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)

It has been demonstrated in animal model of somatic pain that hypothalamic paraventricular nucleus (PVN) participates in acupuncture analgesia, probably by mediation of vasopressin release. The role of PVN in acupuncture analgesia for experimental visceral pain in rats was further investigated in the present study. Experimental results demonstrated that electroacupuncture could inhibit the writhing response, produced by intraperitoneal injection of antimonium potassium tartrate and this inhibitory effect could be enhanced by electrical stimulation of PVN, but decreased by electrolytical lesion of PVN, intracerebroventricular injection of vasopressin antiserum (14 microliters) or the vasopressin antagonist, d(CH2)5Tyr(Me)-AVP (500 ng/5 microliters). Intraperitoneal administration of the latter drug (10 micrograms/kg), however, was ineffective. The above experimental results suggest that vasopressinergic neurons in PVN also participate in the inhibition of visceral pain by electroacupuncture.
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PMID:[Involvement of vasopressinergic neurons of paraventricular nucleus in the electroacupuncture-induced inhibition of experimental visceral pain in rats]. 129 59

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

Recent evidence has indicated that vasopressin (VP) can increase the pain threshold. It is not clear whether the paraventricular nucleus (PVN) of hypothalamus, which is one of the main nuclei that secrete VP in brain, is involved in the acupuncture analgesia (AA). The present study was designed to examine the role of PVN in AA. Experiments were carried out on Wistar rats using tail stimulation vocalization test to measure the pain threshold. The acupoints "Renzhong" and "Chengjiang" were selected for electroacupuncture. Electrical stimulation of PVN could increase significantly the pain threshold and enhance the effect of AA. On the contrary, electrolytical lesion of PVN could decrease the effect of AA obviously, which could be recovered by cerebroventricular injection (ICV) of 300 ng of arginine VP. Pretreatment with AVP-antiserum (ICV) could attenuate the effect of AA. These data indicated that PVN plays an important role in pain modulation and in the effect of AA. This role might be mediated by the VP-containing neurons in PVN.
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PMID:[The role of paraventricular nucleus of hypothalamus in acupuncture analgesia in rats]. 187

This study was undertaken to evaluate the analgesic effect of paraventricular nucleus (PVN) stimulation with tail stimulation-vocalization test. The mechanism of this analgesia was analysed with nuclear lesion and microinjection technique. The main results were as follows: (1) Electrical stimulation of the PVN could significantly enhance the pain threshold and increase the content of AVP in brainstem measured by radioimmunoassay. (2) Solitary tract nucleus (STN) lesion could eliminate the analgesic effect induced by PVN stimulation. (3) Intranuclear microinjection of AVP-antagonist and AVP-antiserum into the STN could block the analgesic effect of PVN stimulation. (4) Intranuclear microinjection of AVP into the STN could mimick the analgesic effect similar to that of PVN stimulation. These results suggest that electrical stimulation of the PVN could produce an analgesic effect. This effect might be mediated by the activation of VP-ergic neurons in PVN and upon releasing VP from the descending fibers, the activities of neurons in the STN are influenced.
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PMID:[Involvement of solitary tract nucleus in analgesic effect produced by paraventricular nucleus stimulation]. 206 81

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

Recent studies have provided several lines of evidence that peripheral administration of oxytocin induces analgesia in human and rodents. However, the exact underlying mechanism of analgesia still remains elusive. In the present study, we aimed to identify which receptor could mediate the analgesic effect of intraperitoneal injection of oxytocin and its cellular mechanisms in thermal pain behavior. We found that oxytocin-induced analgesia could be reversed by d(CH2)5[Tyr(Me)2,Dab5] AVP, a vasopressin-1a (V1a) receptor antagonist, but not by desGly-NH2-d(CH2)5[DTyr2, Thr4]OVT, an oxytocin receptor antagonist. Single cell RT-PCR analysis revealed that V1a receptor, compared to oxytocin, vasopressin-1b and vasopressin-2 receptors, was more profoundly expressed in dorsal root ganglion (DRG) neurons and the expression of V1a receptor was predominant in transient receptor potential vanilloid 1 (TRPV1)-expressing DRG neurons. Fura-2 based calcium imaging experiments showed that capsaicin-induced calcium transient was significantly inhibited by oxytocin and that such inhibition was reversed by V1a receptor antagonist. Additionally, whole cell patch clamp recording demonstrated that oxytocin significantly increased potassium conductance via V1a receptor in DRG neurons. Taken together, our findings suggest that analgesic effects produced by peripheral administration of oxytocin were attributable to the activation of V1a receptor, resulting in reduction of TRPV1 activity and enhancement of potassium conductance in DRG neurons.
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PMID:Oxytocin produces thermal analgesia via vasopressin-1a receptor by modulating TRPV1 and potassium conductance in the dorsal root ganglion neurons. 2952 Jan 70