Pancreatic islet transplantation: utility of ductular obstruction and exocrine atrophy model?

Introduction of 'silent' exocrine atrophy (and endocrine 'enrichment') in pancreatic grafts following ductular blockade may have a role in human diabetes by circumventing currently elusive islet isolation/purification protocols. To explore this potential, pancreatic isografts were performed in 12 pairs of inbred Wistar NIN rats. Donor pancreatectomy was performed after distal clamping and canulation of common bile duct and injection of 0.5 ml. polyacrylamide gel (blocked n = 7) or normal saline (un-blocked n = 5) respectively. One to 2 m.m. fragments of the resulting mildly distended pancreases were transplanted in to 2 sites (renal capsule and iliac fossa subcutaneously) of cach recipient. Post-operative biopsies of the transplanted grafts (unilateral nephrectomy and iliac fossa biopsies) revealed macroscopic and microscopic evidence of necrotizing pancreatitis in both the groups at both the sites (histiocytic and giant cell infiltration, fat necrosis and focal calcification with destruction of exocrine and endocrine cells) as early as 1 and 3 weeks. Possible detrimental factors include: volume and pressure of ductal injection, graft sites (confined spaces), post-operative wound infection and bio-compatibility of the material used for ductular blockade.

Applied aspects of theoretical analysis of pulmonary gas exchange.

This paper gives a summary of the theoretical analysis of the processes of gas exchange in the lungs. It brings out the effect of changes in the rate of equilibration of gases across the membrane due to a variety of factors. It brings out that the length of the capillary over which complete equilibration occurs is infinitesimally small, hence a diffusion defect is seldom a cause of hypoxaemia in disease unless the character of membrane changes like in interstitial fibrosis or pneumoconiosis. The increase in length of capillary for complete equilibrium is significant in hypoxia of high altitude and left ventricular failure causing dilatation of pulmonary capillaries.