Changes of plasma gastrointestinal glucagon concentrations following lethal infusions of E. coli.

We have determined the effect of lethal E. coli infusions in dogs on plasma concentrations of pancreatic and gastrointestinal-derived glucagon and have explored the contributions of each source of glucagon during the early and recovery phases of shock. We examined 18 adult dogs in three protocols: group I received LD100 E. coli alone, group II received LD100 E. coli + tobramycin (TOB), and group III received LD100 E. coli + TOB + methylprednisolone sodium succinate (MPSS). E. coli organisms were infused intravenously during a 1-hour period and each animal was monitored for 6 hours and observed for a 7-day recovery period. Plasma concentrations of pancreatic and gastrointestinal glucagon were determined by specific RIAs. The survival percentages (greater than 7 days) were 0% in group I, 17% in group II, and 83% in group III. Early progressive increases in plasma concentrations of pancreatic and gastrointestinal-derived glucagon, reaching statistical significance by 6 hours following the onset of E. coli administration, were seen in the three groups. The increase in gastrointestinal-derived glucagon was of a greater magnitude than that from the pancreas. Attenuation of the increase appeared to be achieved by corticosteroid infusion during its time of administration (6 hours). Recovery from shock was characterized by an exceptionally slow return (greater than or equal to 7 days) to control levels of glucagon in all recovering animals.