title: Development of cardioplegic solution without potassium: experimental study in rat.
abstract: BACKGROUND
  Myocardial preservation during open heart surgeries and harvesting for transplant are of great importance. The heart at the end of procedure has to resume its functions as soon as possible. All cardioplegic solutions are based on potassium for induction of cardioplegic arrest.
  
  
  OBJECTIVE
  To assess a cardioplegic solution with no potassium addition to the formula with two other commercially available cardioplegic solutions. The comparative assessment was based on cytotoxicity, adenosine triphosphate myocardial preservation, and caspase 3 activity. The tested solution (LIRM) uses low doses of sodium channel blocker (lidocaine), potassium channel opener (cromakalin), and actin/myosin cross bridge inhibitor (2,3-butanedione monoxime).
  
  
  METHODS
  Wistar rats underwent thoracotomy under mechanical ventilation and three different solutions were used for "in situ" perfusion for cardioplegic arrest induction: Custodiol (HTK), Braile (G/A), and LIRM solutions. After cardiac arrest, the hearts were excised and kept in cold storage for 4 hours. After this period, the hearts were assessed with optical light microscopy, myocardial ATP content and caspase 3 activity. All three solutions were evaluated for direct cytotoxicity with L929 and WEHI-164 cells.
  
  
  RESULTS
  The ATP content was higher in the Custodiol group compared to two other solutions (P<0.05). The caspase activity was lower in the HTK group compared to LIRM and G/A solutions (P<0.01). The LIRM solution showed lower caspase activity compared to Braile solution (P<0.01). All solutions showed no cytotoxicity effect after 24 hours of cells exposure to cardioplegic solutions.
  
  
  CONCLUSIONS
  Cardioplegia solutions without potassium are promised and aminoacid addition might be an interesting strategy. More evaluation is necessary for an optimal cardioplegic solution development.
authors.forename: Karla
authors.initials: K
authors.lastname: Reichert
authors.forename: Helison Rafael Pereira do
authors.initials: HR
authors.lastname: Carmo
authors.forename: Fany
authors.initials: F
authors.lastname: Lima
authors.forename: Anali Galluce
authors.initials: AG
authors.lastname: Torina
authors.forename: Karlos Alexandre de Souza
authors.initials: KA
authors.lastname: Vilarinho
authors.forename: Pedro Paulo Martins de
authors.initials: PP
authors.lastname: Oliveira
authors.forename: Lindemberg Mota
authors.initials: LM
authors.lastname: Silveira Filho
authors.forename: Elaine Soraya Barbosa de Oliveira
authors.initials: ES
authors.lastname: Severino
authors.forename: Orlando
authors.initials: O
authors.lastname: Petrucci
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D002314:Cardioplegic Solutions / Q000737:chemistry / Q000494:pharmacology*; D053148:Caspase 3 / Q000032:analysis; D002470:Cell Survival / Q000187:drug effects; D005947:Glucose / Q000737:chemistry / Q000494:pharmacology; D006321:Heart / Q000187:drug effects*; D006324:Heart Arrest, Induced / Q000379:methods*; D008353:Mannitol / Q000737:chemistry / Q000494:pharmacology; D023421:Models, Animal; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D009926:Organ Preservation / Q000379:methods*; D011188:Potassium / Q000737:chemistry / Q000494:pharmacology; D011189:Potassium Chloride / Q000737:chemistry / Q000494:pharmacology; D011343:Procaine / Q000737:chemistry / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015203:Reproducibility of Results; D026941:Sodium Channel Blockers / Q000737:chemistry; D013997:Time Factors
chemical_list: C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D026941:Sodium Channel Blockers; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; C505410:Casp3 protein, rat; D053148:Caspase 3; D005947:Glucose; D011188:Potassium