title: Effect of improved myocardial protection on edema and diastolic properties of the rat left ventricle during acute allograft rejection.
abstract: BACKGROUND
  Studies of myocardial edema and diastolic dysfunction in rat heart transplantation have been flawed by ischemic injury. This study uses improved methods to prevent ischemic contracture.
  
  
  METHODS
  Hearts of 30 ACI rats were transplanted into the abdomen of Lewis rats by use of cold University of Wisconsin solution for improved preservation. Left ventricular diastolic properties were expressed as volume at standardized pressure intervals.
  
  
  RESULTS
  On posttransplantation day 3, mean left ventricular volume at 15 mm Hg in allografts (290 +/- 9 microl, SEM) was not significantly different vs isografts (299 +/- 32 microl), allografts on day 0 (337 +/- 28 ml) or day 1 (324 +/- 20 microl), or native hearts (334 +/- 19 microl). However, volume was reduced to 173 +/- 17 microl on day 4 and to 70 +/- 23 microl on day 5 (p < 0.05). Similar findings were obtained for volume at 5 and 10 mm Hg. Allograft myocardial water content on day 3, 76.3% +/- 5%, similar to allografts on day 0 and 1 and to isografts on day 3, increased to 77.6% +/- 8% on day 4 (NS) and 79.4% +/- 6% on day 5 (p < 0.05 vs day 0). Histologically, rejection in allografts was mild on day 3, moderate on day 4, and severe on day 5.
  
  
  CONCLUSIONS
  Reduced left ventricular filling volume during rejection is only partially explained by edema. Abnormalities of diastolic properties previously attributed to the unloaded state of nonworking heart models may actually reflect inadequate peritransplantation myocardial protection.
authors.affiliation: Department of Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
authors.forename: P F
authors.initials: PF
authors.lastname: Soto
authors.forename: C X
authors.initials: CX
authors.lastname: Jia
authors.forename: Y M
authors.initials: YM
authors.lastname: Carter
authors.forename: D
authors.initials: D
authors.lastname: Rabkin
authors.forename: J P
authors.initials: JP
authors.lastname: Starr
authors.forename: M M
authors.initials: MM
authors.lastname: Amirhamzeh
authors.forename: D T
authors.initials: DT
authors.lastname: Hsu
authors.forename: R
authors.initials: R
authors.lastname: Sciacca
authors.forename: P E
authors.initials: PE
authors.lastname: Fisher
authors.forename: H M
authors.initials: HM
authors.lastname: Spotnitz
mesh_terms: D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002314:Cardioplegic Solutions; D003971:Diastole; D004487:Edema / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D005978:Glutathione; D006084:Graft Rejection / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D016027:Heart Transplantation; D007328:Insulin; D008297:Male; D009926:Organ Preservation; D019188:Organ Preservation Solutions; D011887:Raffinose; D051381:Rats; D011912:Rats, Inbred ACI; D011917:Rats, Inbred Lew; D016042:Transplantation, Heterotopic; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*
chemical_list: D002314:Cardioplegic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose