Kim C H, Zinsmeister A R, Malagelada J R
Gastroenterology Unit, Mayo Clinic, Rochester, Minnesota 55905.
Dig Dis Sci. 1988 Feb;33(2):193-9. doi: 10.1007/BF01535733.
The effect of electrical dysrhythmias on the mechanical activity of the fed stomach was investigated in 5 conscious dogs implanted with Ag-AgCl electrodes and strain gauge force transducers. Each dog was fed 1 can of ALPO and electromechanical activities of the stomach were recorded for the next 120 min. The results show that intraarterial boluses of met-enkephalin (75 micrograms/kg), PGE2 (36 micrograms/kg), and epinephrine (36 micrograms/kg) induced episodes of antral dysrhythmias whereas saline (1 cc) did not. The postcibal antral motility index for the test period was not altered following saline injection, but it was reduced by 61%, 70%, and 81% following the administration of met-enkephalin, epinephrine, and PGE2, respectively (p less than 0.01 vs. baseline period). During periods of normal electrical rhythm, PGE2 and epinephrine significantly reduced the antral motility index (2.07 +/- 0.93 and 3.24 +/- 0.79, respectively) vs. saline (7.92 +/- 0.44) (p less than 0.05 for both drugs) whereas met-enkephalin (4.98 +/- 0.56) did not. In contrast, during episodes of dysrhythmia, met-enkephalin significantly depressed antral motility (1.70 +/- 0.74) (p less than 0.05 vs. periods with normal electrical rhythm) whereas neither epinephrine nor PGE2 caused a further reduction in antral motility from what was seen during periods of normal electrical rhythm (1.84 +/- 0.72 and 1.34 +/- 0.37, respectively). We thus conclude that intraarterial administration of met-enkephalin, PGE2, or epinephrine induce gastric dysrhythmias postcibally and depress antral contractile activity. The relaxatory effect of met-enkephalin on antral contractions is primarily due to its dysrhythmic effect whereas PGE2 and epinephrine inhibit antral motility even when the electrical rhythm is undisturbed.
在5只植入了银-氯化银电极和应变片式力传感器的清醒犬中，研究了心律失常对进食后胃机械活动的影响。每只犬喂食1罐阿尔波宠物食品（ALPO），并在接下来的120分钟记录胃的机电活动。结果显示，动脉内注射甲硫氨酸脑啡肽（75微克/千克）、前列腺素E2（36微克/千克）和肾上腺素（36微克/千克）可诱发胃窦部心律失常发作，而注射生理盐水（1毫升）则不会。注射生理盐水后，测试期的餐后胃窦部运动指数未改变，但注射甲硫氨酸脑啡肽、肾上腺素和前列腺素E2后，该指数分别降低了61%、70%和81%（与基线期相比，p<0.01）。在正常电节律期间，与注射生理盐水相比，前列腺素E2和肾上腺素显著降低胃窦部运动指数（分别为2.07±0.93和3.24±0.79）（两种药物p均<0.05），而甲硫氨酸脑啡肽（4.98±0.56）则无此作用。相反，在心律失常发作期间，甲硫氨酸脑啡肽显著抑制胃窦部运动（1.70±0.74）（与正常电节律期相比，p<0.05），而肾上腺素和前列腺素E2均未使胃窦部运动比正常电节律期进一步降低（分别为1.84±0.72和1.34±0.37）。因此，我们得出结论，动脉内注射甲硫氨酸脑啡肽、前列腺素E2或肾上腺素可在进食后诱发胃节律失常并抑制胃窦部收缩活动。甲硫氨酸脑啡肽对胃窦部收缩的松弛作用主要归因于其致心律失常作用，而前列腺素E2和肾上腺素即使在电节律未受干扰时也能抑制胃窦部运动。
