Low molecular weight dextran in experimental pancreatitis: Effects on pancreatic microcirculation

Abstract

Although low molecular weight (LMW) dextran has been said to decrease the lethality of experimental acute pancreatitis (AP) by reversing stasis in the pancreatic microcirculation, the actual mechanism(s) of action is unknown. This investigation was designed to measure the effects of low molecular weight dextran on pancreatic capillary flow ( Q CAP) and arteriovenous shunt flow ( Q AVS), and on pancreatic oxygen consumption (O 2 C P) following bile-trypsin-induced AP in dogs. Total pancreatic blood flow ( Q T) was measured with an electromagnetic flow probe on the superior pancreaticoduodenal artery (SPDA). Q AVS was measured by liver trapping of 99mTc-albumin microspheres after SPDA injection. Q CAP was calculated as Q T minus Q AVS. Seventeen dogs were treated with lactated Ringer's (LR) solution at 6.5 ml/kg/hr; 10 dogs were treated with LMW dextran 10% in normal saline at 1.5 ml/kg/hr plus LR at 5.0 ml/kg/hr. Mean arterial and central venous pressures remained constant throughout the 4-hr experiment. In the dogs receiving LR only, Q T decreased from 42.7 to 24.4 ml/min ( P < 0.001); Q AVS remained constant at 1.35 ± 0.04 ml/min. During the first 30 min O 2 C P decreased from 1.17 to 0.76 ml O 2/min ( P < 0.05) and remained constant thereafter. LMW dextran treatment altered none of these hemodynamic or metabolic parameters significantly. Conclusions: bile trypsin AP in the dog causes significant decreases in Q T and Q CAP without altering Q AVS. The decrease in O 2 C P in association with a constant Q AVS suggests a metabolic block to oxygen uptake at the cellular level. Continuous infusion of LMW dextran at a dose of 1.5 ml/kg/hr in the dog does not reverse these abnormalities.