Snygg Johan, Aneman Anders, Pettersson Anders, Fändriks Lars
Department of Anaesthesiology and Intensive Care, Sahlgrens University Hospital, Göteborg, Sweden.
Crit Care Med. 2003 Aug;31(8):2198-204. doi: 10.1097/01.CCM.0000080489.67211.1F.
Nitric oxide regulates epithelial permeability and other properties of the intestinal mucosal barrier. It previously has been shown in animals that intestinal mucosal nitric oxide production is impaired during gut hypoperfusion. The study was performed to confirm the presence of intestinal mucosal nitric oxide production in humans and to investigate the effect of gut hypoperfusion due to moderate arterial hypotension on intestinal nitric oxide concentrations.
Open study where each subject served as his own control.
Clinical research laboratory.
Nine healthy volunteers were intubated with a nasogastrointestinal tube for recordings in the distal duodenum. Intestinal nitric oxide output and motility were assessed by tonometry and manometry, respectively. Laser Doppler flowmetry and plasma angiotensin II concentration were used to investigate mucosal perfusion and a vasoregulatory response.
Moderate hypotension was induced with lower body negative pressure over 1 hr.
Intestinal nitric oxide production varied in parallel with the migrating motor complex. Low values were obtained during phase I and peak values during phase III. Lower body negative pressure was initiated at a well-defined point in the migrating motor complex cycle. It was followed by a 40 +/- 6% reduction of laser Doppler flow signal, a 778 +/- 138% increase in angiotensin II, and a reduction in intestinal mucosal nitric oxide production by 48 +/- 8%. After lower body negative pressure, laser Doppler signal and angiotensin II concentrations returned to baseline levels within 1 hr, whereas intestinal nitric oxide output remained decreased.
Intestinal tonometry in humans exhibits a considerable mucosal nitric oxide formation that varies in relation to intestinal motility. Intestinal nitric oxide production is depressed during conditions with lowered mucosal blood perfusion.
一氧化氮调节上皮通透性及肠黏膜屏障的其他特性。此前在动物实验中已表明，肠道低灌注时肠黏膜一氧化氮生成受损。本研究旨在证实人类肠黏膜一氧化氮生成的存在，并探究中度动脉低血压所致肠道低灌注对肠道一氧化氮浓度的影响。
开放性研究，每位受试者作为自身对照。
临床研究实验室。
9名健康志愿者经鼻胃管插管，用于记录十二指肠远端情况。分别通过张力测定法和压力测定法评估肠道一氧化氮输出及蠕动。使用激光多普勒血流仪和血浆血管紧张素II浓度来研究黏膜灌注及血管调节反应。
通过下体负压诱导中度低血压，持续1小时。
肠道一氧化氮生成与移行性运动复合波平行变化。在I期获得低值，在III期获得峰值。在下体负压于移行性运动复合波周期的明确时间点开始后，激光多普勒血流信号降低40±6%，血管紧张素II升高778±138%，肠黏膜一氧化氮生成减少48±8%。下体负压后，激光多普勒信号和血管紧张素II浓度在1小时内恢复至基线水平，而肠道一氧化氮输出仍降低。
人体肠道张力测定显示存在相当数量的黏膜一氧化氮生成，其与肠道蠕动相关。在黏膜血流灌注降低的情况下，肠道一氧化氮生成减少。
