Hepatic nitric oxide generation as a putative mechanism for failure of intrahepatic islet cell grafts.

PRIMARY non function of islet allografts and chronic failure of intrahepatic islet autografts has been observed in large animals and humans, bringing into question the liver as the ideal site for islet transplantation. Our hypothesis is that inflammatory mediators released in the microenvironment at the transplant site might result in impaired islet engraftment. The L-arginine~ependent nitric oxide (NO) pathway, which is known to inhibit rodent islet primary function.! is a putative cytotoxic mediator.