Pain and stress: correlation of stress hormone release to pain modulation in man.
The contribution of stress-induced and opioid-dependent mechanisms to the modulation of experimental pain was studied in man under different conditions. The contribution of these mechanisms to the possible attenuation of acute cardiac pain in human patients was also studied. According to the present series of investigations, stress-induced mechanisms might be involved in the modulation of pain caused by physical exercise but not by concurrent subacute pain or transcutaneous nerve stimulation. The lack of any negative correlation between the pain intensity and the release of stress hormones indicates that stress mechanisms do not attenuate acute ischaemic pain of the cardiac origin. The use of an opioid-antagonist, naloxone, and the measurement of plasma levels of beta-endorphin did not reveal any contribution of endogenous opinoids to pain modulation in the current study.
D003327:Coronary Disease / Q000503:physiopathology; D004723:Endorphins / Q000502:physiology; D006801:Humans; D009270:Naloxone; D009490:Neurosecretory Systems / Q000378:metabolism*; D010146:Pain / Q000503:physiopathology* / Q000523:psychology; D005082:Physical Exertion; D013312:Stress, Physiological / Q000503:physiopathology*; D013315:Stress, Psychological / Q000503:physiopathology*; D004561:Transcutaneous Electric Nerve Stimulation; D001615:beta-Endorphin / Q000097:blood
D004723:Endorphins; D009270:Naloxone; D001615:beta-Endorphin