Hepatocellular dysfunction after severe hypotension in the absence of blood loss is associated with the increased IL-6 and PGE2

Academic Article

Abstract

  • Although hepatocellular dysfunction occurs following trauma and hemorrhagic shock, whether severe hypotension even in the absence of blood loss depresses hepatocellular function remains unknown. The aim of this study, therefore, was to determine whether chemically induced severe hypotension causes hepatocellular dysfunction and, if so, whether IL-6 and PGE2 are associated with this dysfunction. To study this, hypotension was induced in adult male rats by intravenous infusion of a high dosage of ATP- MgCl2 solution (3.2 ± 0.45 μmol/min/kg body wt) for 60 min. Blood pressure decreased from 108 ± 6 mm Hg to an average of 43 mm Hg during the infusion period and returned to normal levels immediately after the completion of ATP- MgCl2 infusion. At 0 and 4 h after hypotension, hepatocellular function [i.e., maximum velocity of indocyanine green clearance (V(max)) and its efficiency (K(m)] was measured using a fiberoptic catheter and in vivo hemoreflectometer. Cardiac output was determined by dye dilution. Microvascular blood flow was assessed by laser Doppler flowmetry. Plasma levels of PGE2 and IL-6 were measured by radioimmunoassay and bioassay, respectively. The results indicate that severe hypotension in the absence of any blood loss depresses hepatocellular function (i.e., decreased V(max) and K(m)) despite stable cardiac output and hepatic perfusion at 0 and 4 h after the completion of hypotension. Moreover, severe hypotension resulted in significantly increased plasma levels of PGE2 (only at 0 h) and IL-6. Thus, chemically induced severe hypotension in the absence of any blood loss, which does not significantly reduce cardiac output and hepatic perfusion, depresses hepatocellular function and upregulates IL-6 and PGE2 production.
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    Author List

  • Wang P; Ba ZF; Cioffi WG; Bland KI; Chaudry IH
  • Start Page

  • 136
  • End Page

  • 142
  • Volume

  • 80
  • Issue

  • 2