Cullen J J, Caropreso D K, Hemann L L, Hinkhouse M, Conklin J L, Ephgrave K S
Department of Surgery and Internal Medicine, University of Iowa College of Medicine and VAMC, Iowa City 52242, USA.
Dig Dis Sci. 1997 Apr;42(4):731-7. doi: 10.1023/a:1018847626936.
We hypothesized that the inhibitory neurotransmitters nitric oxide (NO) and vasoactive intestinal peptide (VIP) may play a role in the disrupted gastrointestinal motility of endotoxemia. Strain gauge transducers on the stomach and small intestine of dogs determined interdigestive gastrointestinal motility. Tissue levels of NO synthase and VIP and serum levels of nitrite/nitrate (NO(2)-/NO(3)-) and VIP were measured. Following completion of the baseline studies, dogs were given a single dose of E. coli lipopolysaccharide, 200 microg/kg intravenously, and the studies were repeated for the next three days. Following endotoxin bolus, the migrating motor complex (MMC) was delayed for two days while serum VIP was increased on postendotoxin day 1 and serum NO(2)-/NO(3)- was increased on postendotoxin day 2. There were no changes in gut smooth muscle levels of NO synthase or VIP. We conclude that a single, sublethal dose of endotoxin results in prolongation of the MMC with distinct but independent increases in serum levels of VIP and NO(2)-/NO(3)-.
我们推测,抑制性神经递质一氧化氮(NO)和血管活性肠肽(VIP)可能在内毒素血症所致胃肠动力紊乱中发挥作用。通过应变片传感器测定犬胃和小肠的消化间期胃肠动力。检测组织中一氧化氮合酶和血管活性肠肽水平以及血清中亚硝酸盐/硝酸盐(NO₂⁻/NO₃⁻)和血管活性肠肽水平。在完成基线研究后,给犬静脉注射单剂量200μg/kg的大肠杆菌脂多糖,随后三天重复进行研究。注射内毒素后,移行性运动复合波(MMC)延迟两天,同时内毒素注射后第1天血清血管活性肠肽升高,内毒素注射后第2天血清NO₂⁻/NO₃⁻升高。肠道平滑肌中一氧化氮合酶或血管活性肠肽水平无变化。我们得出结论,单剂量亚致死量内毒素导致MMC延长,同时血清血管活性肠肽和NO₂⁻/NO₃⁻水平有明显但独立的升高。