title: Fluorocarbon simulation of myocardial ischaemia and reperfusion: studies of relationships between force and intracellular calcium.
abstract: OBJECTIVE
  The aim was to compare the effects of simulated ischaemia-reperfusion with those of hypoxia-reoxygenation in isolated muscle preparations from the ferret right ventricle.
  
  
  METHODS
  Ischaemia was simulated using fluorocarbon immersion plus hypoxia. Intracellular calcium transients were determined from aequorin luminescence during isometric contractions.
  
  
  RESULTS
  Hypoxia in fluorocarbon and physiological saline solution resulted in a similar reversible depression of the peak of the calcium transient. Peak active tension, however, was more depressed in fluorocarbon than in physiological salt solution. The dissociation between peak light and peak active tension was most pronounced on reoxygenation, with near complete recovery of peak light, while there was little recovery of tension in fluorocarbon. When fluorocarbon was then replaced by physiological salt solution, peak active tension recovered promptly. A prolongation of the decay of the calcium transient was seen in both fluorocarbon and physiological salt solution during hypoxia, which shortened promptly on reoxygenation. The time to the peak of the calcium transient was most prolonged during hypoxia in fluorocarbon and there was gradual recovery on reoxygenation.
  
  
  CONCLUSIONS
  While some changes in the calcium transient during simulated ischaemia are rapidly reversible with reoxygenation (in fluorocarbon), suggesting an effect of hypoxia, others are incompletely reversed or only reversed with physiological salt solution, suggesting an effect of metabolite accumulation. The pronounced dissociation between peak light and peak active tension during reoxygenation in fluorocarbon is promptly reversed by changing to physiological salt solution, suggesting that metabolite retention in the postischaemic period may contribute to depressed myocardial function after reperfusion.
authors.affiliation: Department of Veterans Affairs Medical Center, Boston, MA 02130.
authors.forename: O H
authors.initials: OH
authors.lastname: Bing
authors.forename: Y
authors.initials: Y
authors.lastname: Kihara
authors.forename: W W
authors.initials: WW
authors.lastname: Brooks
authors.forename: C H
authors.initials: CH
authors.lastname: Conrad
authors.forename: J P
authors.initials: JP
authors.lastname: Morgan
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000187:drug effects; D005289:Ferrets; D005466:Fluorocarbons / Q000494:pharmacology*; D000860:Hypoxia / Q000378:metabolism; D007424:Intracellular Fluid / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*
chemical_list: D005466:Fluorocarbons; D007773:Lactates; D019344:Lactic Acid; D000252:Calcium-Transporting ATPases; D002118:Calcium