title: Diastolic properties, myocardial water content, and histologic condition of the rat left ventricle: effect of varied osmolarity of a coronary perfusate.
abstract: BACKGROUND
  Although myocardial edema is known to impair diastolic filling of the left ventricle, the interrelation of edema, histologic condition, and function has not been quantitated sufficiently for extrapolation to studies of multifactorial influences on diastolic properties.
  
  
  METHODS
  Accordingly, ACI rat hearts arrested at 4 degrees C underwent coronary artery perfusion with a cardioplegia solution that was either unaltered (288 mOsm/L, P288 group, n = 6), diluted (144 mOsm/L, P144 group, n = 6), or concentrated (380 mOsm/L, P380 group, n = 6). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. Myocardial samples were fixed in varying dilutions of glutaraldehyde. After dehydration and paraffin embedding, edema was graded subjectively (0 to 5), and myocardial interstitial spaces were determined by use of a semiquantitative method.
  
  
  RESULTS
  Mean normalized left ventricular filling volume at 20 mm Hg filling pressure in the P144 group, 189 +/- 16 microliters (SEM), was reduced versus both the P288 (278 +/- 26 microliters) and the P380 (332 +/- 18 microliters) groups (p < 0.05, ANOVA). Mean myocardial water content in the P144 group, 80.7% +/- 1%, was increased versus the P380 (76.7% +/- 0.4%, p < 0.05) but not versus the P288 group (78.4% +/- 0.8%). In hearts preserved with 2.5% glutaraldehyde, mean edema grade and interstitial space in the P144 group (4.0 +/- 0.3) were increased versus the P380 (1.8 +/- 0.3, p < 0.05) but not the P288 group (2.7 +/- 0.5). Derived linear regressions relate water content to filling volume and histologic condition.
  
  
  CONCLUSIONS
  Coronary perfusate osmolarity is thus associated with predictable changes in myocardial water content, left ventricular filling volume, and edema. These correlations allow definition of new hypotheses for the study of cardiac allograft rejection in patients and experimental animals.
authors.affiliation: Department of Surgery, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA.
authors.forename: Y M
authors.initials: YM
authors.lastname: Carter
authors.forename: C X
authors.initials: CX
authors.lastname: Jia
authors.forename: P F
authors.initials: PF
authors.lastname: Soto
authors.forename: J P
authors.initials: JP
authors.lastname: Starr
authors.forename: D G
authors.initials: DG
authors.lastname: Rabkin
authors.forename: D T
authors.initials: DT
authors.lastname: Hsu
authors.forename: P E
authors.initials: PE
authors.lastname: Fisher
authors.forename: H M
authors.initials: HM
authors.lastname: Spotnitz
mesh_terms: D000818:Animals; D001834:Body Water / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism*; D003971:Diastole; D004489:Edema, Cardiac / Q000378:metabolism / Q000473:pathology; D005976:Glutaral / Q000494:pharmacology; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism*; D009994:Osmolar Concentration; D010477:Perfusion; D051381:Rats
chemical_list: D005976:Glutaral