Intragastric nitric oxide is abolished in intubated patients and restored by nitrite
Intragastric nitric oxide is abolished in intubated patients and restored by nitrite
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DOI：
10.1097/01.ccm.0000171304.59502.aa
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发表时间：
2005-08-01
影响因子：
8.8
通讯作者：
Weitzberg, E
中科院分区：
文献类型：
--
作者：
Björne, H;Govoni, M;Weitzberg, E
目标。唾液中的亚硝酸盐在酸性胃中被还原为一氧化氮（NO），该一氧化氮可能具有胃保护功能。我们研究了健康对照者和气管插管重症监护病房患者在补充维生素c前后的胃内NO水平。nitrite.Design。前瞻性观察性研究，包括患者和对照组。环境：混合重症监护病房和大学实验室。患者和受试者。8名健康志愿者和10名插管、机械通气的重症监护病房患者。干预措施：首先在体外评估血压计导管，然后用于所有NO测量。在空腹对照组中，在唾液消耗期间和胃内亚硝酸盐输注后反复测量胃NO水平。在患者胃内亚硝酸盐输注后，测量胃内NO、血浆和胃液中亚硝酸盐以及胃液中s -亚硝基硫醇水平的变化。测量和主要结果：血压计导管的恢复率为80%，具有较高的类内和类间相关性。健康志愿者的中位基线NO水平为21.6 ppm（四分位数范围11.4-22.3 ppm），在唾液消耗25-50分钟期间下降90%至3.3 ppm （2.0-5.2 ppm）。亚硝酸盐灌胃可恢复一氧化氮水平。患者的基线NO水平几乎消失（0.1 ppm [0.07-0.4 ppm]），但在胃内亚硝酸盐输注期间迅速增加到124 ppm（范围，65-180 ppm）。血浆亚硝酸盐水平从0.18 +/- 0.03 μ M增加到1.3 +/- 0.2 μ M (p < 0.01)，胃液中s -亚硝基硫醇水平从0.12 +/- 0.09 μ M增加到6.7 +/- 1.8 μ M。胃内生成一氧化氮需要持续输送含亚硝酸盐的唾液，在危重患者中几乎被消除。然而，肠道补充亚硝酸盐可以完全恢复胃NO水平。未来的研究将揭示低NO水平是否会导致这些患者中常见的应激性溃疡和胃细菌过度生长，以及用亚硝酸盐恢复胃NO是否可能是一种有用的治疗方法。
Objective. Nitrite in saliva is reduced to nitric oxide (NO) in the acidic stomach, and this NO may serve gastroprotective functions. We studied intragastric NO levels in healthy controls and in intubated intensive care unit patients before and after supplementation with. nitrite.Design. Prospective observational study involving patients and controls.Setting: A mixed intensive care unit and a university laboratory.Patients and Subjects. Eight healthy volunteers and ten intubated, mechanically ventilated intensive care unit patients.Interventions: A tonometric catheter was first evaluated in vitro and then used for all NO measurements. In fasting controls, gastric NO levels were measured repeatedly during periods of saliva depletion and after an intragastric nitrite infusion. In patients, changes in levels of intragastric NO, nitrite in plasma and gastric juice, and S-nitrosothiols in gastric juice were measured in response to an intragastric nitrite infusion.Measurements and Main Results: The tonometric catheter had a recovery of 80% with a high intraclass and interclass correlation. Median baseline NO levels in healthy volunteers were 21.6 ppm (interquartile range, 11.4-22.3 ppm) and decreased by 90% to 3.3 ppm (2.0-5.2 ppm) during 25-50 mins of saliva depletion. The NO level was restored by an intragastric nitrite infusion. Baseline NO levels in patients were almost abolished (0.1 ppm [0.07-0.4 ppm]) but increased rapidly to 124 ppm (range, 65-180 ppm) during intragastric nitrite infusion. Nitrite levels in plasma increased from 0.18 +/- 0.03 to 1.3 +/- 0.2 mu M (p < .01), and levels of, S-nitrosothiols in gastric juice increased from 0.12 +/- 0.09 to 6.7 +/- 1.8 ILM.Conclusions. Intragastric generation of NO requires continuous delivery of nitrite-containing saliva and is almost abolished in critically ill, intubated patients. Enteral supplementation with nitrite could however fully restore gastric NO levels. Future studies will reveal if low NO levels contribute to stress ulcers and gastric overgrowth of bacteria often seen in these patients and in turn if restoring gastric NO with nitrite could be a useful therapeutic approach.