Fraser R, Horowitz M, Dent J
Gastroenterology Unit, Royal Adelaide Hospital, South Australia.
Gut. 1991 May;32(5):475-8. doi: 10.1136/gut.32.5.475.
The motor correlates of the delay in gastric emptying produced by hyperglycaemia were investigated in 11 healthy volunteers. Fasting gastroduodenal motility was measured during euglycaemia (blood glucose concentration 3-5 mmol/l) and during hyperglycaemia induced by intravenous dextrose (blood glucose concentration 12-16 mmol/l). Antral, pyloric, and proximal duodenal pressures were recorded by a sleeve/sidehole manometric assembly positioned across the pylorus, with the aid of measurements of transmucosal potential difference. During hyperglycaemia there was stimulation of isolated pyloric pressure waves when compared with the euglycaemia period (p less than 0.05). This was associated with inhibition of antral pressure waves (p less than 0.05). In nine of the 11 subjects an episode of duodenal 'phase III like' activity occurred within 15 minutes of the onset of hyperglycaemia. It is proposed that the stimulation of localised pyloric contractions and inhibition of antral contractions contribute to the delayed gastric emptying induced by hyperglycaemia. Abnormal gastric motility in patients with diabetes mellitus may be the result of hyperglycaemia itself, rather than irreversible autonomic neuropathy.
在11名健康志愿者中研究了高血糖导致胃排空延迟的运动相关性。在血糖正常(血糖浓度3 - 5 mmol/l)和静脉输注葡萄糖诱导的高血糖(血糖浓度12 - 16 mmol/l)期间测量空腹胃十二指肠运动。借助跨黏膜电位差测量,通过横跨幽门放置的袖带/侧孔测压组件记录胃窦、幽门和十二指肠近端压力。与血糖正常期相比,高血糖期间孤立的幽门压力波受到刺激(p < 0.05)。这与胃窦压力波受抑制有关(p < 0.05)。11名受试者中有9名在高血糖发作后15分钟内出现十二指肠“类似Ⅲ期”活动。有人提出,局部幽门收缩的刺激和胃窦收缩的抑制导致了高血糖引起的胃排空延迟。糖尿病患者的胃动力异常可能是高血糖本身所致,而非不可逆的自主神经病变。