We studied the pancreatic high-energy
phosphates in two models of
acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo.
Alcoholic pancreatitis was induced by acute
ethanol intoxication and an obstruction-hyperstimulation mechanism.
Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10%
taurocholate-Na+. In addition to the obligate control groups, a simple
ischemia experiment was performed. The high-energy
phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of
taurocholate showed an increase in
inorganic phosphate with a concomitant decrease in
ATP levels, similar to pancreatic
ischemia. This irreversible decrease was accompanied histologically by severe pancreatic
hemorrhage. After induction of alcoholic
acute pancreatitis a reversible decrease in
ATP was occasionally seen. Even when
alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy
phosphates seems to occur as a result of pancreatic cell death rather than being a cause of
pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in
acute pancreatitis.