46b showed superior cardioprotective properties according to postischemic hemodynamic recovery and biochemical markers compared to HTK in failing rat hearts.
authors: Ludwig Boltzmann Cluster for Cardiovascular Research, Medical University Vienna, Vienna, Austria.
authors: K
authors: K
authors: Trescher
authors: M
authors: M
authors: Hasun
authors: A
authors: A
authors: Baumgartner
authors: W
authors: W
authors: Dietl
authors: M
authors: M
authors: Wolfsberger
authors: S
authors: S
authors: Hallström
authors: B K
authors: BK
authors: Podesser
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D006348:Cardiac Surgical Procedures / Q000379:methods*; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D004195:Disease Models, Animal; D005947:Glucose / Q000494:pharmacology; D006324:Heart Arrest, Induced / Q000379:methods*; D006333:Heart Failure / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D011189:Potassium Chloride / Q000494:pharmacology; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D005947:Glucose