TY - JOUR
T1 - Visceral pain and public speaking stress
T2 - Neuroendocrine and immune cell responses in healthy subjects
AU - Lucas, A.
AU - Holtmann, G.
AU - Gerken, G.
AU - Pietsch, A.
AU - Braun-Lang, U.
AU - Gilani, K.
AU - Strassburger, K.
AU - Gesing, S.
AU - Janssen, O. E.
AU - Kavelaars, A.
AU - Heijnen, C. J.
AU - Schedlowski, M.
AU - Elsenbruch, S.
N1 - Funding Information:
This work was funded by the Deutsche Forschungsgemeinschaft (DFG) (DFG Sche 341/11-1) and the Netherland Organization for Scientific Research (NWO).
PY - 2006/1
Y1 - 2006/1
N2 - Whereas responses to psychological stressors are well-characterized, little is known regarding responses to painful visceral stimuli. We analyzed the emotional, cardiovascular, neuroendocrine, and cellular immune responses to painful rectal stimulation and psychological stress in healthy individuals. Eleven healthy subjects were studied in three conditions on separate days: painful rectal distension, public speaking stress, and rest. Blood was drawn for endocrinological and immunological analyses; heart rate and blood pressure were measured continuously; state anxiety was assessed with a questionnaire (STAI-S). Anxiety scores were highest in the rectal distension condition. This was evident following rectal distension (mean STAI-S scores: 44.2 ± 3.5 post-distension vs. 36.6 ± 3.8 post-speech, p < .05), but anxiety was also elevated at baseline (41.6 ± 3.9 vs. 32 ± 3.2 recovery, p < .01). This anticipatory effect was reflected by elevated baseline cortisol (p < .05) and baseline ACTH (p < .01) levels, as well as circulating lymphocytes and lymphocyte subsets, including decreased basal CD3 +CD4+ cells (p < .05) and increased CD16 +CD56+ cells (p = .06) compared to rest. Both public speech and rectal distension induced cardiovascular activation, but the effect was more pronounced following rectal distension (+63.8 ± 9.4 mmHg in response to distension vs. +36.4 ± 6.2 mmHg in response to speech for systolic BP, p < .05). Different response patterns were also observed in the distribution of circulating leukocytes and lymphocyte subsets, including CD16+CD56+ cells (p < .05). An acute visceral pain stimulus causes profound emotional, neuroendocrine, and immune cell responses, which are markedly affected by anticipatory anxiety. These findings may have implications for conditions associated with visceral hyperalgesia.
AB - Whereas responses to psychological stressors are well-characterized, little is known regarding responses to painful visceral stimuli. We analyzed the emotional, cardiovascular, neuroendocrine, and cellular immune responses to painful rectal stimulation and psychological stress in healthy individuals. Eleven healthy subjects were studied in three conditions on separate days: painful rectal distension, public speaking stress, and rest. Blood was drawn for endocrinological and immunological analyses; heart rate and blood pressure were measured continuously; state anxiety was assessed with a questionnaire (STAI-S). Anxiety scores were highest in the rectal distension condition. This was evident following rectal distension (mean STAI-S scores: 44.2 ± 3.5 post-distension vs. 36.6 ± 3.8 post-speech, p < .05), but anxiety was also elevated at baseline (41.6 ± 3.9 vs. 32 ± 3.2 recovery, p < .01). This anticipatory effect was reflected by elevated baseline cortisol (p < .05) and baseline ACTH (p < .01) levels, as well as circulating lymphocytes and lymphocyte subsets, including decreased basal CD3 +CD4+ cells (p < .05) and increased CD16 +CD56+ cells (p = .06) compared to rest. Both public speech and rectal distension induced cardiovascular activation, but the effect was more pronounced following rectal distension (+63.8 ± 9.4 mmHg in response to distension vs. +36.4 ± 6.2 mmHg in response to speech for systolic BP, p < .05). Different response patterns were also observed in the distribution of circulating leukocytes and lymphocyte subsets, including CD16+CD56+ cells (p < .05). An acute visceral pain stimulus causes profound emotional, neuroendocrine, and immune cell responses, which are markedly affected by anticipatory anxiety. These findings may have implications for conditions associated with visceral hyperalgesia.
KW - Gastrointestinal pain
KW - Psychological stress
KW - Public speaking stress
KW - Rectal distension
KW - Visceral pain
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U2 - 10.1016/j.bbi.2005.03.009
DO - 10.1016/j.bbi.2005.03.009
M3 - Article
C2 - 16364816
AN - SCOPUS:29144447516
SN - 0889-1591
VL - 20
SP - 49
EP - 56
JO - Brain, behavior, and immunity
JF - Brain, behavior, and immunity
IS - 1
ER -