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Am J Physiol Gastrointest Liver Physiol 276: G1507-G1514, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 6, G1507-G1514, June 1999

Effect of diaspirin cross-linked hemoglobin on normal and postischemic microcirculation of the rat pancreas

Ernst von Dobschuetz1, Tomas Hoffmann2, Clemens Engelschalk3, and Konrad Messmer1

1 Institute for Surgical Research and 3 Institute for Clinical Chemistry, Klinikum Grosshadern, Ludwig-Maximilians University, D-81366 Munich; and 2 Maria-Theresia Klinik, D-80336 Munich, Germany

Microcirculatory alterations with reduced nutritive supply to the pancreas could be the cause of hyperamylasemia, which occurs in some patients receiving the vasoactive oxygen carrier diaspirin cross-linked hemoglobin (DCLHb) in clinical studies. Therefore, the effects of DCLHb on rat pancreas microcirculation were evaluated. Anesthetized Sprague-Dawley rats received one of the following treatments during baseline conditions (n = 7 rats/group): 10% hydroxyethyl starch (HAES) (0.4 ml/kg), DCLHb (400 mg/kg), or DCLHb (1,400 mg/kg). After 1 h of complete, reversible pancreatic ischemia, other animals received 10% HAES (0.4 ml/kg) or DCLHb (400 mg/kg) during the onset of reperfusion. The number of red blood cell-perfused capillaries (functional capillary density, FCD) and the level of leukocyte adherence in postcapillary venules in the pancreas were assessed by means of intravital microscopy during 2 h after treatment. In the nonischemic groups, FCD was 18% greater after DCLHb (1,400 mg/kg) than after 10% HAES treatment without any increase in leukocyte adherence. In the inschemia-reperfusion (I/R) 10% HAES group, FCD was significantly (P < 0.05) lowered, leukocyte adherence enhanced, and mean arterial pressure (MAP) reduced by 31% compared with nonischemic animals. DCLHb treatment in the I/R group resulted in a slight increase in FCD, a significant (P < 0.05) reduction of leukocyte adherence, and a complete restoration of MAP compared with the animals of the I/R control group. Thus our data provide no evidence for a detrimental effect on the pancreatic microcirculation or an enhanced risk of postischemic pancreatitis by DCLHb.

hemoglobin solutions; blood substitute; endothelin; nitric oxide; shock treatment


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