Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The emotional responses induced when individuals are confronted with noxious or threatening stimuli, or with a disadvantageous environment, must be a signal of alertness, usually accompanied by an analgesic effect which might be elicited by activation of intrinsic pain-inhibitory systems (stress-induced analgesia, SIA), as one of the basic adaptive mechanisms of animals and humans. In this report, the author will present the involvement of opioid or non-opioid mediated mechanism, role of the emotional responses, endocrinological implication such as hypothalamus-pituitary-adrenal cortex-axis and hypothalamus-sympatho-adrenal medulla-axis, and relation to classical neurotransmitters and their receptors, in the production of analgesia induced by exposure to stresses, especially footshock, forced swimming and psychological stresses. Furthermore, the author also will discuss the possible underlying mechanism in the blockade of the development of tolerance to morphine analgesia by concurrent exposure to footshock or psychological stress, which is one of our recent findings.
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PMID:[Stress-induced analgesia]. 184 52

The analgesic effect induced by exposure to psychological stress, using a communication box (psychological stress-induced analgesia, PSY-SIA), was completely antagonized by 10 min pretreatment with 0.5, 1 and 2 mg/kg of nor-binaltorphimine and with 0.5 and 1 mg/kg of Mr2266, selective kappa-opioid receptor antagonists, in the tail pinch method. Neither footshock (FS)- nor forced swimming (SW)-SIA was affected by these antagonists. The selective delta-opioid receptor antagonist naltrindole, at doses up to 20 mg/kg, had no appreciable effect on PSY-SIA. Daily morphine treatment, 10 mg/kg, s.c., resulted in tolerance to the analgesic effect, and concurrent exposure to PSY-stress suppressed the development of morphine tolerance. The substitution of treatment with U-50,488H for PSY-stress still resulted in analgesia on the initial day; and likewise, the suppression by U-50,488H of the development of morphine tolerance was replicated by PSY-stress. Pretreatment with nor-binaltorphimine antagonized the suppressive effect of PSY-stress on the development of morphine tolerance without affecting the analgesic effect of morphine per se. These results provide further evidence that PSY-SIA involves the mediation by kappa-opioid receptor mechanisms.
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PMID:Further evidence for the implication of a kappa-opioid receptor mechanism in the production of psychological stress-induced analgesia. 217 Jul 23

Psychological (PSY) stress using the communication box produced a short-lasting antinociceptive effect which was less potent than that induced by physical stress such as footshock (FS) and forced swimming (SW) in mice. Naloxone completely antagonized PSY-stress induced analgesia (SIA) when the analgesia was measured by the tail pinch (TP) method; however, the antagonist did not reverse the effect in the tail flick (TF) assay. On the other hand, FS-SIA was antagonized by naloxone in both methods, while naloxone failed to reverse SW-SIA in either TF or TP assessment. Daily exposure to psychological stress developed tolerance to the analgesia. One-way cross-tolerance between PSY-SIA and morphine and the naloxone antagonism of PSY-SIA by the tail pinch method lead to the suggestion that an endogenous opioid system may be involved in the underlying mechanism for its production. On the contrary, from the findings of cross-tolerance between SW- or FS-SIA and the lack of naloxone antagonism in the TF method, the involvement of a more complicated mechanism is suggested in PSY-SIA. In both tests, U-50488H, a selective kappa-agonist, produced profound analgesia; however, no appreciable antagonism of naloxone was found in the TF test, whereas the effect was completely blocked by naloxone in the TP test. From the similarity in naloxone antagonism of PSY-stress and U-50488H induced analgesia, the participation of a common mechanism which may be mediated by kappa-opioid receptors, is suggested in the production of PSY-SIA.
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PMID:Implication of endogenous opioid mechanism in the production of the antinociceptive effect induced by psychological stress in mice. 282 8

In the runner study, as measured by tourniquet ischemic pain, exercise stress produced hypoalgesia 20 minutes post-run, followed by hyperalgesia and euphoria at 30 minutes. The hypoalgesia and euphoria were reversed by naloxone. Exercise stress also produced a decrease in P(A), suggesting hypoalgesia to the thermal cutaneous stimulation. However, this analgesia was not naloxone reversible. Nor did exercise stress produce analgesia to cold-pressor pain. In the acupuncture study, noxious electrical stimulation of classical acupuncture sites failed to produce analgesia either during or after stimulation. However, expectation did produce a change in the pain report criterion, but only in the acupunctured arm. Noxious electrical stimulation (TENS) of the median nerve produced no analgesia outside of the related segmental area, that is, acute electrical pain did not produce generalized hypoalgesia. Thus, the effects of the stress produced by noxious electrical stimulation differ from that produced by exercise. In contrast to the results of the acute pain studies, chronic clinical pain, which combines mental stress and pain stress, produced strong hypoalgesia and anesthesia. Again, in contrast to the acute experimental pain studies, the emotional stress of mental illness produces hypoalgesia, but not anesthesia. Finally, the somatosensory system is not the only the sensory system affected by stress. Cold-pressor pain decreases visual sensitivity both during and for a few minutes following stimulation, and does not interfere with short-term (supra-digit span) memory.
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PMID:Altered pain and visual sensitivity in humans: the effects of acute and chronic stress. 294 86

Exposure to footshock (2 mA, 1-sec duration, 0.2 Hz for 15 min; FS), forced swimming (water at 20 degrees C for 3 min, SW) or psychological stress (using a communication box for 5 min, PSY) produced antinociceptive effects (stress-induced analgesia, SIA). Intracerebroventricular (i.c.v.) injection of glibenclamide (10-40 micrograms/mouse), an ATP-sensitive K+ (KATP) channel blocker, antagonized FS-SIA, while SW- and PSY-SIA were unaffected by the compound. Cromakalim (0.1-10 micrograms/mouse, i.c.v.), a KATP-channel opener, did not affect FS-, SW- or PSY-SIA. Thus, we provided evidence that central KATP channels participate in the production of FS-SIA but not production of SW- or PSY-SIA; and we suggest that glibenclamide, through closing of KATP channels, suppresses mu-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of mu-receptors.
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PMID:Implication of ATP-sensitive K+ channels in various stress-induced analgesia (SIA) in mice. 885 12

Psychological stress is believed to be implicated in the etiology of affective disorders such as anxiety and depression. To date, a wide range of behavioral responses including analgesia and motor suppression induced by various physiological stressors such as footshock, forced swimming and immobilization have been investigated in animals. However, there is little information concerning behavioral changes in psychological stress. This article describes the experimental procedures and the characteristics of motor suppression in psychological stress, defined as conditioned fear stress (CFS). Mice exhibit a marked suppression of motility when they are re-placed in the same environment in which they had previously received an electric footshock. This motor suppression is regarded as a conditioned emotional response to the environment associated with previous footshock. The motor suppression in CFS is attenuated by sigma receptor agonists such as (+)-N-allylnormetazocine and dextromethorphan, whereas typical anxiolytics (diazepam and chlordiazepoxide) and antidepressants (imipramine and fluoxetine) have no effect. These findings suggest that the CFS model may be useful for investigating the pathogenesis of affective disorders, particularly those considered to be treatment resistant, and for developing their novel therapeutic drugs.
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PMID:[The psychological stress model using motor suppression]. 1020 85

This study investigated the combined effect of neonatal maternal separation and acute psychological stress on pain responses in adult rats. Long-Evans dams and their male pups were reared under two conditions: 1) 180 min daily maternal separation (MS180) on postnatal days 2-14 or 2) no handling or separation (NH). At 2 mo of age, visceromotor responses to graded intensities of phasic colorectal distension (10-80 mmHg) at baseline as well as following acute 60 min water avoidance stress (WA) were significantly higher in MS180 rats. Both groups showed similar stress-induced visceral hyperalgesia in the presence of naloxone (20 mg/kg ip). MS180 rats had smaller stress-induced cutaneous analgesia in the tail-flick test compared with NH rats, with a residual naloxone-resistant component. MS180 rats showed an enhanced fecal pellet output following WA or exposure to a novel environment. These data suggest that early life events predispose adult Long-Evans rats to develop visceral hyperalgesia, reduced somatic analgesia, and increased colonic motility in response to an acute psychological stressor, mimicking the cardinal features of irritable bowel syndrome.
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PMID:Neonatal maternal separation alters stress-induced responses to viscerosomatic nociceptive stimuli in rat. 1180 52

Surgery is associated with immune alterations, which are the combined result of tissue damage, anesthesia, postoperative pain, and psychological stress. In the present study, we compared the effects of several postoperative pain management techniques on postoperative immune function. Patients hospitalized for abdominal surgery were randomly assigned to one of three postoperative pain management techniques: opiates on demand (intermittent opiate regimen [IOR]), patient-controlled analgesia (PCA), and patient-controlled epidural analgesia (PCEA). Postoperative pain was assessed. Blood samples were collected before and 24, 48, and 72 h after surgery. Production of interleukin (IL)-1beta, IL-2, and IL-6, natural killer cell cytotoxicity, and lymphocyte mitogenic responses were assessed. Patients of the PCEA group exhibited lower pain scores in the first 24 h after surgery compared with patients of the IOR and PCA groups. Mitogenic responses were suppressed in all groups in the first 24 h, returned to preoperative values by 72 h in the PCEA group, but remained suppressed in the PCA group. Production of IL-1beta and IL-6 increased in the IOR and PCA groups, whereas it remained almost unchanged in the PCEA group. Patients receiving an epidural mixture of opiate and local anesthetics (PCEA group) exhibited reduced suppression of lymphocyte proliferation and attenuated proinflammatory cytokine response in the postoperative period.
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PMID:The effects of postoperative pain management on immune response to surgery. 1293 9

Hypothalamo-pituitary-adrenal (HPA)-axis activation is a response of the organism to psychological and physical stress, resulting in elevated levels of glucocorticoids, mainly cortisol in humans. In our previous studies we found post-mortem blood and cerebrospinal fluid (CSF) cortisol levels to be up to 20-fold higher than in vivo levels. Since clinical observations point to similar strong elevations of cortisol in fatally ill patients, we suggested that the high post-mortem cortisol levels might be due to the stress during the process of dying. We hypothesized that if the cortisol rise during dying is due to the psychological stress of the impending death, then the rise in cortisol should be inversely proportional to the degree of dementia, and that high-dose morphine giving analgesia, sedation, and sleep would suppress this response. Therefore, we measured the cortisol levels by radioimmunoassay (RIA) in the post-mortem CSF of 85 Alzheimer patients and 52 controls. In addition, post-mortem serum cortisol of 17 subjects from the Alzheimer group and nine from the control group were measured. The Alzheimer patients were subdivided according to their degree of dementia, as scored on the Reisberg Scale, before their death. All groups were further analyzed for the effect of morphine treatment, as well as for the effects of the confounding factors like age, gender, time, and season of death. Alzheimer patients had significantly higher cortisol levels than controls, both in CSF (mean (nmol/l)+/-SEM: 482+/-32 vs 285+/-30, respectively, p<0.001) and in serum (2854+/-279 vs 1533+/-395, p=0.011). Mean CSF cortisol level of the severely demented Alzheimer group was even significantly higher than that of mildly demented group (508+/-35 vs 225+/-65, p=0.024) and controls (p<0.001). Cortisol levels correlated positively with the degree of dementia in the Alzheimer group (r=0.236, p=0.035). High-dose morphine did not cause a suppression of cortisol rise, neither in controls nor in Alzheimer patients. Our results indicate that the extreme elevations of cortisol levels during dying are rather due to the organic stress of the organism than to psychological stress of the patient, and is not suppressed by high-dose morphine.
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PMID:Stress of dying is not suppressed by high-dose morphine or by dementia. 1295 97

Acute stress has been shown to increase latencies of nociceptive reflexes, and this effect is considered evidence for stress-induced analgesia. However, tests for nociception that rely on motivated operant escape assess cerebral processing of pain and could be modulated independent of reflex responses. We therefore compared the effects of an acute stressor (restraint) on escape responses and lick/guard reflexes to stimulation of the paws by a thermally regulated floor. Testing sessions included a pre-test exposure to 36 degrees C, followed by a test trial in which either escape from 44 or 36 degrees C or reflex responses to 44 degrees C were observed. Behavioral responses to stress were assessed during a three day period, with baseline testing on day 1, post-stress or control testing on day 2, and evaluation of long-term stress effects on day 3. On day 2, half the animals received 15 min of restraint stress, followed by 15-min pre-test and test trials. Licking and guarding responses to thermal stimulation during 44 degrees C test trials were significantly reduced by restraint stress, confirming previously reported stress effects on nociceptive reflexes. In contrast, learned escape responses to the same thermal stimulus were significantly enhanced after stress. The increase in operant sensitivity suggests that acute restraint, a form of psychological stress, produces hyperalgesia for a level of thermal stimulation that preferentially activates C nociceptors. These results are discussed in relation to studies involving physical or psychological forms of stress, different nociceptive stimuli, and assessment strategies used to evaluate thermal pain sensitivity.
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PMID:Differential effects of stress on escape and reflex responses to nociceptive thermal stimuli in the rat. 1449 66


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