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 present study confirms that N-terminal fragments of ACTH have an affinity for rat brain opiate receptors in vitro. Such peptides, devoid of corticotrophic activity, were found to inhibit morphine-induced analgesia if they also possessed affinity for opiate receptors in vitro. The structure-activity relationship for these two parameters is comparable to that observed for the same peptides on the induction of excessive grooming.
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PMID:Interaction between ACTH fragments, brain opiate receptors and morphine-induced analgesia. 18 67

Maternal plasma ACTH, cortisol and TSH concentrations were determined during the course of the induced labours of 20 normal parturients. Alternate mothers were given segmental epidural analgesia for pain relief during the first stage of labour. The remaining parturients served as controls. The ACTH level rose in same way in both groups, reaching its peak at the moment of delivery and decreasing rapidly thereafter. Cortisol secretion reached its maximum during the first stage of labour in the moment of delivery. After delivery the cortisol level decreased more rapidly in the epidural group tha. in the control gro,p. Umbilical venous cortisol concentration was the same in both groups. The maternal TSH level did not change significantly during labour in either group.
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PMID:The effect of segmental epidural analgesia on maternal ACTH, cortisol and TSH during labour. 18 74

Both C-terminal fragments of lipotropin (beta-LPH) (endorphins) and N-terminal fragments (e.g., ACTH 4-10) delayed extinction of pole-jumping avoidance behavior in rats. After subcutaneous injection Met5-enkephalin appeared to be as active as ACTH 4-10 whereas beta-LPH 61-69, alpha- and beta-endorphin were more potent in delaying extinction of pole-jumping avoidance behavior (approximate ED50 of alpha-endorphin 4 x 10(-11) M rat.) However, the potency of beta-LPH 61-69 and alpha-endorphin appeared to be approximately the same whereas that of beta-endorphin was less than that of ACTH 4-10 after intraventricular administration (approximate ED50 of alpha-endorphin 0.2 x 10(-11) M rat). alpha-Endorphin and ACTH 4-10, administered subcutaneously in a dose which markedly delayed extinction of pole-jumping avoidance behavior, had only slight effects on open field behavior and on responsiveness to electric footshock. A 5 times higher dose of both peptides facilitated passive avoidance behavior. Morphine in two doses significantly delayed extinction of pole-jumping avoidance behavior but the effect was not dose dependent. The specific opiate antagonist naltrexone, however, markedly facilitated extinction of the avoidance response. ACTH 4-10, alpha- and beta-endorphin and a behaviorally potent ACTH 4-9 analog (Org 2766) restored pole-jumping avoidance behavior of rats pretreated with naltrexone. Treatment with a similar dose of naltrexone blocked beta-endorphin-induced analgesia. These results suggest that the influence of peptides related to C-terminal and N-terminal fragments of lipotropin on extinction of avoidance behavior may be dissociated from those exerted on opiate receptor sites. Subcutaneously injected beta-LPH 61-69 or intraventricularly administered beta-endorphin induced a shift from lower to higher frequencies of hippocampal theta rhythm during paradoxical sleep in the same way as that found after ACTH 4-10. This effect is interpreted as indicating an increased arousal state in certain midbrain limbic structures. This may, as has been postulated for ACTH 4-10, alter the motivational value of environmental stimuli (e.g., aversive stimulation).
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PMID:Behavioral and electrophysiological effects of peptides related to lipotropin (beta-LPH). 20 66

These experiments characterized the analgesia resulting from exposure to certain noxious and/or stressful manipulations. Rats exposed either to electric grid shock (0.35-2.0 mA for 10-30 sec) or to 5 min of presumably non-painful centrifugal rotation (about 7.0 transverse g's) were analgesic as measured by tail-flick, hot plate and responses to applications of a calibrated paw pinch or alligator clip. Analgesia produced by shock (SA) or centrifugal rotation (RA) persisted after termination of these manipulations. Neither SA nor RA were attended by generalized sensory, attentional or motoric deficits. Intraperitoneal injection of hypertonic saline also increased tail-flick latencies. Exposure to brief ether anesthesia or horizontal oscillation, both of which have been reported to increase ACTH secretion (a commonly used indicator of stress), did not produce analgesia as measured by the tail-flick test. The use of classical conditioning procedures to pair shock with environmental stimuli resulted in increased tail-flick latencies. The narcotic antagonist naloxone (1 mg/kg, i.p.) did not reduce the tail-flick inhibition produced by shock, rotation, hypertonic saline or classical conditioning. Chlordiazepoxide (5 mg/kg, i.p.) also failed to antagonize the increased tail-flick latencies produced by shock or conditioning. Tail-flick inhibition produced by shock or rotation was markedly reduced by complete spinal cord transection at thoracic levels. These results suggest that: (1) the selective modulation of nociceptive input at the level of the spinal cord can be mediated by a supraspinal system or systems physiologically distinct from those involved in analgesia produced by the administration of opiates; (2) non-narcotic modulation of nociceptive input occurring within the spinal cord can be learned by exposure to classical conditioning procedures; and (3) noxious stimuli are sufficient but not necessary to produce a non-narcotic analgesia; stress alone, however, is not always sufficient to produce this analgesia.
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PMID:Behavioral and physiological studies of non-narcotic analgesia in the rat elicited by certain environmental stimuli. 68 16

Surgical stress leads to reproducible physiological metabolic and hormonal responses, characterized by on altered carbohydrate metabolism, a net loss of protein and an increased lipolysis. They are due to an increased secretion of catecholamines, ACTH, cortisol and cytokines. Epidural analgesia prevents the hyperglycaemic, cortisol and adrenocortical responses to surgery. The lipolysis and the loss of protein are also attenuated. This effect only occurs in lower abdominal surgery, with an epidural blockade extending from T4 to S5, carried out with local anesthetic agents and started before the skin incision. However, such a blockade abates, but does not suppress, the metabolic response to upper abdominal or thoracic surgery, probably because of persistent vagal afferences, the incomplete blockade of somatic afferents, and a stimulation of the diaphragm and peritoneal free nerve endings. Likewise, epidural morphine does not modify the intraoperative metabolic and hormonal responses. The main reason is most probably the failure of opioids to block the sympathetic system, as well as their insignificant effects on fast conducting fibers.
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PMID:[Epidural anesthesia and metabolic response to surgical stress]. 130 61

Potentials in the final sector of the afferent pathway from the acupuncture point (AP) were enhanced by intraperitoneal 0.5 mg/kg morphine without changing the threshold of AP stimulation and greatly decreased by hypophysectomy. The decreased potentials were restored to the control level by morphine (0.5 mg/kg, IP). Potentials evoked in the final sector of the afferent pathway from the nonacupuncture point (NAP) by NAP stimulation after lesion of the analgesia inhibitory system were greatly enhanced by corticotropin (ACTH) (0.25 mg/kg, IP) and greatly decreased by hypophysectomy. Diminished potentials were restored to the control level by ACTH (0.25 mg/kg, IP). Both morphine (0.5 mg/kg, IP) and ACTH (0.25 mg/kg, IP) produced analgesia, but morphine did not affect acupuncture analgesia (AA) and ACTH did not affect nonacupuncture point stimulation-produced analgesia (NAA). All analgesia, that due to 0.5 mg/kg morphine or 0.25 mg/kg ACTH, AA, and NAA were abolished by hypophysectomy. The abolished AA and NAA were restored by 0.5 mg/kg morphine and 0.25 mg/kg ACTH, respectively. Hence, beta-E and ACTH liberated from the pituitary gland by stimulation of an AP and NAP may act as positive feedback on the AA and NAA afferent pathways, respectively.
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PMID:Positive feedback action of pituitary beta-endorphin on acupuncture analgesia afferent pathway. 132 98

Analgesia (NAA) caused by nonacupuncture point (abdominal muscle) stimulation after lesioning the analgesia inhibitory system (AIS) or treating the subject with proglumide was abolished by hypophysectomy or adrenalectomy. The final sector of the NAA afferent pathway from the nonacupuncture point to the pituitary gland and the initial sector of the descending pain inhibitory system were found in the anterior and posterior arcuate nucleus (A-HARN and P-HARN), respectively. Analgesia caused by ACTH microinjected into the P-HARN disappeared after denervation of the A-HARN, but that caused by dopamine did not. Firing rates of P-HARN neurons were increased by nonacupuncture point simulation (NAPS) after lesion of the AIS or treatment with proglumide. The NAPS responsive neurons also responded to ultramicroinjected dopamine, but not to ultramicroinjected ACTH. Both NAA and NAPS responsive neuron activity that were abolished by hypophysectomy were restored by concurrent application of NAPS and intraperitoneal ACTH. Reduction of sodium ions due to adrenalectomy was found to abolish NAA. It was concluded that NAA production involves dopaminergic transmission in the HARN and ACTH acting presynaptically on this transmission.
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PMID:Analgesia produced by pituitary ACTH and dopaminergic transmission in the arcuate. 165 17

Twenty-eight patients undergoing upper abdominal operations (mainly selective proximal vagotomy [SPV]) were referred for assessment of the hormonal metabolic reaction (adrenocorticotropic hormone [ACTH], arginine vasopressin [AVP], cortisol, and glucose), the postoperative pain reaction, and respiration according to the method of anesthesia (group 1: neuroleptanesthesia [NLA], group 2: NLA in combination with epidural opiate analgesia, group 3: NLA in combination with local anesthesia). To alleviate postoperative pain piritramide was systematically administered in group 1, whereas in groups 2 and 3 a thoracic epidural catheter was injected with morphine or bupivacaine. Postoperative analgesia was better in patients with epidural administration than in those with systemic application. On the 1st and 2nd postoperative days the vital capacity was statistically significantly higher by 10%-15% in groups 2 and 3 than in group 1. As expected, the neurohormonal and metabolic stress response was highest in all patients in the intraoperative and immediate postoperative phases: ACTH, AVP, and glucose levels were in most cases significantly higher compared with the initial values. However, cortisol levels decreased intraoperatively, probably as a result of the generally used induction agent etomidate. Comparison of the three methods of anesthesia revealed that all mean hormone levels analyzed in group 2 patients were lower both intraoperatively and 2 h postoperatively, which implies that epidurally administered morphine reduces the stress reaction, probably indirectly through additional selective alleviation of pain at the spinal cord level. The various differences in hormonal reactions of patients in groups 1 and 3 gave no clear evidence, however, of possible mitigation of the stress reaction by epidural local anesthetics in upper abdominal operations.
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PMID:[The effect of combination epidural anesthesia techniques in upper abdominal surgery on the stress reaction, pain control and respiratory mechanics]. 175 31

Lesion of the preoptic area (POA) or medial arcuate nucleus (M-HARN) abolished acupuncture analgesia (AA). Potentials in the median eminence (ME) evoked by stimulation of the acupuncture point (AP) were not affected by lesion of either the POA or M-HARN alone, but were abolished by concurrent lesion of both. No analgesia was produced by stimulation of the POA. Analgesia produced by stimulation of the M-HARN was abolished by lesion of the POA, and the abolished analgesia was restored by concurrent stimulation of the POA and M-HARN, hence POA and M-HARN outputs might converge in the ME to produce AA. Similar convergence from the anterior arcuate nucleus (A-HARN) and POA to the ME was observed in analgesia (NAA) produced by stimulation of a nonacupuncture point (NAP). Two pathways diverged from the lateral hypothalamus in the AA afferent pathway and two from the lateral periaqueductal central gray (L-PAG) in the NAA afferent pathway. POA potentials evoked by stimulation of the AP were reversed by naloxone, and those evoked by stimulation of the AP were reversed by dexamethasone. ACTH sensitive sites were found in both the L-PAG and the anterior hypothalamus.
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PMID:Convergence from the preoptic area and arcuate nucleus to the median eminence in acupuncture and nonacupuncture point stimulation analgesia. 193 97

Effects of prenatal stress on stress-induced behavioral and hormonal responses were investigated in preweanling rats at two ages. Prenatal stress treatments involved the application of uncontrollable electric shocks to pregnant rats every other day throughout gestation. Offspring of undisturbed rats in home cages served as controls. When male pups were 14 and 21 days old, ultrasonic vocalizations and freezing were recorded in 10-min tests involving isolation, and isolation with the application of electric foot shocks at either 0.5- or 2.0-mA intensity. Immediately before and after each test, tail-flick latencies were measured in order to assess alterations in stress-induced analgesia. Stress-induced secretion of ACTH was measured in plasma obtained after the second tail-flick test. Results indicated that 14-day-old prenatally stressed pups emitted significantly fewer ultrasonic vocalizations and exhibited significantly lower percent increases in tail-flick latencies than control pups. Plasma ACTH, however, was significantly elevated in prenatally stressed rats, suggesting that exposure to different tests was a stress-inducing event. At 21 days of age, prenatally stressed rats no longer differed significantly from control males in the exhibition of ultrasonic vocalizations, defensive freezing, and tail-flick latencies. Plasma ACTH content, however, was significantly lower in prenatally stressed than control males after exposure to the isolation with 2.0-mA shock test. The involvement of motivational, maturational, and mediational factors is examined in order to account for these age-dependent and stressor-dependent differences in behavioral and hormonal responses occurring between prenatally stressed and control pups.
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PMID:Ontogeny of behavioral and hormonal responses to stress in prenatally stressed male rat pups. 215 65


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