Increase In Plasma Beta-endorphin Levels Research Articles

Voluntary alcohol consumption and plasma beta-endorphin levels in alcohol-preferring rats chronically treated with naltrexone

It is well known that alcohol consumption leads to an increase in the levels of beta-endorphin (an endogenous opioid), which can contribute to the reinforcing effect of alcohol. Our previous studies have shown that repeated treatment with naltrexone, a nonselective opioid antagonist, results in increased plasma beta-endorphin levels. Ample studies in animals and humans have shown that naltrexone diminishes ethanol consumption. The aim of the present study in alcohol-preferring rats (Warsaw High Preferring; WHP) was to investigate the effect of 10 days of naltrexone treatment (2 mg/kg i.p.) on voluntary alcohol intake and on changes in plasma beta-endorphin levels while alcohol was available and 10 days after imposed abstinence. It was observed that voluntary alcohol intake induces an increase in plasma beta-endorphin levels in WHP rats. After a 10-day period of alcohol withdrawal, the levels of this peptide were significantly reduced compared with the levels in rats with free access to ethanol and in control alcohol-naïve rats. In chronic naltrexone-treated rats with free access to alcohol, an increase in the levels of this peptide was also observed; however, voluntary alcohol intake was diminished. A similar increase in plasma beta-endorphin levels was observed in naltrexone-treated rats that did not have access to ethanol. As the endogenous opioid system has an important role in the development of a craving for alcohol, it is likely that chronic naltrexone treatment may have a beneficial effect leading to a compensatory increase in the beta-endorphin concentration and ameliorating its deficiency during ethanol withdrawal. Restoring the alcohol-induced deficiency of beta-endorphin may be an important factor in the prevention of craving and maintenance of abstinence. This finding supports the proposition that the endogenous opioid system plays an important role in developing a craving for alcohol.

Psychophysical responses to a speech stressor: Correlation of plasma beta-endorphin levels at rest and after psychological stress with thermally measured pain threshold in patients with coronary artery disease

Objectives. We tested the hypothesis that psychological stress alters plasma levels of opioid peptides and that these plasma levels are related to pain perception in patients with coronary artery disease.Background. Public speaking psychological stress has previously been shown to be associated with silent ischemia.Methods. After instrumentation and a 30-min rest period, venous blood samples for beta-endorphin were obtained before and immediately after psychological stress in 20 patients with coronary artery disease. Pain threshold was then assessed using a thermal probe technique at baselin and immediately after stress. Patients gave three brief speeches lasting a total of 15 min about real-life hassle situations.Results. Psychological stress significantly increases plasma beta-endorphin levels (4.3 ± 0.9 pmol/liter [mean ± SE] at rest to 8.3 ± 2 pmol/liter after stress, p < 0.05). There was a significant positive correlation between pain threshold and beta-endorphin levels after stress (r = 0.577, p = 0.008). This significant positive correlation was still present while rest blood pressure and change in blood pressure during stress were controlled for by analysis of covariance techniques.Conclusions. In patients with coronary artery disease and exercise-induced ischemia, public speaking produces psychological stress manifested by increased cardiovascular reactivity and causes an increase in plasma beta-endorphin levels that is significantly correlated with pain thresholds. These findings may explain the predominance of silent ischemia during psychological stress in patients with coronary artery disease.

Beta-Endorphin and blood pressure in multiple trauma victims.

In addition to pain and stress, endogenous opiates and in particular beta-endorphin could be involved in the modulation of cardiovascular parameters. Several studies have thus shown increases in plasma beta-endorphin levels in the course of septic or hypovolemic shock. Our study involving 44 multiple trauma patients indicates that even in the absence of any hemodynamic disorders, there is a correlation between systolic blood pressure and plasma beta-endorphins. These results argue in favor of the existence of feedback between systolic blood pressure and plasma beta-endorphins.

Plasma endogenous opioid levels in acute myocardial infarction patients, with and without pain.

Plasma levels of beta-endorphin, met-enkephalin and dynorphin were assessed in acute myocardial infarction (AMI) patients, with and without pain (group I: no pain, N = 12; group II: severe pain, N = 16). Plasma opioid peptide concentration was measured on admission to hospital (between 1 and 3 h after the myocardial infarction onset), at 7, 12, 24 h and at 2, 3 and 4 days. A transient increase in plasma beta-endorphin levels was found in AMI patients with severe pain, the levels normalizing within 12-18 h when pain had ceased. No changes in beta-endorphin concentration were observed in AMI patients without pain. Compared with healthy subjects, low levels of met-enkephalin were found in both groups of AMI patients throughout the study. Low levels of dynorphin were observed in patients with no pain while in the other patients initial low levels of dynorphin normalized when pain ceased. Blood pressure, heart rate and central venous pressure values were normal and did not correlate with plasma opioid levels. The results suggest that endogenous opioids do not affect pain in the early phase of myocardial infarction. The rise in beta-endorphin concentration observed in patients with severe pain seems to be induced by pain stress.

Depression and type A behavior pattern in patients with coronary artery disease: relationships to painful versus silent myocardial ischemia and beta-endorphin responses during exercise.

A sample of 45 patients with a history of coronary heart disease and documented myocardial ischemia during exercise testing were evaluated in an investigation of the possible relationships between psychological factors (depression and Type A behavior pattern), plasma beta-endorphin response and pain experience during maximal exercise-induced ischemia. Depression was assessed using the MMPI-D subscale, while Type A was evaluated using the Structured Interview. All patients developed ischemia during exercise as defined by ST-segment depression; however, only 18 patients reported anginal pain. Patients with high depression scores (MMPI-D greater than or equal to 70; n = 13) showed lesser increases in plasma beta-endorphin levels, tended more often to report anginal pain and rated pain as more severe during exercise than patients with low depression scores (MMPI-D less than 60; n = 18). Hemodynamic responses and severity of ischemia (assessed by ejection fraction changes and wall-motion abnormalities) did not differ between depression groups. Even after adjustment for group differences in exercise duration, depression was significantly associated with a lesser beta-endorphin response in the sample as a whole and, among patients reporting angina, with earlier pain onset and greater pain duration and severity. In contrast, when Type A versus B/X subgroups were compared, no differences in pain experience, beta-endorphin response or measures of ischemia were obtained. These findings suggest that in patients with ischemic heart disease, there may be a relationship between depression and anginal pain which may in part involve a blunted or absent beta-endorphin response.

Plasmatic beta-endorphin levels and thalamic surgery for pain.

Plasma beta-endorphin levels were found to be significantly lower in patients suffering from chronic pain of malignant etiology than in a control group. After a bilateral stereotactic cryothalamotomy in Centrum Medianum and Parafascicularis nuclei, a good clinical result and a significant increase in plasma beta-endorphin levels were obtained.