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Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy
DOES THE AUTONOMIC SYSTEM CONTRIBUTE TO PAIN-RELATED ENDOTHELIAL DYSFUNCTION ?
Abstract number: S01
PAOLETTI1 G, VARANINI2 M, CARLI1 G, BALOCCHI2 R, MORIZZO3 C, PALOMBO3 C, SANTARCANGELO4 EL
1Department of Physiology, University of Siena
2Institute of Clinical Physiology, National Council of Research, Pisa
3Department of Internal Medicine
4Department of Physiological Sciences, University of Pisa (Italy)
Aim:
Studies (Jambrik et al 2004; 2005) on flow-mediated vascular dilation (FMD) in subjects with high (Highs) and low (Lows) hypnotizability showed lower reduction of FMD ("endothelial dysfunction") in Highs during nociceptive stimulation with (AN) and without suggestions for analgesia (PAIN) and during mental computation (MC). The experiment investigates the role of hemodynamic factors possibly modulating shear stress differentially and, thus, accounting for the hypnotizability-related FMD differences. The cardiovascular correlates of pain imagery (IM) were also studied because they might affect the shift from acute to chronic pain.
Methods:
Heart rate, blood pressure and skin blood flow were monitored during basal conditions, PAIN, AN, MC and IM (2 min each) in non hypnotized Highs (n=20) and Lows (n=20).
Results:
The results did not show any difference between Highs and Lows in the stimulation-related changes in heart rate and blood pressure, while the skin mean blood flow changed only in Lows.
Conclusions:
The local activity of vasoactive factors, i. e. nitric oxide and endothelin 1, rather than sympathetically-mediated control, is responsible for the hypnotizability-related FMD differences observed. Results do not confirm that High may be more prone than Lows to a shift from acute to chronic pain because of a more pronounced autonomic response to pain imagery and indirectly support the hypothesis of a lower vulnerability of Highs to cardiovascular disease.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :S01