Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: a selective role for endogenous opioids.
Ischemic pain was produced by a blood pressure cuff placed to the arm of healthy human subjects for 15 min which produced a mean pain score of 59% (visual analogue scale). Ischemia induced a significant dental pain threshold elevation (mean 67%) and 2 mg of naloxone did not reduce it. Thermal sensitivity of the upper lip had a tendency to reduction during ischemia and 2 mg of naloxone reduced this effect. Tactile thresholds in the forehead or in the contralateral arm were not markedly elevated. Neither ACTH nor prolactin level in the plasma was related to the dental pain threshold elevation during ischemia. The findings of the present study suggest that ischemic pain nonsegmentally produces a predominant inhibition of responses to thin afferents. Endogenous opioids may markedly contribute to the reduction of thermal sensitivity induced by ischemia, but their contribution to dental pain threshold elevations seems to be less important. Stress or other adenohypophyseal mechanisms involving the release of ACTH or prolactin do not explain the effects of ischemia found in the present study.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001132:Arm / Q000098:blood supply; D001794:Blood Pressure; D004723:Endorphins / Q000502:physiology*; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D009270:Naloxone; D010146:Pain / Q000503:physiopathology*; D011388:Prolactin / Q000097:blood; D012039:Regional Blood Flow; D014111:Tourniquets
D004723:Endorphins; D009270:Naloxone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin