Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on endogenous beta-endorphins of a new synthetic protease inhibitor was studied in acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Plasma beta-endorphin concentrations and cardiovascular function were measured. Ten dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 3 mg/kg/h of a new synthetic protease inhibitor, E-3123 (4-(2-succinimidoethylthio)4-geranidinobenzoate methanesuLfonate), in lactate Ringer's solution soon after the induction of pancreatitis. Plasma beta-endorphin concentrations in the control group increased significantly. However, plasma beta-endorphin levels in the protease inhibitor group did not increase as in the control group. The protease inhibitor infusion improved hypotension, myocardial depression, and plasma lactate, suggesting that the inhibitory effect of the protease inhibitor on beta-endorphin release contributed to the improvement.
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PMID:Effect of a new synthetic protease inhibitor on beta-endorphin release during acute pancreatitis in dogs. 187

120 SD rats were randomly divided into three groups: the sham operation group, the AP (acute pancreatitis) group, the naloxon treated group. AP was induced by intraductal injection of 5% sodium taurocholate solution. Naloxon was given intramuscularly at the dosage of 0.1 g/100 gw immediately after the injection and 90 minutes later. The survival rate and the mean survival time of the rats during 3 days after the induction of AP were determined. The pancreata were sampled for semiquantitative histopathologic evaluation. By using the fractional indicator distribution technique with 86 RB, QP/CO and pancreatic tissue perfusion performed 1 and 6 hours after the induction of AP, the amount of beta-endorphin in the hypothalamus and pituitary was measured 1 and 4 hours after the induction of AP. It was found in the naloxon treated group, the pancreatic blood flow and tissue perfusion was greatly increased, the mortality rate was decreased, and the rats survival time was significantly prolonged. The results suggest that: (1) The hemodynamic changes play an important role in the pathogenesis of AP. (2) Beta-Endorphin may play a role in the pathophysiological process of AP. (3) naloxon has good therapeutic effects on AP.
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PMID:[An experimental study on the role of beta-endorphin in the pathogenesis of acute pancreatitis and the effects and mechanisms of naloxone]. 226 55

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.
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PMID:Plasma beta-endorphin and the effect of naloxone on hemodynamic changes during experimental acute pancreatitis in dogs. 254 May 37

The therapeutic effect of a new synthetic protease inhibitor on hemodynamic changes was studied in experimental acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligating the accessory duct. Plasma beta-endorphin concentrations and cardiovascular function were measured. Seventeen dogs (control group) were given 10 ml/kg/hr of lactate Ringer's solution intravenously 1 hr before the induction of pancreatitis and throughout the experiment. Seven dogs (the low protease inhibitor group) were given an intravenous bolus injection of 0.4 mg/kg of a new synthetic protease inhibitor, E-3123 (4-(2-succiminido-ethylthio)4-geranidinobenzoate methanesulfate) 30 min after the induction of pancreatitis and then a continuous intravenous infusion at 3 micrograms/kg/min throughout the experiment. Seven dogs (the high protease inhibitor group) received an intravenous bolus injection of 3 mg/kg and a continuous intravenous infusion at 50 micrograms/kg/min of E-3123 according to the same method as in the low protease inhibitor group. The mortality rate during the experiment was 41% (7/17) in the control group, 28.5% (2/7) in the high protease inhibitor group and 0% in the low protease inhibitor group. The increase in the plasma beta-endorphin levels in the control group was statistically significant. When E-3123 was given 30 min after the induction of pancreatitis, the increase in the plasma beta-endorphin levels in the high protease inhibitor group was also found to be increased statistically significant, compared with preinduction levels, but the increase was statistically significantly lower than that in the control group. Plasma beta-endorphin levels in the low protease inhibitor group, however, did not increase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The therapeutic effect of a new synthetic protease inhibitor (E-3123) on hemodynamic changes during experimental acute pancreatitis in dogs. 844 Apr 25

Bradykinin and beta-endorphin increases during acute pancreatitis are thought to contribute to the development of hypotension and myocardial depression in acute pancreatitis. beta-Endorphin release is mediated by trypsin-like enzymes and bradykinin from the pituitary gland. This study was undertaken to investigate the effect of a long-acting bradykinin receptor antagonist on bradykinin and beta-endorphin release and on hemodynamic changes during acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Serum bradykinin and plasma beta-endorphin levels and cardiovascular function were measured. Twelve dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 0.6 mg/kg/h of a new bradykinin receptor antagonist, HOE 140, D-Arg-[Hyp3, Thi5, D-Tic, Oic8]-bradykinin, in lactate Ringer's solution soon after the induction of pancreatitis. Six of twelve dogs in the control group, and none of the six dogs in the bradykinin receptor antagonist group, died during the experiments. Serum bradykinin levels in both groups increased until 1 h after the induction of pancreatitis, but thereafter the levels in the bradykinin receptor antagonist group decreased gradually until 5 h after induction, and levels were significantly lower than those in the control group (p < 0.05). Plasma beta-endorphin levels in the control group increased significantly, to 291.8 pg/ml (+/- 6.6 SEM) 5 h after the induction of pancreatitis, from the mean levels of 47.8 pg/ml before the induction of pancreatitis, while the mean beta-endorphin level in the bradykinin receptor antagonist group did not increase after the induction of pancreatitis. Infusion of the bradykinin receptor antagonist improved survival rates, hypotension, myocardial depression, and plasma lactate, suggesting that the bradykinin receptor antagonist inhibited the release of bradykinin and beta-endorphin, which contributed to the clinical improvement.
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PMID:Effects of bradykinin receptor antagonist on the release of beta-endorphin and bradykinin and on hemodynamic changes in a canine model of experimental acute pancreatitis. 892 25

Ten dogs with pituitary-dependent hyperadrenocorticism (PDH) received 2 mg/kg of L-Deprenyl once daily for 6 months. Monthly patient assessment consisted of evaluation of the owner's daily observation protocol, a standardized owner questionnaire, physical examination, CBC, biochemical profile, determination of the urine cortisol/creatinine ratio (UC/C), low-dose dexamethasone suppression (LDDS) test, corticotropin releasing hormone (CRH) test, and adrenal ultrasonography. At the beginning and the end of the study, an adrenocorticotropic hormone (ACTH) stimulation test and computed tomography also were performed. Two dogs developed neurologic signs and 2 dogs developed acute pancreatitis. An increase in activity, decrease in polyphagia, and decrease in panting were reported by 6, 4, and 2 owners, respectively. Seven owners believed that water intake decreased, but this was confirmed in only 3 dogs. Water intake increased in 2 dogs and remained unchanged in 5 dogs. The condition of the hair coat and skin improved in 2 dogs, worsened in 3, and remained unchanged in 5. Urine specific gravity, urine osmolality, ACTH test results, UC/C, and adrenal gland size did not change significantly throughout the study. In 4 of 8 dogs, LDDS was abnormal at the start of the study but normal at the end of the study, and in 2 dogs, the opposite occurred. Marked individual variation was noted in the CRH test, with a tendency for smaller increases in ACTH toward the end of the study. A marked increase in hypophyseal tumor size occured in 4 dogs. Treatment with L-Deprenyl resulted in improvement, deterioration, and stagnation of clinical signs in 2, 4, and 4 dogs, respectively. The results of this study indicate that L-Deprenyl cannot be recommended as the sole treatment for canine PDH.
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PMID:The efficacy of L-Deprenyl in dogs with pituitary-dependent hyperadrenocorticism. 1044 18