Jakob S M, Parviainen I, Ruokonen E, Uusaro A, Takala J
Department of of Anaesthesiology and Intensive Care Medicine, Kuopio University Hospital, Kuopio, Switzerland.
Acta Anaesthesiol Scand. 2005 Mar;49(3):390-6. doi: 10.1111/j.1399-6576.2005.00651.x.
Histamine(2) (H(2))-blocking agents can attenuate intragastric CO(2)-production by reducing gastric acid secretion and preventing the interaction between H(+) and bicarbonate. However, gastric acid production may be impaired in acute circulatory failure due to poor mucosal perfusion, and H(2)-blockade could further impair mucosal perfusion.
Forty patients with acute circulatory and/or respiratory failure, age 61 +/- 16 years (mean +/- SD), APACHE II score 21 +/- 7, and SOFA score 8 +/- 3, received randomly either ranitidine, 50 mg (R) or placebo (P) every 8 h. Gastric intraluminal pH (gpH; antimony probe with external reference electrode) and mucosal pCO(2) (prCO(2), semicontinuous air-tonometry) were measured during 24 h, and blood gases were taken at 6-h intervals.
Gastric intraluminal pH was 4.3 +/- 2.4 in P and 5.1 +/- 1.6 in R (NS). Mean prCO(2) was 6.8 +/- 2.7 kPa in P and 7.4 +/- 2.1 kPa in R, and mucosal-arterial pCO(2) gradient (Delta pCO(2)) was 2.2 +/- 2.9 kPa and 2.4 +/- 2.4 kPa, respectively (NS). Within-patient variabilities of gpH and prCO(2) were not influenced by ranitidine. A posthoc analysis revealed that non-survival in R was associated with a low mucosal pHi after 24 h (P = 0.002). This was explained by a low arterial pH but not by differences in gpH or prCO(2).
In acute respiratory and circulatory failure, H(2) blockade has an inconsistent impact on gpH and does not reduce variabilities of gpH or prCO(2).
组胺2(H₂)受体阻滞剂可通过减少胃酸分泌并防止H⁺与碳酸氢盐相互作用来减弱胃内二氧化碳生成。然而,由于黏膜灌注不良,急性循环衰竭时胃酸分泌可能受损,而H₂受体阻滞可能会进一步损害黏膜灌注。
40例急性循环和/或呼吸衰竭患者,年龄61±16岁(均值±标准差),急性生理与慢性健康状况评分系统(APACHE II)评分为21±7,序贯器官衰竭评估(SOFA)评分为8±3,随机每8小时接受雷尼替丁50 mg(R组)或安慰剂(P组)治疗。在24小时内测量胃腔内pH值(gpH;带有外部参比电极的锑电极探头)和黏膜PCO₂(prCO₂,半连续空气张力测定法),并每隔6小时采集血气样本。
P组胃腔内pH值为4.3±2.4,R组为5.1±1.6(无显著差异)。P组平均prCO₂为6.8±2.7 kPa,R组为7.4±2.1 kPa,黏膜-动脉PCO₂梯度(ΔPCO₂)分别为2.2±2.9 kPa和2.4±2.4 kPa(无显著差异)。雷尼替丁对患者胃腔内pH值和prCO₂的个体内变异性无影响。事后分析显示,R组未存活与24小时后黏膜内pH值低有关(P = 0.002)。这是由动脉pH值低所致,而非胃腔内pH值或prCO₂的差异。
在急性呼吸和循环衰竭中,H₂受体阻滞对胃腔内pH值的影响不一致,且不会降低胃腔内pH值或prCO₂的变异性。