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RISS 인기검색어
- 검색키워드
- 저자 : ( G. F. Gebhart ) (검색결과 3 건)
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Adenosine Receptor Agonists Modulate Visceral Hyperalgesia in the Rat
( Chong Il Sohn ),( Hyo Jin Park ),( G. F. Gebhart ) 대한소화기기능성질환·운동학회 2008 Gut and Liver Vol.2 No.1
Background/Aims: Adenosine is an endogenous modulator of nociception. Its role in visceral nociception, particularly in visceral hyperalgesia, has not been studied. The aim of this study was to determine the effects of adenosine receptor agonists in a model of visceral hyperalgesia. Methods: The visceromotor response (VMR) in rats to colorectal distension (CRD; 80 mmHg, 20 seconds) was quantified by electromyographic recordings from the abdominal musculature. Three hours after the intracolonic administration of zymosan (25 mg/mL, 1 mL), VMRs to CRD were measured before and after either subcutaneous or intrathecal administration of an adenosine receptor agonist. Results: Subcutaneous injection of 5`-N-ethylcarboxyamidoadenosine (NECA; an A1 and A2 receptor agonist), R(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA; a selective A1 receptor agonist), or CGS-21680 hydrochloride (a selective A2a receptor agonist) dose-dependently (10-100 mg/kg) attenuated the VMR to CRD, although hindlimb weakness occurred at the higher doses tested. Intrathecal administration of NECA or R-PIA dose-dependently (0.1-1.0μg/kg) decreased the VMR, whereas CGS-21680 hydrochloride was ineffective over the same concentration range. Higher intrathecal doses of the A1/A2 receptor agonist NECA produced motor weakness. Conclusions: Adenosine receptor agonists are antihyperalgesic, but also produce motor weakness at high doses. However, activation of the spinal A1 receptor significantly attenuates the VMR to CRD without producing motor weakness. (Gut and Liver 2008;2:39-46)
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Gebhart, G.F. 대한소화관운동학회 2003 Journal of Neurogastroenterology and Motility (JNM Vol.9 No.3
The physiology of visceral afferent pathways was the emphasis of study in the recent past, and we now understand much better how mechanoreceptors contribute to acute noxious events in the viscera. The pathophysiology of visceal sensory neurons is not as well understood, but it is clear that they share with their somatic counterparts the ability to sensitize. In the cutaneous sensory realm, however, only nociceptors sensitize, whereas both low- and high- threshold mecha-nosensitive visceral sensory neurons sensitize. Accordingly, both mechanosensitive populations in the viscera can contribute to discomfort and pain, Knowledge about the potential contribution of the nonmechanosensitive population of visceral receptors in mucosa, muscle, and/or serosa to visceral pain and visceral hyperalgesia is limited at present. However, given the approximately fourfold greater size of the low-threshold population of mechanosensitive afferent fibers, acute inflammatory events in the viscera are conceivably represented in the central nervous system by a greatly increased afferent input relative to normal. Because these receptors are polymodal, intraluminal chemical or mechanical visceral stimuli in the physiological range have the potential to contribute significantly to altered sensations arising from the viscera.
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