AJP - Renal Physiology, Vol 251, Issue 6 969-F977, Copyright © 1986 by American Physiological Society
Renal failure in dogs with experimental acute pancreatitis: role of hypovolemia
M. Levy, R. Geller and S. Hymovitch
The factors causing a decline in renal perfusion were studied in
anaesthetized dogs with acute pancreatitis 4 h after the forceful injection
of bile into the pancreatic duct. In 11 such dogs, glomerular filtration
rate (GFR) decreased by 40.4% from the control state (P less than 0.05),
whereas the clearance of para-aminohippurate (CPAH) declined by 50.2%.
These changes were associated with a 15.3% decline in cardiac output (P
less than 0.05) and a 26.2% fall in plasma volume. Glomerular morphology
was entirely normal. When hypovolemia was prevented by infusing homologous
plasma over the 4-h period of observation, the normally observed decline in
GFR, CPAH, and cardiac output was prevented. The decline in plasma volume,
associated with a rising hematocrit and declining plasma protein
concentration, and the associated decrement in renal perfusion, could be
entirely duplicated by the infusion of trypsin, chymotrypsin, elastase, and
phospholipase A2 (but not lipase or amylase) into normal dogs. These
perturbations also were prevented by the concurrent infusion of 4% albumin
in saline. At 24 h, however, the renal failure became unresponsive to
volume replenishment. We conclude that the decline in renal perfusion in
dogs at 4 h with acute pancreatitis is entirely due to hypovolemia, induced
by the release of specific enzymes from the inflamed gland, which causes
the loss of protein-rich plasma from the vascular space.
