title: Rabbit ventricular myocyte volume changes as a direct result of crystalloid cardioplegia in congestive heart failure induced by aortic regurgitation.
abstract: OBJECTIVE
  We hypothesized that the cell volume of ventricular myocytes isolated from hearts in volume-overload congestive failure would respond differently to hypothermic cardioplegia than would sham-operated cohorts.
  
  
  METHODS
  Adult rabbits underwent either valvotomy and aortic regurgitation-induced heart failure or sham surgery. Congestive failure was confirmed clinically and by means of echocardiography. Cell volumes of isolated myocytes were measured by digital video microscopy. After equilibration in 37 degrees C physiologic solution, cells were suprafused with 9 degrees C standard or low-Cl(-) St Thomas' Hospital solution followed by reperfusion in 37 degrees C physiologic solution.
  
  
  RESULTS
  Exposure to cold St Thomas' Hospital solution for 20 minutes caused sham myocytes to swell by 8% (n = 9); cell volumes fully recovered on normothermic reperfusion. In contrast, congestive failure myocytes (n = 9) maintained their cell volume in cold St Thomas' Hospital solution and during reperfusion. Lowering the [K(+)][Cl(-)] product of St Thomas' Hospital solution by partially replacing Cl(-) with an impermeant anion prevented cellular edema in the sham group (n = 8) but caused a 4% swelling in failure myocytes (n = 10) on reperfusion. Osmotically shrinking the failure cells (n = 9) converted their behavior to that of sham cells.
  
  
  CONCLUSIONS
  In the absence of ischemia, congestive failure myocytes are less sensitive to cardioplegia-induced edema than sham cells. Low-Cl(-) cardioplegia, which prevents edema and protects the normal heart, induced swelling and may be detrimental in myopathic hearts. Differences in volume regulation in failure and sham myocytes may be due to activation of volume-sensitive channels that are turned off by osmotic shrinkage.
authors.affiliation: Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA.
authors.forename: J S
authors.initials: JS
authors.lastname: Danetz
authors.forename: R D
authors.initials: RD
authors.lastname: Davies
authors.forename: H F
authors.initials: HF
authors.lastname: Clemo
authors.forename: C M
authors.initials: CM
authors.lastname: Baumgarten
mesh_terms: D000818:Animals; D001022:Aortic Valve Insufficiency / Q000150:complications*; D001639:Bicarbonates; D002122:Calcium Chloride; D002314:Cardioplegic Solutions; D048429:Cell Size; D004452:Echocardiography; D006324:Heart Arrest, Induced; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D006352:Heart Ventricles / Q000473:pathology*; D066298:In Vitro Techniques; D008274:Magnesium; D018715:Microscopy, Video; D011189:Potassium Chloride; D011817:Rabbits; D012965:Sodium Chloride
chemical_list: D001639:Bicarbonates; D002314:Cardioplegic Solutions; C041711:St. Thomas' Hospital cardioplegic solution; D012965:Sodium Chloride; D011189:Potassium Chloride; D008274:Magnesium; D002122:Calcium Chloride