Non invasive analysis of hemodynamic changes in dogs with acute pancreatitis

To elucidate the hemodynamic changes in the course of acute pancreatitis in dogs, various parameters were monitored non-invasively and real-timely by the ultrasonic flow probes which had been placed in advance. The dogs were divided into two groups, i.e., control group (CG) and infusion group (IG). In the infusion group, lactated Ringer solution was infused intravenously for 12 hours in order to maintain LAP or CVP at the mean +/- 1 mmHg of its control value before inducing pancreatitis. In the control group, lactated Ringer solution was not infused. Cardiac output (CO) and LV dp/dt abruptly decreased in a few hours and remained low levels in a control group (CG), but not in an infusion group (IG). It shows that the decreased CO was caused by a decrease in preload but not by a depression of contractility. Gastroduodenal arterial flow (GDAF) and GDAF/CO decreased in a few hours and kept low level in CG, but not in IG. Therefore, a decrease in GDAF is mainly caused by an increase in vascular resistance due to an increase in Hematocrit. Superior pancreatico-duodenal venous flow (SPDVF) and SPDVF/CO decreased immediately in both groups, revealing that there is severely depressive outflow from pancreas because of hemorrhage and destruction of pancreatic parenchyma immediately after the onset of pancreatitis. In CG, Total hepatic flow (THF) and Portal vein flow (PVF) gradually decreased in a few hours and kept low levels, but Common hepatic arterial flow (CHAF) did not decrease. This suggests that decrease of THF is due to decrease of PVF. THF/CO increased in CG. PVF/CO decreased in CG, while CHAF/CO increased in both groups. The increased CHAF compensated for the decreased PVF, which may play an important role in protecting the liver.