• J. Surg. Res. · Dec 2000

    E- and P-selectin expression depends on the resuscitation fluid used in hemorrhaged rats.

    • H B Alam, L Sun, P Ruff, B Austin, D Burris, and P Rhee.
    • Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.
    • J. Surg. Res. 2000 Dec 1;94(2):145-52.

    BackgroundE- and P-selectins are adhesion molecules that effect neutrophil-mediated reperfusion injury. Our hypothesis was that the expression of E- and P-selectins is dependent on the type of fluid used for resuscitation and that lactated Ringer's (LR) solution would result in an early upregulation of these molecules.MethodsMale Sprague-Dawley rats (n = 36) were subjected to a 27 ml/kg hemorrhage over 5 min followed by a 1-h shock period and 1-h of resuscitation. The animals were randomized into the following resuscitation groups: (1) sham; (2) hemorrhage, no resuscitation; (3) whole blood (27 ml/kg); (4) 3:1 lactated Ringer's (81 ml/kg); (5) sham hemorrhage, infusion of lactated Ringer's (81 ml/kg); (6) 7. 5% hypertonic saline (9.7 ml/kg). Immediately after resuscitation, the spleen and lung were harvested for measurement of E- and P-selectin mRNA expression with reverse transcriptase- polymerase chain reaction (RT-PCR), and protein expression with immunostaining.ResultsLR resuscitation and LR infusion without prior hemorrhage significantly increased the E- and P-selectin mRNA in the lung and spleen. Immunostaining demonstrated that the adhesion molecule expression was mainly located in perivascular/peribronchial areas in the lung, and the marginal and trabecular areas in the spleen. Pulmonary edema and inflammatory cell infiltration were observed only in the animals that were hemorrhaged and resuscitated with LR. No resuscitation and resuscitation with whole blood caused no significant increase in selectin expression.ConclusionLR resuscitation and LR infusion without hemorrhage are associated with early increased expression of E- and P-selectin molecules in the lung and spleen.Copyright 2000 Academic Press.

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