beta-endorphin and Hepatic-Encephalopathy

To observe the therapeutic effect of acupuncture at thirteen evil acupoints in patients with hepatic encephalopathy, and to explore its possible mechanism.. Patients with hepatic encephalopathy were randomly divided into acupuncture group (. Following the treatment, of the 36 and 38 hepatic encep-halopathy patients in the western medicine and acupuncture groups, 12 and 18 experienced a marked improvement in their symptoms, 13 and 16 were effective, and 11 and 4 invalid, with the effective rates being 69.4% and 89.5%, respectively. Compared with pre-treatment, the levels of serum aspartate aminotransferase, alanine aminotransferase, total bilirubin, and plasma β-endo-rphin and blood ammonia were significantly lower in both western medicine and acupuncture groups(. Treatment of acupuncture at thirteen evil acupoints combined with western medicine can enhance the curative effect of hepatic encephalopathy, improve patients' liver function and decrease the levels of plasma ammonia and β-endorphin.

Topics: Acupuncture Points; Acupuncture Therapy; Ammonia; beta-Endorphin; Hepatic Encephalopathy; Humans

Opioid peptides may contribute to some of the manifestations of hepatic encephalopathy. To address the role of the opioid system in the pathogenesis of hepatic encephalopathy, three representative opioid ligands were measured in plasma and cerebrospinal fluid of patients with hepatic encephalopathy.. Plasma and cerebrospinal fluid were obtained in three groups of patients: group 1: patients with hepatic encephalopathy; group 2: patients with lumbar back pain; group 3: healthy controls. Met-enkephalin, leu-enkephalin and beta-endorphin levels were measured in extracted plasma and cerebrospinal fluid samples by radioimmunoassay.. Plasma met-enkephalin levels were 656% (p<0.05) and 301% (p<0.05) and cerebrospinal fluid met-enkephalin levels were 1481% (p<0.01) and 645% (p<0.05) higher when compared to healthy control and pain control patients, respectively. Although plasma and cerebrospinal leu-enkephalin levels were elevated in patients with hepatic encephalopathy, the increases were not statistically significant. Plasma and cerebrospinal beta-endorphin levels were similar in the three study groups.. The results of this study support accumulating data on the role of the delta opioid receptor ligand met-enkephalin in the pathogenesis of hepatic encephalopathy, and provide a rationale for the use of opioid receptor antagonists in the treatment of hepatic encephalopathy.

Topics: beta-Endorphin; Enkephalin, Leucine; Enkephalin, Methionine; Hepatic Encephalopathy; Humans; Ligands; Radioimmunoassay; Receptors, Opioid

Although plasma levels of Met-enkephalin and beta-endorphin are elevated in patients suffering from liver failure, it is not known whether central nervous system (CNS) opioidergic neurotransmission is altered in these patients. Such changes may contribute to the motor dysfunction, psychiatric abnormalities and CNS depression observed in hepatic encephalopathy (HE). Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. Pituitary and brainstem dynorphin A levels increased whereas plasma levels decreased in rats with thioacetamide-induced fulminant hepatic failure. Both striatal Met- and Leu-enkephalin levels increased and hypothalamic concentrations decreased in HE. Concurrent with the increase in striatal Met-enkephalin levels was a 26 to 48% decrease in the density of striatal and hypothalamic delta receptors. No change in either the density or affinity of radioligand binding to mu or delta receptors was observed in the CNS. Finally, administering (+/-)-naloxone (5 and 10 mg/kg) or (+/-)-naltrexone (5-15 mg/kg), but not (+)-naloxone (10 mg/kg), significantly increased the motor activity of rats with Stage III HE. Whereas elevated plasma levels of opioid peptides may play a role in the peripheral manifestations of hepatic failure (ascites and hypotension), increased CNS levels of these peptides may be involved in the neuropsychiatric abnormalities characteristic of HE. Thus, opioid antagonists may be effective in ameliorating some of the neurological manifestations of HE.

Topics: Animals; beta-Endorphin; Brain Chemistry; Dynorphins; Enkephalin, Leucine; Enkephalin, Methionine; Hepatic Encephalopathy; Male; Motor Activity; Narcotic Antagonists; Opioid Peptides; Rats; Rats, Sprague-Dawley; Thioacetamide

Clinical observation has indicated a supersensitivity to morphine in patients with hepatic encephalopathy. With the aim of clarifying the issue, radioreceptor binding studies of opiate receptors were performed in frontal cortex and hypothalamus of 6 dogs with mild portal-systemic encephalopathy induced by chronic treatment with dimethylnitrosamine followed by porto-caval shunt end-to-side. beta-Endorphin assays were performed in the same areas with radioimmunoassay. Opiate receptors labeled with [3H]naloxone in both areas showed a significant increase in the receptor densities (Bmax) without changes in the dissociation constant (KD). In parallel beta-endorphin levels showed a decline during the development of encephalopathy in both areas. The increased densities of opiate receptors in the mild stage of encephalopathy may explain the supersensitivity to morphine in patients with liver diseases.

Topics: Animals; beta-Endorphin; Brain; Cerebral Cortex; Dogs; Endorphins; Female; gamma-Aminobutyric Acid; Hepatic Encephalopathy; Hypothalamus; In Vitro Techniques; Kinetics; Male; Naloxone; Receptors, Opioid