Methods for detecting focal intestinal ischemic anaerobic metabolic acidosis by PCO2
Methods for detecting focal intestinal ischemic anaerobic metabolic acidosis by PCO2
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DOI：
10.1152/jappl.1996.81.4.1834
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发表时间：
1996-10-01
影响因子：
3.3
通讯作者：
Schlichtig, R
中科院分区：
文献类型：
--
作者：
Rozenfeld, RA;Dishart, MK;Schlichtig, R
肠缺血通常通过在与组织PCO 2平衡后，在盐水填充的球囊眼压计中由动脉血浆HCO 3-和PCO 2计算假想的组织间质pH（Pti（CO2））来评估。Pti（CO2）可替代地被假定为等于该肠道区域中的静脉PCO 2（Pv（CO2））。这个想法是，随着血流量减少，肠道Pti（CO2）和Pv（CO2）将增加到最大有氧值，即，最大呼吸Pv（CO2）（Pv（CO2 rmax））。在“临界”无氧阈值以上，通过滴定组织HCO 3-产生乳酸盐（La-），应将Pti（CO2）提高到Pv（CO2 rmax）以上。在6只戊巴比妥麻醉猪的渐进式选择性全肠流量减少过程中，我们使用PCO 2电极来检验以下假设：粘膜中比浆膜中更早达到临界Pti（CO2），并且使用体外模型计算的Pv（CO2 rmax）预测临界Pti（CO2）。我们将临界Pti（CO2）定义为Pti（CO2）-Pv（CO2）与O-2输送（QO（2））曲线的拐点。O-2摄取的临界QO（2）为12.55 +/- 2 ml。kg（-1）。min（-1）。粘膜和浆膜的临界Pti（CO2）在相似的全肠QO（2）（13.90 +/- 5和13.36 +/- 5 ml）时达到。kg（-1）。min（-1），P = NS）。临界Pti（CO2）（129 +/- 24和96 +/- 21 Torr）超过Pv（CO2 rmax）（62 +/- 3 Torr）。在缺血期间，La-排泄到门静脉血中与K+排泄相匹配，导致Pv（CO2）仅略微增加，尽管Pti（CO2）上升到380 +/- 46（粘膜）和280 +/- 38（浆膜）Torr。这些结果表明，粘膜和浆膜成为dysocompatibility同时，缺血性dysocompatibility肠基本上是未灌注，并在体外预测的Pv（CO2 rmax）低估了临界Pti（CO2）。
Gut ischemia is often assessed by computing an imaginary tissue interstitial pH from arterial plasma HCO3- and PCO2 in a saline-filled balloon tonometer after equilibration with tissue PCO2 (Pti(CO2)). Pti(CO2) may alternatively be assumed equal to venous PCO2 (Pv(CO2)) in that region of gut. The idea is that as blood flow decreases, gut Pti(CO2) and Pv(CO2) will increase to the maximum aerobic value, i.e., maximum respiratory Pv(CO2) (Pv(CO2rmax)). Above a "critical" anaerobic threshold, lactate (La-) generation, by titration of tissue HCO3-, should raise Pti(CO2) above Pv(CO2rmax). During progressive selective whole intestinal flow reduction in six pentobarbital-anesthetized pigs, we used PCO2 electrodes to test the hypotheses that critical Pti(CO2) is achieved earlier in mucosa than in serosa and that Pv(CO2rmax), computed using an in vitro model, predicts critical Pti(CO2). We defined critical Pti(CO2) as the inflection of Pti(CO2)-Pv(CO2) vs. O-2 delivery (QO(2)) plots. Critical QO(2) for O-2 uptake was 12.55 +/- 2 ml . kg(-1). min(-1). Critical Pti(CO2) for mucosa and serosa was achieved at similar whole intestine QO(2) (13.90 +/- 5 and 13.36 +/- 5 ml . kg(-1). min(-1), P = NS). Critical Pti(CO2) (129 +/- 24 and 96 +/- 21 Torr) exceeded Pv(CO2rmax) (62 +/- 3 Torr). During ischemia, La- excretion into portal venous blood was matched by K+ excretion, causing Pv(CO2) to increase only slightly, despite Pti(CO2) rising to 380 +/- 46 (mucosa) and 280 +/- 38 (serosa) Torr. These results suggest that mucosa and serosa become dysoxic simultaneously, that ischemic dysoxic gut is essentially unperfused, and that in vitro predicted Pv(CO2rmax) underestimates critical Pti(CO2).