Plasma beta-endorphin and the effect of naloxone on hemodynamic changes during experimental acute pancreatitis in dogs.

The effect of endogenous pituitary and pancreatic beta-endorphins in the physiopathologic factors of acute pancreatitis and the effect of opiate antagonist naloxone in these conditions were studied. Pancreatitis was induced by the injection of 0.5 milligram per kilogram of autologous bile mixed with 10,000 units per kilogram of trypsin into the main duct after ligating the accessory duct. After the induction of acute pancreatitis, plasma beta-endorphin concentrations in systemic and portal blood and cardiovascular function were measured. Ten dogs (control group) were given an intravenous injection of 10 milliliters per kilogram per hour of lactate Ringer's solution one hour before the induction of acute pancreatitis. Six (naloxone group) received an intravenous bolus injection of 2 milligrams per kilogram of naloxone at one hour after the induction of acute pancreatitis and then an intravenous infusion of 2 milligrams per kilogram per hour of naloxone was given under the same conditions as for those in the control group. Beta-endorphin in systemic and portal venous blood in those in the control group increased significantly during the experiments. Beta-endorphin and adrenocorticotropin hormone in systemic venous blood both in the control and naloxone groups increased simultaneously. However, blood pressure, pulse pressure and cardiac output improved quickly after the bolus injection of naloxone and were well maintained during intravenous infusion of naloxone. Also, naloxone improved the survival time from acute pancreatitis and decreased plasma lactate concentrations. Our data show that beta-endorphin, released mainly from the pituitary gland and not from the pancreas, may have an important role in subsequent cardiovascular depression. Also the opiate antagonist naloxone may be effective in the treatment of acute pancreatitis.