Hasler W L, Kim M S, Chey W D, Stevenson V, Stein B, Owyang C
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0362, USA.
Am J Physiol. 1995 Apr;268(4 Pt 1):G539-47. doi: 10.1152/ajpgi.1995.268.4.G539.
Motion sickness is associated with gastric slow wave disruption. Animal models of slow wave disturbances show dependence on neural and prostaglandin pathways. Roles of these pathways in circular vection-evoked gastric dysrhythmias and nausea were tested. Eight volunteers with histories of motion sickness underwent vection (60 degrees/s), during which nausea (0 = none to 3 = severe) and electrogastrographic parameters were assessed. Tachygastric activity was expressed as the signal percentage at frequencies of > 4.5 cycles/min. Circular vection induced a maximal nausea score of 2.8 +/- 0 at 513 +/- 66 s. Tachygastric activity increased from 18 +/- 2 to 37 +/- 4% (P < 0.05) and peaked before maximal nausea. Atropine reduced nausea scores to 0 +/- 0 (P < 0.01) with no increase in tachygastric activity (14 +/- 6%). In contrast, the peripheral muscarinic antagonist methscopolamine did not reduce tachygastric activity (46 +/- 4%), nausea (1.8 +/- 0.5), or time to maximal tachygastric activity (504 +/- 80 s) with vection. Phentolamine reduced nausea (1.5 +/- 0.3, P < 0.01) and tachygastric activity, and delayed their onset, whereas propranolol and naloxone had no effect. Pretreatment with oral indomethacin (50 mg) three times daily for 3 days had no effect on vection-evoked tachygastric activity or nausea. To conclude, circular vection evokes gastric dysrhythmias that correlate temporally with maximal nausea and are suppressed by atropine, but not methscopolamine, and are reduced by phentolamine. In contrast to other models of slow wave disruption, endogenous prostaglandins play no role. Thus central cholinergic pathways mediate vection-evoked dysrhythmias with additional modulation by alpha-adrenergic pathways.
晕动病与胃慢波紊乱有关。慢波干扰的动物模型显示其依赖于神经和前列腺素途径。测试了这些途径在圆周性视动诱发的胃节律失常和恶心方面的作用。八名有晕动病史的志愿者接受视动（60度/秒），在此期间评估恶心程度（0 = 无至3 = 严重）和胃电图参数。快胃活动以频率>4.5次/分钟时的信号百分比表示。圆周性视动在513±66秒时诱发的最大恶心评分为2.8±0。快胃活动从18±2%增加到37±4%（P<0.05），并在最大恶心之前达到峰值。阿托品将恶心评分降至0±0（P<0.01），而快胃活动没有增加（14±6%）。相比之下，外周毒蕈碱拮抗剂甲基东莨菪碱对视动时的快胃活动（46±4%）、恶心程度（1.8±0.5）或达到最大快胃活动的时间（504±80秒）没有影响。酚妥拉明减轻了恶心程度（1.5±0.3，P<0.01）和快胃活动，并延迟了它们的发作，而普萘洛尔和纳洛酮则没有效果。每天三次口服吲哚美辛（50毫克），连续3天，对视动诱发的快胃活动或恶心没有影响。总之，圆周性视动诱发胃节律失常，其在时间上与最大恶心程度相关，且被阿托品抑制，但不被甲基东莨菪碱抑制，并被酚妥拉明减轻。与其他慢波干扰模型不同，内源性前列腺素不起作用。因此，中枢胆碱能途径介导视动诱发的节律失常，并受到α-肾上腺素能途径的额外调节。
