title: Fluosol cardioplegia results in complete functional recovery: a comparison with blood cardioplegia.
abstract: Blood cardioplegia is considered by many to be the preferred solution for myocardial protection. Proposed benefits include the ability to deliver oxygen and the ability to maintain metabolic substrate stores. However, the decreased capacity of blood to release oxygen at hypothermic conditions as well as the presence of deleterious leukocytes, platelets, and complement may limit complete functional recovery. Fluosol is an asanguineous solution with the ability to bind and release oxygen linearly at low temperatures. Neonatal piglet hearts (24 to 48 hours old) were excised and supported on an isolated, blood-perfused working heart model. After baseline stroke-work index was determined, hearts were arrested with either normocalcemic blood cardioplegia (group 1, n = 8) or normocalcemic Fluosol cardioplegia (group 2, n = 8). Cold cardioplegia was administered at 45 mm Hg every 20 minutes for 2 hours. Hearts were then reperfused with whole blood. Functional recovery, expressed as percent of control stroke-work index, was determined 60 minutes after reperfusion at left atrial pressures of 3, 6, 9, and 12 mm Hg. Functional recovery at 60 minutes was similar between group 1 (95%, 93%, 93%, 88%) and group 2 (100%, 94%, 94%, 95%) at left atrial pressures of 3, 6, 9, and 12 mm Hg, respectively. Mean lactate consumption 5 minutes after reperfusion was significantly greater (p = 0.0001) in group 1 (31.8 +/- 6.3 micrograms.min-1 x g-1) than in group 2 (-0.59 +/- 0.1 microgram.min-1 x g-1), indicating superior metabolic recovery in the blood cardioplegia hearts. Edema formation, as determined both by water content (group 1, 81.10%; group 2, 81.63%) and by electron microscopy, was not significantly different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Surgery, University of California, Los Angeles.
authors.forename: J M
authors.initials: JM
authors.lastname: Pearl
authors.forename: H
authors.initials: H
authors.lastname: Laks
authors.forename: D C
authors.initials: DC
authors.lastname: Drinkwater
authors.forename: A
authors.initials: A
authors.lastname: Meneshian
authors.forename: S M
authors.initials: SM
authors.lastname: Martin
authors.forename: M
authors.initials: M
authors.lastname: Curzan
authors.forename: P A
authors.initials: PA
authors.lastname: Chang
mesh_terms: D000255:Adenosine Triphosphate / Q000737:chemistry; D000818:Animals; D001769:Blood; D001774:Blood Chemical Analysis; D004353:Drug Evaluation, Preclinical; D004487:Edema / Q000175:diagnosis / Q000473:pathology; D004734:Energy Metabolism; D005466:Fluorocarbons / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006324:Heart Arrest, Induced / Q000379:methods* / Q000592:standards; D006439:Hemodynamics; D007773:Lactates / Q000737:chemistry / Q000378:metabolism; D019344:Lactic Acid; D008854:Microscopy, Electron; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D009929:Organ Size; D010725:Phosphocreatine / Q000737:chemistry; D013318:Stroke Volume; D013552:Swine; D014655:Vascular Resistance
chemical_list: D005466:Fluorocarbons; D007773:Lactates; D010725:Phosphocreatine; D019344:Lactic Acid; C050455:fluosol; D000255:Adenosine Triphosphate