Rigaud D, Chastre J, Accary J P, Bonfils S, Gibert C, Hance A J
Chest. 1986 Jul;90(1):58-63. doi: 10.1378/chest.90.1.58.
The ability of H2 receptor antagonists and continuous enteral alimentation to maintain high intragastric pH in patients with chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation was evaluated by continuously monitoring intragastric pH prior to and following sequential addition of ranitidine or continuous enteral alimentation (or both) to their therapeutic regimen. Prior to therapy, intragastric pH was less than 4.0 for 75 +/- 10 percent of the time, but never less than 1.0. Nevertheless, this moderate gastric acidity was associated with evidence of mucosal injury. Ranitidine failed to continuously maintain a high intragastric pH (pH less than 4.0 for 35 +/- 11 percent of the time; p greater than 0.2 compared to patients treated with placebo). Following administration of continuous enteral alimentation, intragastric pH fell, and ranitidine therapy only partially blocked this increase in gastric acidity induced by continuous enteral alimentation. We conclude that without treatment, patients with COPD who have acute respiratory failure may develop gastric mucosal injury despite the presence of only moderate intragastric acidity; however, ranitidine and continuous enteral alimentation are not effective in maintaining a high intragastric pH.
通过在慢性阻塞性肺疾病(COPD)需要机械通气的患者治疗方案中依次添加雷尼替丁或持续肠内营养(或两者都添加)之前和之后连续监测胃内pH值,评估了H2受体拮抗剂和持续肠内营养维持高胃内pH值的能力。治疗前,胃内pH值在75±10%的时间内低于4.0,但从未低于1.0。然而,这种中度胃酸与黏膜损伤的证据有关。雷尼替丁未能持续维持高胃内pH值(胃内pH值在35±11%的时间内低于4.0;与接受安慰剂治疗的患者相比,p>0.2)。给予持续肠内营养后,胃内pH值下降,雷尼替丁治疗仅部分阻断了由持续肠内营养引起的胃酸增加。我们得出结论,未经治疗的急性呼吸衰竭COPD患者,尽管仅存在中度胃酸,仍可能发生胃黏膜损伤;然而,雷尼替丁和持续肠内营养在维持高胃内pH值方面无效。