De Ponti F, Azpiroz F, Malagelada J R
Gastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota 55905.
Dig Dis Sci. 1989 Jun;34(6):873-81. doi: 10.1007/BF01540272.
The viscerovisceral reflex control of gastric tone remains poorly characterized. We have previously demonstrated physiological variations in gastric tone that occur during fasting and after feeding. These variations are neurally regulated. We have now compared the reflex mechanisms modulating gastric tone that are elicited by esophageal or duodenal distension in fasted, conscious dogs. To determine the pathways involved in these reflexes, we combined the technique of vagal blockade (by cooling the supradiaphragmatic vagi isolated within a surgically implanted cooling jacket) with the administration of autonomic drugs. Gastric tone was measured as the air volume within an intragastric bag maintained at a constant, low pressure by an electronic barostat. Standardized distensions were performed by means of an inflatable balloon-catheter positioned either in the mid-esophagus (in three dogs) or in the distal duodenum (in three dogs). A profound and consistent gastric relaxation was induced by distension of either the esophagus (247 +/- 21 ml delta volume, P less than 0.05) or the duodenum (238 +/- 29 ml, P less than 0.05). Supradiaphragmatic vagal cooling abolished the gastric relaxatory response to duodenal distension and significantly reduced, but did not completely suppress, the response to esophageal distension. Neither cholinergic stimulation (intravenous bethanechol) nor adrenergic blockade (combined intravenous phentolamine and propranolol) had any significant effect on either gastric relaxatory response. Combined adrenergic and cholinergic (intravenous atropine) blockade induced gastric relaxation, but failed to suppress the gastric responses. We conclude that both esophageal and duodenal distension elicit gastric relaxation by a noncholinergic vagal mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
胃张力的内脏-内脏反射控制目前仍未得到充分描述。我们之前已经证明了禁食期间和进食后胃张力会出现生理变化。这些变化受到神经调节。我们现在比较了在禁食、清醒的犬中,由食管或十二指肠扩张引发的调节胃张力的反射机制。为了确定这些反射所涉及的通路,我们将迷走神经阻断技术(通过冷却手术植入的冷却套中分离出的膈上迷走神经)与自主神经药物的给药相结合。胃张力通过置于胃内袋中的空气量来测量,该胃内袋由电子恒压器维持在恒定的低压。通过将可充气的球囊导管置于食管中部(三只犬)或十二指肠远端(三只犬)来进行标准化扩张。食管(247±21ml容积变化,P<0.05)或十二指肠(238±29ml,P<0.05)的扩张均诱导出显著且持续的胃松弛。膈上迷走神经冷却消除了胃对十二指肠扩张的松弛反应,并显著降低但未完全抑制对食管扩张的反应。胆碱能刺激(静脉注射氨甲酰甲胆碱)或肾上腺素能阻断(静脉联合注射酚妥拉明和普萘洛尔)对任何一种胃松弛反应均无显著影响。肾上腺素能和胆碱能联合阻断(静脉注射阿托品)诱导胃松弛,但未能抑制胃反应。我们得出结论,食管和十二指肠扩张均通过非胆碱能迷走神经机制引发胃松弛。(摘要截取自250字)