beta-endorphin and Chest-Pain

Adenosine is a neuromodulator with both excitatory and inhibitory effects in different organs. High-dose adenosine infusion provokes chest pain in patients and healthy volunteers. This study examines the nature of chest pain and whether it is modified by the mu opioid receptor agonist (beta-endorphin) or a nonselective opioid antagonist (naloxone). Ten healthy volunteers with a mean age of 26 +/- 3 years participated in the study. The study was performed during 3 sessions. During every session the subjects were given a high dose of adenosine infusion (140 microg/kg/min) for 22 minutes. After 5 minutes, the subjects were randomized in a double-blind order on 1 of the 3 categories: (1) as placebo, NaCl bolus for 2 minutes followed by NaCl infusion for 15 minutes; (2) beta-endorphin bolus followed by infusion; and (3) naloxone bolus followed by NaCl infusion. Hemodynamic and pain parameters were monitored. During adenosine infusion, all volunteers experienced chest pain with oscillations of pain intensity. The oscillations continued during beta-endorphin and naloxone. There were no significant differences between hemodynamic and pain parameters during beta-endorphin or naloxone compared to adenosine infusion. High-dose infusion of adenosine provokes chest pain with oscillations of algesia and pain-free intervals. Peripheral opioid administration did not influence the adenosine-provoked chest pain.. Adenosine-induced oscillations of pain and pain-free intervals could theoretically be a sign of neuronal reflex activity dependent on spatiotemporal summation of adenosine excitatory and inhibitory properties. This could contribute to the complex nature of angina pectoris. Peripheral opioid receptors might not be involved in the oscillations.

Topics: Adenosine; Adult; Analgesics; beta-Endorphin; Chest Pain; Double-Blind Method; Humans; Male; Naloxone; Narcotic Antagonists; Periodicity

Adenosine is a neuromodulator with both excitatory and inhibitory effects dependent in part upon preconditions; it can act as an algesic or an analgesic agent. Previously we found variations of pain intensity during constant infusion of adenosine. We therefore quantified pain intensity during constant infusion of adenosine at a rate of 140 microg/kg/min intravenously in healthy volunteers, placebo controlled, double blind, and the relation to hemodynamic, vasomotor and sudomotor responses of the sympathetic nervous system and to the role of peripheral beta-endorphin response. The perceived chest pain during adenosine infusion showed an oscillatory pattern. Painful periods of about 30s were interrupted by painfree periods, and pain was always preceded by an increase in vasomotor sympathetic activity and by increased sudomotor activity. Plasma beta-endorphin values were heterogenous but exhibited an increase during infusion.

Topics: Adenosine; Adult; beta-Endorphin; Chest Pain; Double-Blind Method; Electrophysiology; Heart Rate; Hemodynamics; Humans; Injections, Intravenous; Male; Oscillometry; Severity of Illness Index; Sweating; Sympathetic Nervous System; Vasomotor System

The endogenous peptide B-endorphin (B-EP) is closely connected with different aspects of homeostasis, behavior, and in particular with the perception of pain. The purpose of this study was to investigate the correlation between: the level of plasma B-EP and the intensity of pain in acute myocardial infarction (AMI); and the B-EP and specific enzymes for AMI serum glutamic oxolo-acetic transferase, lactate dehydrogenase, and creatine phosphokinase and some stress hormones (cortisol, growth hormone). Twenty-six patients hospitalized in the CCU for acute MI were studied during the first 72 hours from the onset of symptoms. Seven normal subjects served as controls. Blood was taken for hormone and B-EP evaluation before treating the patients by opiates. Plasma B-EP levels were determined using the protocol of the Immunonuclear Corporation (Stillwater, MN). Statistical analysis of the results showed: Nonsignificant differences between B-EP levels of all MI patients and control group. Unaltered B-EP levels in patients with acute MI suffering from moderate pain. Significant differences in drop of B-EP in the group with most severe pain (p less than 0.025). A tendency toward decreased B-EP in patients suffering from more prolonged pain (greater than 6 hours). Significant negative correlation was shown between B-EP and chest pain intensity (0-4 graduation) (r = 0.8, p less than 0.01); lactate dehydrogenase (r = 0.7, p less than 0.01); serum glutamic oxolo-acetic transferase (r = 0.6, p less than 0.01); creatine phosphokinase (r = 0.6, p less than 0.05; plasma cortisol level (r = 0.5, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aspartate Aminotransferases; beta-Endorphin; Chest Pain; Creatine Kinase; Endorphins; Female; Growth Hormone; Humans; Hydrocortisone; L-Lactate Dehydrogenase; Male; Myocardial Infarction