title: Ischemia affects cardiac proteins in healthy animals less severely than in human patients.
abstract: BACKGROUND
  Recently, our group showed that in human hearts proteins are extremely sensitive to ischemic injury. The purpose of this investigation was to evaluate the effects of ischemia on contractile and cytoskeletal proteins in rabbit and pig hearts and to compare these findings with those obtained in humans.
  
  
  METHODS
  Rabbit hearts were arrested by perfusion with Euro-Collins solution at different temperatures. Hearts perfused with buffer served as controls. Tissue samples were incubated for varying time intervals and processed for immunohistochemistry and electron microscopy. Porcine hearts were treated in the same manner. Changes in the localization of myosin, desmin, and tropomyosin antibodies were evaluated and the degree of ischemic injury was determined by electron microscopy.
  
  
  RESULTS
  Healthy animal hearts tolerate ischemia better than human hearts. Cardiac proteins are more sensitive to ischemia than the ultrastructural cellular organelles. Temperatures as low as 0 degree C produce more cell damage than 4 degrees C and should therefore be avoided. The Euro-Collins solution protects the myocardium better than buffer.
  
  
  CONCLUSIONS
  We conclude that healthy animal hearts are more resistant to ischemia than diseased human hearts and that results from experimental studies should be interpreted with caution with regard to the human situation.
authors.affiliation: Max-Planck-Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Bad Nauheim, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Sprengel
authors.forename: B
authors.initials: B
authors.lastname: Münkel
authors.forename: F
authors.initials: F
authors.lastname: Robicsek
authors.forename: T N
authors.initials: TN
authors.lastname: Masters
authors.forename: J
authors.initials: J
authors.lastname: Schaper
mesh_terms: D000818:Animals; D002021:Buffers; D002314:Cardioplegic Solutions; D003080:Cold Temperature / Q000009:adverse effects; D003598:Cytoskeletal Proteins / Q000378:metabolism* / Q000648:ultrastructure; D003893:Desmin / Q000378:metabolism / Q000648:ultrastructure; D004195:Disease Models, Animal; D006801:Humans; D006982:Hypertonic Solutions; D007150:Immunohistochemistry; D008297:Male; D008854:Microscopy, Electron; D009124:Muscle Proteins / Q000378:metabolism* / Q000648:ultrastructure; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009218:Myosins / Q000378:metabolism / Q000648:ultrastructure; D015388:Organelles / Q000378:metabolism / Q000648:ultrastructure; D011817:Rabbits; D013552:Swine; D013696:Temperature; D014335:Tropomyosin / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D002021:Buffers; D002314:Cardioplegic Solutions; D003598:Cytoskeletal Proteins; D003893:Desmin; C037096:Euro-Collins' solution; D006982:Hypertonic Solutions; D009124:Muscle Proteins; D014335:Tropomyosin; D009218:Myosins