PMID- 7888260
OWN - NLM
STAT- MEDLINE
DCOM- 19950417
LR  - 20190503
IS  - 0007-0769 (Print)
IS  - 0007-0769 (Linking)
VI  - 73
IP  - 1
DP  - 1995 Jan
TI  - Activation and inhibition of the endogenous opioid system in human heart failure.
PG  - 41-8
AB  - BACKGROUND: In a canine model of congestive heart failure beta endorphin 
      concentrations were high and opioid receptor antagonists exerted beneficial 
      haemodynamic effects. In humans previous studies have suggested that opioid 
      peptides may modify the perception of breathlessness and fatigue in heart 
      failure. METHODS: Plasma concentrations of beta endorphin were measured in 
      patients with acute and chronic heart failure and cardiogenic shock. A subgroup 
      of eight patients with New York Heart Association (NYHA) class III-IV heart 
      failure was assessed for acute haemodynamic effects of naloxone, an opioid 
      receptor antagonist. A separate group of 10 patients with class II-III heart 
      failure, was randomised to a double blind placebo controlled study of the effects 
      of intravenous naloxone on cardiopulmonary exercise performance. RESULTS: Plasma 
      concentrations of beta endorphin were usually normal in patients with chronic 
      heart failure and did not correlate with severity as assessed by NYHA class. In 
      29% of patients with acute heart failure and 71% of those with cardiogenic shock 
      beta endorphin concentrations were high. The median concentration in the 
      cardiogenic shock group was significantly higher than in either of the two heart 
      failure groups and there was some evidence of a relation between beta endorphin 
      concentrations and survival. At the doses tested, naloxone was unable to modify 
      systemic haemodynamics, exercise performance, or symptoms in patients with 
      chronic congestive heart failure. CONCLUSIONS: Circulating concentrations of beta 
      endorphin are usually normal in patients with chronic congestive heart failure. 
      Inhibition of the endogenous opioid system is unlikely to have therapeutic 
      potential in heart failure.
FAU - Oldroyd, K G
AU  - Oldroyd KG
AD  - Department of Medical Cardiology, Royal Infirmary, Glasgow.
FAU - Gray, C E
AU  - Gray CE
FAU - Carter, R
AU  - Carter R
FAU - Harvey, K
AU  - Harvey K
FAU - Borland, W
AU  - Borland W
FAU - Beastall, G
AU  - Beastall G
FAU - Cobbe, S M
AU  - Cobbe SM
LA  - eng
PT  - Clinical Trial
PT  - Comparative Study
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br Heart J
JT  - British heart journal
JID - 0370634
RN  - 36B82AMQ7N (Naloxone)
RN  - 60617-12-1 (beta-Endorphin)
SB  - IM
MH  - Acute Disease
MH  - Adult
MH  - Aged
MH  - Chronic Disease
MH  - Double-Blind Method
MH  - Exercise Test
MH  - Female
MH  - Heart Failure/*blood/drug therapy
MH  - Hemodynamics/drug effects
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Naloxone/blood/*therapeutic use
MH  - Shock, Cardiogenic/*blood
MH  - Stroke Volume
MH  - Ventricular Function, Left/physiology
MH  - beta-Endorphin/*blood
PMC - PMC483754
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
PMCR- 1995/01/01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PHST- 1995/01/01 00:00 [pmc-release]
AID - 10.1136/hrt.73.1.41 [doi]
PST - ppublish
SO  - Br Heart J. 1995 Jan;73(1):41-8. doi: 10.1136/hrt.73.1.41.