Raybould H E, Plourde V, Zittel T, Bover J, Quintero E
CURE/UCLA Digestive Diseases Center, VA Wadsworth Medical Center 90073.
Dig Dis Sci. 1994 Nov;39(11):2301-5. doi: 10.1007/BF02087642.
Severe gastric complications occur in uremic patients, yet few studies have addressed the effect of chronic renal failure (RF) on gastric physiology. In the present study, we investigated: (1) the effect of RF on gastric emptying of liquids and solids in awake rats, (2) the motor function in the gastric corpus, and (3) the role of nitric oxide in any alterations in gastric motor function in uremic rats. RF was induced by partial kidney infarction. RF had no effect on gastric emptying of liquids but significantly inhibited gastric emptying of solids by 68%. N-Nitro-L-arginine, an inhibitor of nitric oxide (NO) synthesis, had no effect on the reduced gastric emptying of solids in RF rats. RF rats showed an altered pattern of gastric motility compared to sham-operated rats. These data suggest that RF induced an inhibition of gastric emptying of solids, but not liquids. However, NO does not seem to play a role in this inhibition.
尿毒症患者会出现严重的胃部并发症,但很少有研究探讨慢性肾衰竭(RF)对胃生理的影响。在本研究中,我们调查了:(1)RF对清醒大鼠液体和固体胃排空的影响;(2)胃体的运动功能;(3)一氧化氮在尿毒症大鼠胃运动功能改变中的作用。通过部分肾梗死诱导RF。RF对液体胃排空没有影响,但显著抑制固体胃排空达68%。一氧化氮(NO)合成抑制剂N-硝基-L-精氨酸对RF大鼠固体胃排空减少没有影响。与假手术大鼠相比,RF大鼠的胃运动模式发生了改变。这些数据表明,RF诱导了固体胃排空的抑制,但对液体胃排空没有影响。然而,NO似乎在这种抑制中不起作用。