title: Beneficial effect of fluorocarbon reperfusion on postoperative cardiac dysfunction of transplanted heart.
abstract: Fluosol DA 20% (Fluosol) perfusion was used to protect ischemic donor hearts of mongrel dogs from reperfusion injury. Fifteen orthotopically transplanted hearts, eight in the control group and seven in the Fluosol group, were studied for 3 hours after weaning from cardiopulmonary bypass. Donor hearts were arrested and immersed in 4 degrees C St. Thomas's Hospital Solution for 4 hours. The mean total ischemic time was 323 minutes (range, 298 to 345 minutes). In the Fluosol group, 200 ml of oxygenated Fluosol (37 degrees C; PO2 650 mm Hg; PCO2 35 mm Hg) was infused into the aortic root at approximately 100 ml/min just before aortic unclamping. Coronary sinus blood was analyzed for the MB fraction of creatine kinase, reduced glutathione, and oxidized glutathione. Hemodynamic and biochemical results were obtained at 30 minutes, 1 hour, and 3 hours after bypass. In the control group, during the second 30 minutes of the period after bypass, left ventricular end-diastolic pressure and stroke volume showed progressive deterioration, 54.8% increased (p less than 0.01) and 28.4% decreased (p less than 0.05), respectively. The MB fraction of creatine kinase and oxidized glutathione were increased, and reduced glutathione had declined, from 39.3 to 135.3 IU/L (p less than 0.01), from 28.0 to 33.4 micrograms/ml (p less than 0.05) and from 4.4 to 2.5 micrograms/ml (p less than 0.01), respectively. These parameters failed to recover during the next 2 hours, and massive mitochondrial degeneration was observed by electron microscopy. In the Fluosol group, these parameters maintained their baseline values, and electron microscopy showed well-preserved mitochondria. The data suggested that, in the control group, initial mitochondrial dysfunction was profound, persistent for at least 3 hours, and associated with membrane hyperpermeability, leading to cardiac dysfunction. Oxygenated Fluosol perfusion better preserved cardiac and mitochondrial function.
authors.affiliation: Department of Surgery, Saitama Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Genda
authors.forename: I
authors.initials: I
authors.lastname: Hirata
authors.forename: M
authors.initials: M
authors.lastname: Shimada
authors.forename: T
authors.initials: T
authors.lastname: Shibata
authors.forename: T
authors.initials: T
authors.lastname: Ueda
authors.forename: R
authors.initials: R
authors.lastname: Omoto
mesh_terms: D000818:Animals; D001639:Bicarbonates; D001802:Blood Substitutes / Q000494:pharmacology*; D002122:Calcium Chloride; D002314:Cardioplegic Solutions; D003402:Creatine Kinase / Q000378:metabolism; D004285:Dogs; D004338:Drug Combinations; D005466:Fluorocarbons / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D016027:Heart Transplantation / Q000502:physiology*; D006895:Hydroxyethyl Starch Derivatives; D007527:Isoenzymes; D008274:Magnesium; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D011189:Potassium Chloride; D012965:Sodium Chloride; D013997:Time Factors
chemical_list: D001639:Bicarbonates; D001802:Blood Substitutes; D002314:Cardioplegic Solutions; D004338:Drug Combinations; D005466:Fluorocarbons; D006895:Hydroxyethyl Starch Derivatives; D007527:Isoenzymes; C041711:St. Thomas' Hospital cardioplegic solution; D012965:Sodium Chloride; D011189:Potassium Chloride; C017323:glucose, glycerol, hydroxyethyl starch, perfluorodecalin, perfluorotripropylamine, pluronic F-68, salts, yolk phospholipids drug combination; D003402:Creatine Kinase; D005978:Glutathione; D008274:Magnesium; D002122:Calcium Chloride