title: Replacing potassium with nicorandil in cold St. Thomas' Hospital cardioplegia improves preservation of energetics and function in pig hearts.
abstract: BACKGROUND
  To determine whether the adenosine triphosphate-sensitive potassium channel opener nicorandil, instead of potassium in cold crystalloid cardioplegia, may enhance cardioprotection, crystalloid cardioplegia with nicorandil, magnesium, and procaine was compared with standard crystalloid cardioplegia in terms of left ventricular performance and efficiency.
  
  
  METHODS
  Sixteen pigs were randomly assigned to receive cold hyperkalemic crystalloid cardioplegia (n = 8) or nicorandil in cold saline (n = 8). Cold (4 degrees C) cardioplegic solutions were given antegradely and intermittently, with a cross-clamp time of 60 minutes. The preload recruitable stroke work relationship (PRSW), pressure-volume area (PVA), and myocardial oxygen consumption (MVO(2)) were calculated at baseline and at one and two hours following cross-clamp release, using combined pressure-volume conductance catheters, coronary flow probes, and O(2)-content differences.
  
  
  RESULTS
  The left ventricular contractility expressed in PRSW was reduced to 58% (standard deviation [SD]: 20) of baseline in the crystalloid group and to 89% (SD: 20) in the nicorandil group two hours after cross-clamp release (p = 0.044). The slope of the MVO(2)-PVA relationship increased in the crystalloid group from 1.59 (SD: 0.22) before cardioplegia to 2.55 (SD: 0.73) afterwards, significantly more than in the nicorandil group, where the slope changed from 1.69 (SD: 0.30) to 1.95 (SD: 0.47) (p = 0.027).
  
  
  CONCLUSIONS
  Nicorandil in a crystalloid cardioplegic solution was easily employed and contractility was significantly better than after standard hyperkalemic cardioplegia. The smaller shift of the slope in the MVO(2)-PVA relationship in the nicorandil group shows improved efficiency in oxygen to mechanical transfer compared with the crystalloid group.
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway. tors@fagmed.uit.no
authors.forename: Tor
authors.initials: T
authors.lastname: Steensrud
authors.forename: Dag
authors.initials: D
authors.lastname: Nordhaug
authors.forename: Kjell V
authors.initials: KV
authors.lastname: Husnes
authors.forename: Ebrahim
authors.initials: E
authors.lastname: Aghajani
authors.forename: Dag G
authors.initials: DG
authors.lastname: Sørlie
mesh_terms: D000818:Animals; D001639:Bicarbonates; D002122:Calcium Chloride; D002314:Cardioplegic Solutions / Q000737:chemistry; D003080:Cold Temperature; D004734:Energy Metabolism; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D008274:Magnesium; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D011188:Potassium; D015221:Potassium Channels / Q000378:metabolism; D011189:Potassium Chloride; D011343:Procaine; D012965:Sodium Chloride; D013552:Swine
chemical_list: D001639:Bicarbonates; D002314:Cardioplegic Solutions; D015221:Potassium Channels; C041711:St. Thomas' Hospital cardioplegic solution; D012965:Sodium Chloride; D011343:Procaine; D011189:Potassium Chloride; D008274:Magnesium; D002122:Calcium Chloride; D011188:Potassium