Guzman J A, Kruse J A
Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA.
Crit Care Med. 1997 Mar;25(3):533-7. doi: 10.1097/00003246-199703000-00025.
To test a novel device for continuous monitoring of gut intramucosal PCO2 and pH and to compare its use with conventional intermittent saline balloon-tonometry in a model of hemorrhagic shock.
A prospective animal study.
A university research laboratory.
Eight anesthetized, mechanically ventilated mongrel dogs.
Two balloon-tip tonometry catheters, one conventional and one modified for continuous recirculating gas tonometry, were inserted into each animal's stomach by the oral route. Gastric intramucosal PCO2 was recorded continuously by capnometric recirculating gas tonometry throughout the experiment. After a baseline period of 90 mins, vital signs, arterial and mixed venous blood gases, and intramucosal PCO2 values were obtained by recirculating gas tonometry and by the conventional method. Using a modified Wiggers' model, the animals were then subjected to hemorrhage of up to 45 mL/kg, or the volume required to effect a decrease in mean arterial pressure to < 30 mm Hg. After 30 mins, the shed blood was reinfused and the experiment continued for an additional 30 mins. Vital signs, arterial and mixed venous blood samples, saline tonometry samples, and recirculating gas tonometry readings were obtained immediately before and 30 mins after reinfusion of blood.
Mean +/- SD baseline intramucosal PCO2 was 47.6 +/- 9.5 torr (6.3 +/- 1.3 kPa) by capnometric recirculating gas tonometry and 45.8 +/- 3.4 torr (6.1 +/- 0.5 kPa) by conventional saline tonometry (p = NS). By 5 mins after inducing hemorrhage, intramucosal PCO2 by recirculating gas tonometry had increased significantly (49.3 +/- 9.7 torr [6.6 +/- 1.3 kPa]; p < .05), and by 30 mins, it had increased to 59.7 +/- 11.3 torr (8.0 +/- 1.5 kPa; p < .001 compared with baseline). After 30 mins of hemorrhage, the conventional method showed an increase in intramucosal PCO2 to 63.0 +/- 20.9 torr (8.4 kPa +/- 2.8 kPa; p = NS vs. baseline by conventional method; p = NS vs. corresponding recirculating gas tonometry values). Gastric intramucosal pH, as determined by recirculating gas tonometry, decreased significantly at 5 mins after starting hemorrhage (7.13 +/- 0.10 to 7.10 +/- 0.10, p < .02). After 30 mins of hemorrhage, intramucosal pH decreased to 6.88 +/- 0.14 (from 7.10 +/- 0.10) by the conventional saline tonometry technique (p < .01) and to 6.89 +/- 0.10 by recirculating gas tonometry (p < .001 vs. baseline). Intramucosal PCO2 by both techniques remained significantly increased above baseline values 30 mins after reinfusion of the shed blood.
Capnometric recirculating gas tonometry allows continuous and automated assessment of gastrointestinal tract perfusion by providing on-line measurements of intramucosal PCO2, which can also be used to derive intramucosal pH. The technique is able to detect changes in intramucosal PCO2 in response to an induced insult over intervals as short as 5 mins.
测试一种用于连续监测肠道黏膜PCO₂和pH值的新型装置，并在失血性休克模型中将其与传统的间歇性生理盐水球囊测压法进行比较。
前瞻性动物研究。
大学研究实验室。
8只麻醉、机械通气的杂种犬。
通过口腔途径将两根球囊尖端测压导管插入每只动物的胃内，一根为传统导管，另一根为改良的用于连续循环气体测压的导管。在整个实验过程中，通过二氧化碳测定循环气体测压法连续记录胃黏膜PCO₂。在90分钟的基线期后，通过循环气体测压法和传统方法获取生命体征、动脉和混合静脉血气以及黏膜内PCO₂值。使用改良的维格斯模型，然后使动物失血多达45 mL/kg，或使平均动脉压降至<30 mmHg所需的血量。30分钟后，回输 shed blood（原文有误，推测为shed blood，意为失血）并将实验再持续30分钟。在回输血前和回输血后30分钟立即获取生命体征、动脉和混合静脉血样本、生理盐水测压样本以及循环气体测压读数。
通过二氧化碳测定循环气体测压法测得的平均±标准差基线黏膜内PCO₂为47.6±9.5托（6.3±1.3千帕），通过传统生理盐水测压法测得为45.8±3.4托（6.1±0.5千帕）（p =无显著性差异）。在诱导出血后5分钟内，通过循环气体测压法测得的黏膜内PCO₂显著升高（49.3±9.7托[6.6±1.3千帕]；p<.05），到30分钟时，已升至59.7±11.3托（8.0±1.5千帕；与基线相比p<.001）。出血30分钟后，传统方法显示黏膜内PCO₂升至63.0±20.9托（8.4千帕±2.8千帕；与传统方法的基线相比p =无显著性差异；与相应的循环气体测压值相比p =无显著性差异）。通过循环气体测压法测定，胃黏膜pH值在开始出血后5分钟时显著下降（从7.13±0.10降至7.10±0.10，p<.02）。出血30分钟后，通过传统生理盐水测压技术，黏膜内pH值降至6.88±0.14（从7.10±0.10）（p<.01），通过循环气体测压法降至6.89±0.10（与基线相比p<.001）。在回输失血30分钟后，两种技术测得的黏膜内PCO₂仍显著高于基线值。
二氧化碳测定循环气体测压法通过提供黏膜内PCO₂的在线测量值，能够连续、自动地评估胃肠道灌注，该测量值也可用于推算黏膜内pH值。该技术能够在短至5分钟的时间间隔内检测到因诱导损伤而导致的黏膜内PCO₂变化。
