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      Local somatothermal stimulation inhibits the motility of sphincter of Oddi in cats, rabbits and humans through nitrergic neural release of nitric oxide.

      Life Sciences
      Animals, Arginine, pharmacology, Atropine, Benzodiazepinones, Body Temperature, Cats, Devazepide, Female, Hormone Antagonists, Humans, Male, Manometry, Muscle Contraction, drug effects, Muscle Relaxation, NG-Nitroarginine Methyl Ester, Neurons, Efferent, metabolism, Nitric Oxide, Phentolamine, Propranolol, Rabbits, Sphincter of Oddi, physiology, Sympatholytics

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          Abstract

          To examine whether and how local somatothermal stimulation inhibits the function of the sphincter of Oddi (SO) in humans and in animals with different types of SO, we measured the activity of SO in anesthetized cats and rabbits by using continuously perfused open-tip manometric methods. Local somatothermal stimulation was achieved by applying an electroheating rod 0.5 cm away from the skin area near the right subcostal region. A heating pad was applied to the corresponding area in patients undergoing endoscopic retrograde cholangiopancreatography and biliary manometry. The motility of the biliary tract in cats, in terms of gall bladder pressure, tonic and phasic contraction pressure and frequency of SO before and during local heat were significantly different, respectively. The local heat-induced SO relaxation was not inhibited by pretreatment with atropine, propranolol, phentolamine or anti-cholecystokinin-octapeptide, but was almost completely blocked by infiltration of local anesthetics. Pretreatment with a nitric oxide synthesis inhibitor also blocked the relaxation, which was reversed by pretreatment with L-arginine, but not by D-arginine. The inhibition of SO motility by local heat in rabbits was also blocked by pretreatment with L-NAME, and this blockade was reversed by L-arginine. Application of local heat on patients demonstrated obvious inhibitory SO responses. We conclude that local somatothermal stimulation inhibits the SO motility in animals with different types of SO through the activation of heat-sensitive neural release of nitric oxide. This procedure may represent a simplified approach for the treatment of diseases with hypofunction of the L-arginine/NO pathway.

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