title: Effects of isotonic crystalloid resuscitation on fluid compartments in hemorrhaged rats.
abstract: Redistribution of fluid after isotonic crystalloid resuscitation from hemorrhage may result not only in interstitial edema but also in cellular edema. We measured the extent to which shock and resuscitation altered fluid compartments in different organs. Nephrectomized, anesthetized rats were randomly divided into a Control group (n = 10) and a Hemorrhage plus Resuscitation group (H/R, n = 10). Rats were subjected to 60 min hemorrhagic hypotension (50 mmHg) followed by a 60 min resuscitation period with .9% NaCl infused as needed to maintain mean arterial pressure at 80% of baseline. A 2 h 51Cr-EDTA distribution space was used to estimate extracellular fluid volume (ECFV) and a 5 min 125I-albumin distribution space was used to measure plasma volume (PV). After euthanasia, total tissue water was measured by wet/dry weight analysis and interstitial fluid volume (ISFV) and cell water were calculated for selected organs. Resuscitation volume was two times the shed blood volume, but resulted in a PV equal to that of the Controls. There were no significant differences in whole animal ECFV or ISFV, although the mean values in the H/R group were greater than that of the Control group. The mean values for total tissue water for each tissue in the H/R group were larger than the respective means of the Control tissues but was significantly greater for only the heart (3639 +/- 56 microL/g vs. 3493 +/- 24 microL/g, mean +/- S.E., p < .05). In all H/R tissues, mean values for ISFV were also larger; this difference was significant for only the liver and small intestines (744 +/- 62 vs. 518 +/- 29 microL/g and 1117 +/- 155 vs. 706 +/- 58 microL/g, respectively). Heart cell water was significantly larger in H/R than Controls (2900 +/- 60 microL/g vs. 2738 +/- 27 microL/g). These data suggest that resuscitation of hemorrhage using isotonic crystalloid normalizes overall PV and ECFV but also causes interstitial expansion in selected gut tissues and cellular edema in the heart.
authors.affiliation: Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA.
authors.forename: P F
authors.initials: PF
authors.lastname: Moon
authors.forename: M A
authors.initials: MA
authors.lastname: Hollyfield-Gilbert
authors.forename: T L
authors.initials: TL
authors.lastname: Myers
authors.forename: G C
authors.initials: GC
authors.lastname: Kramer
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004487:Edema; D006339:Heart Rate; D006400:Hematocrit; D008297:Male; D008954:Models, Biological; D009392:Nephrectomy; D010953:Plasma Volume; D051381:Rats; D017208:Rats, Wistar; D012119:Respiration; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*; D012965:Sodium Chloride / Q000008:administration & dosage / Q000627:therapeutic use; D013997:Time Factors; D014882:Water-Electrolyte Balance
chemical_list: D012965:Sodium Chloride