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组织间液积聚不影响家兔小肠对氧气的摄取。

Interstitial fluid accumulation does not influence oxygen uptake in the rabbit small intestine.

作者信息

Ostgaard G, Reed R K

机构信息

Department of Physiology, University of Bergen, Norway.

出版信息

Acta Anaesthesiol Scand. 1995 Feb;39(2):167-73. doi: 10.1111/j.1399-6576.1995.tb04037.x.

Abstract

Crystalloid resuscitation increases interstitial fluid volume. Intestinal ischemia and impaired barrier function may contribute to the precipitation of multiple organ failure. Accordingly, the intestine was chosen as target organ to test whether interstitial oedema impairs oxygen extraction by the tissue. The portal vein in anaesthetized rabbits was partially obstructed for 30 min along with an intravenous infusion of 0.9% saline 60-90 ml kg-1 (oedema group, n = 7). Total water content of the small intestine increased from 3.4 ml g-1 dry weight in control (n = 8) to 3.9 ml g-1 in the oedema group (P = 0.049). Small intestinal O2 uptake was calculated from the arteriovenous O2 content and electromagnetic flow measurements in the superior mesenteric artery. Mesenteric flow was reduced stepwise by a snare occluder around the artery. Intestinal oxygenation was monitored indirectly as well, by means of mesenteric venous lactate, arterial base excess and by mucosal pH (pHi) assessed tonometrically. The oxygen extraction ratios were similar in the oedema and control group at similar oxygen supplies. After a 45 min flow reduction to 15% of baseline mesenteric venous lactate and pHi did not differ between the groups. pHi averaged 7.31 and fell to 6.74. Below an intestinal O2 uptake of 2.5 ml min-1, pHi correlated somewhat better with O2 uptake (r = 0.66) than did arterial base excess (r = 0.50). The results indicate that acute elevation of extracellular volume to the extent in the present study, does not impede oxygen uptake in the gut.

摘要

晶体液复苏会增加组织间液容量。肠道缺血和屏障功能受损可能促使多器官功能衰竭的发生。因此,选择肠道作为靶器官,以测试组织间水肿是否会损害组织对氧的摄取。对麻醉兔的门静脉进行30分钟的部分阻断,同时静脉输注0.9%生理盐水60 - 90 ml·kg-1(水肿组,n = 7)。小肠的总含水量从对照组(n = 8)的3.4 ml·g-1干重增加到水肿组的3.9 ml·g-1(P = 0.049)。小肠的氧摄取量通过肠系膜上动脉的动静脉氧含量和电磁血流测量来计算。通过围绕动脉的圈套器逐步减少肠系膜血流。还通过肠系膜静脉乳酸、动脉碱剩余以及通过张力测定法评估的黏膜pH(pHi)间接监测肠道氧合情况。在相似的氧供应条件下,水肿组和对照组的氧摄取率相似。在肠系膜血流减少至基线的15%持续45分钟后,两组之间的肠系膜静脉乳酸和pHi没有差异。pHi平均为7.31,降至6.74。在小肠氧摄取量低于2.5 ml·min-1时,pHi与氧摄取量的相关性(r = 0.66)比动脉碱剩余(r = 0.50)稍好。结果表明,在本研究中细胞外液量急性升高至该程度,并不妨碍肠道对氧的摄取。

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