A controlled comparison of drug effects on escape from conditioned aversive stimulation (“anxiety”) and from continuous shock

James A. Dinsmoor; James C. Bonbright; Daniel R. Lilie

doi:10.1007/bf00406871

A controlled comparison of drug effects on escape from conditioned aversive stimulation (“anxiety”) and from continuous shock

Psychopharmacology ◽

10.1007/bf00406871 ◽

1971 ◽

Vol 22 (4) ◽

pp. 323-332 ◽

Cited By ~ 6

Author(s):

James A. Dinsmoor ◽

James C. Bonbright ◽

Daniel R. Lilie

Keyword(s):

Drug Effects ◽

Aversive Stimulation ◽

Continuous Shock

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Reduction in Pain Sensitivity from Pharmacological Elevation of Blood Pressure in Persons with Chronically Low Blood Pressure

Journal of Psychophysiology ◽

10.1027/0269-8803.23.3.104 ◽

2009 ◽

Vol 23 (3) ◽

pp. 104-112 ◽

Cited By ~ 12

Author(s):

Stefan Duschek ◽

Heike Heiss ◽

Boriana Buechner ◽

Rainer Schandry

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Pain Sensitivity ◽

Pain Threshold ◽

Pain Perception ◽

Drug Effects ◽

Pressure Effects ◽

Double Blind ◽

Low Blood Pressure ◽

Present Trial

Recent studies have revealed evidence for increased pain sensitivity in individuals with chronically low blood pressure. The present trial explored whether pain sensitivity can be reduced by pharmacological elevation of blood pressure. Effects of the sympathomimetic midodrine on threshold and tolerance to heat pain were examined in 52 hypotensive persons (mean blood pressure 96/61 mmHg) based on a randomized, placebo-controlled, double-blind design. Heat stimuli were applied to the forearm via a contact thermode. Confounding of drug effects on pain perception with changes in skin temperature, temperature sensitivity, and mood were statistically controlled for. Compared to placebo, higher pain threshold and tolerance, increased blood pressure, as well as reduced heart rate were observed under the sympathomimetic condition. Increases in systolic blood pressure between points of measurement correlated positively with increases in pain threshold and tolerance, and decreases in heart rate were associated with increases in pain threshold. The findings underline the causal role of hypotension in the augmented pain sensitivity related to this condition. Pain reduction as a function of heart rate decrease suggests involvement of a baroreceptor-related mechanism in the pain attrition. The increased proneness of persons with chronic hypotension toward clinical pain is discussed.

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