26 October 2006

Pain and cocaine

Blockade of tolerance to morphine analgesia by cocaine
Misra, et al.
Tolerance to morphine was induced in male Sprague-Dawley rats by s.c. implantation of a morphine base pellet (75 mg) on the first and second day and determining the magnitude of tolerance 72 h after the first implant by s.c. injection of a test dose of morphine (5 mg/kg). Implantation of a cocaine hydrochloride pellet (25 mg), concurrently with morphine pellets or of a cocaine hydrochloride (50 mg) pellet after the development of tolerance, blocked both the development and expression of morphine analgesic tolerance. In morphine-pelleted animals pretreatment for 3 days with desipramine or zimelidine or phenoxybenzamine but not haloperidol produced no significant morphine tolerance. Pretreatment with a combination of desipramine and zimelidine, however, was as effective as cocaine in blocking morphine tolerance. ?-Methyl-p-tyrosine methyl ester counteracted the effect of cocaine in blocking morphine tolerance and potentiated the tolerance development. Blockade of morphine tolerance by cocaine was reinforced and facilitated by pretreatment with fenfluramine or p-chlorophenylalanine ethyl ester and to a lesser extent by clonidine and haloperidol. Acute administration of fenfluramine or zimelidine or a combination of desipramine and zimelidine or ?-methyl-p-tyrosine methyl ester or p-chlorophenylalanine ethyl ester did not significantly affect morphine analgesia. The study suggests an important role of the concomitant depletion of both central noradrenaline and serotonin in the blockade of morphine tolerance by cocaine and stresses the importance of the counter-balancing functional relationship between these two neurotransmitters in the central nervous system.
(c) 1989 Elsevier Science

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24 October 2006

Exercise-induced stress analgesia?

Exercise-induced analgesia: fact or artifact?
Padawer and Levine
This study critically examines the reported exercise-induced previous termanalgesianext term effect in view of the potential previous termstressnext term-induced previous termanalgesianext term of pain testing itself. Two designs were used to test whether previous findings of previous termanalgesianext term were induced by the exercise procedures or by the previous termstressnext term of the pain testing procedures themselves used in such experiments. In the first design, post-test cold pressor pain ratings were obtained from college students following exercise (bicycle ergometry) and two control tasks (minimal exercise and non-exercise). No significant differences between these groups were found. In the second design, exercise and non-exercise groups pre-exposed to cold pressor pain testing were compared to groups that were not pre-exposed to pain testing. There were no significant effects for exercise; however, significant previous termanalgesianext term effects for pain test pre-exposure were demonstrated. Therefore previous research claiming exercise-induced previous termanalgesianext term may have confounded the effects of exercise with the effects of pre-exposure to pain testing itself.
(c)1992 Elsevier Science

Pain 48 (2) 1992, 131-135
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15 October 2006

Age differences in endogenous analgesia

Age-related differences in the endogenous analgesic response to repeated cold water immersion in human volunteers
Washington, et al.
Recent animal studies using stress-induced analgesia have suggested a general age-related decline in endogenous pain inhibitory systems.
The aim of the current study was to examine age-related differences in the magnitude of endogenous analgesia in human volunteers, using
psychophysical measures of neuroselective electrical, and thermal CO2 laser induced pain thresholds, before, immediately after and 1 h after
repeated cold water immersion of the hand. Sensory detection thresholds did not differ between age groups indicating that the functional
integrity of primary afferent sensory ®bres appears to be intact in older people. Consistent with many previous studies, older adults required a
higher intensity of noxious stimulation in order to ®rst report the presence of pain. The cold water immersion task was effective in eliciting a
powerful analgesic response, regardless of age; pain thresholds were shown to increase by up to 100% immediately after the cold pressor test.
This effect was relatively transient with thresholds returning to baseline within 1 h. The magnitude of analgesic response, however, was found
to be signi®cantly less in older people. Age differences in the ef®cacy of endogenous analgesic systems may be expected to reduce the ability
of older adults to cope with severe persistent pain states and may help explain some of the variation in the literature on pain report.
(c) 2000 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.
Pain 89 (2000) 89-96
PII: S0304-3959(00)00352-3
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10 October 2006

Negative affect and pain

Negative affect: effects on an evaluative measure of human pain
Rhudy, et al.
Prior work indicates that exposure to fear-inducing shock inhibits finger-withdrawal to radiant heat in humans (hypoalgesia), whereas
anxiety induced by threat of shock enhances reactivity (hyperalgesia; Pain 84 (2000) 65–75). Although finger-withdrawal latencies are
thought to reflect changes in pain sensitivity, additional measures of pain are needed to determine whether pain perception is altered. The
present study examined the impact of negative affect on visual analog scale (VAS) ratings of fixed duration thermal stimuli. One hundred
twenty-seven male and female human subjects were randomly assigned to one of three emotion-induction conditions: (1) negative affect
induced by exposure to three brief shocks; (2) negative affect elicited by the threat of shock without presentation; and (3) neutral affect, with
no intervention. VAS ratings were tested before and after emotion-induction. Results suggest that both negative affect manipulations reduced
pain. Manipulation checks indicated that the emotion-induction treatments induced similar levels of fear but with different arousal levels.
Potential mechanisms for affect induced changes in pain are discussed.
(c) 2003 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.

Pain 104 (2003) 617-626

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05 October 2006

Stress-induced analgesia

Cigarette smoking, stress-induced analgesia and pain perception in men and women
Girdler, et al.
This study examined gender differences in smoking-related analgesia and stress-induced analgesia (SIA), as a function of pain modality. Forty men (20 smokers, 20 nonsmokers) and 37 women (17 smokers) were tested twice for pain sensitivity to tourniquet ischemia, thermal heat, and cold pressor tests; once following mental stress and once following rest control, counterbalancing order. Cardiovascular and neuroendocrine responses to mental stress were also examined. While expected gender differences in pain sensitivity were observed, women smokers had greater threshold and tolerance times to ischemic pain than women nonsmokers (P!0.05) when pain testing followed rest. Male smokers had greater threshold and tolerance to cold pressor pain than male nonsmokers (P!0.05) after both rest and stress Only women showed evidence for SIA, since women nonsmokers demonstrated greater ischemic pain threshold and tolerance following mental stress versus rest (P!0.05), and all women reported lower thermal heat pain unpleasantness after stress versus rest (PZ0.05). Only nonsmokers showed expected inverse relationships between sympathetic and hypothalamic–pituitary–adrenal (HPA) axis reactivity measures and sensitivity to pain. Smokers showed evidence for blunted HPA-axis function at rest and stress. These results indicate that analgesia related to both being a smoker and stress is influenced by gender and pain modality. The reduced pain perception in smokers and absence of relationships between endogenous pain regulatory mechanisms and pain sensitivity may reflect a maladaptive response to chronic smoking.
(c) 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Pain 114(2005) 372-385

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