Weaver F C
Department of Biology, Saint John's University, Collegeville, Minnesota 56321.
Pancreas. 1988;3(6):688-99. doi: 10.1097/00006676-198812000-00010.
Although it is known that ducts remain intact in the atrophied pancreata of rats rendered dietarily copper-deficient, no information is available that characterizes the ductal angioarchitecture of the experimentally altered gland. Furthermore, since the vascular relationship between pancreatic ducts and the parenchyma of the normal gland has not been well defined, this atrophy model was used to examine blood flow to ducts in the atrophied gland where acinar tissue undergoes selective necrosis. Scanning electron microscopy (SEM) of pancreatic corrosion casts produced from Mercox-injected rats was used. SEM was compared with light microscopic study of stain-injected cleared pancreata and correlated with histological and ultrastructural studies. The results indicate that duct cells and ductal vasculature remain unaffected by surrounding acinar cell necrosis and glandular lipomatous atrophy. Furthermore, the results support a largely autonomous blood supply for the ductal system by arterial blood that flows directly from major extralobular arteries of the pancreas or their interlobular branches. In the same manner, venous blood draining the ductal system returns to major extralobular veins or by way of their interlobular branches. No evidence could be established for manifest acinoductal or ductoacinar portal systems. There were, however, places in the route of both ductal and acinar vessels where the vessels were found to anastomose. These places were found near the source of major arteries or veins that supply and drain confluent acinar and ductal tissues. It is concluded that, while some acinoductal or ductoacinar exchange may take place, the role of these putative portal systems would appear less significant than the direct route of blood to and from pancreatic ducts.
