Pathophysiological aspects of experimental fat necrosis and its relation to acute pancreatic necrosis (Hebrew)

An experimental model was devised to correlate the pathogenesis of fat necrosis and of acute pancreatitis early in the course of development. Intrabiliary injection of taurocholate produced necrotic changes in the pancreatic parenchyma within 24 hr with affection of the surrounding fat. The addition of vasoactive substances, such as theophylline and epinephrine, resulted in vascular changes with the appearance of focal fat necrosis. However, these drugs did not increase the intensity of the pancreatic necrosis. It is concluded that theophylline and epinephrine interfere with the regional blood supply to the fat, resulting in anoxia and eventually in the death of fat cells. The old concept of the pancreatic lipase in the degradation of triglycerides during fat necrosis is questioned. It is now known that pancreatic lipase is rapidly inactivated either by the presence of bile salts or by a decrease of pH of the medium. However, the possibility of eventual participation of intracellular lipase in fat tissue necrosis activated through cAMP by the vasoactive drugs is considered. It appears that in its early phases the pathogenesis of fat necrosis differs from that of pancreatic necrosis, although in the later stages differentiation between the two phenomena becomes impossible.