Knichwitz G, Rötker J, Möllhoff T, Richter K D, Brüssel T
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Westfälische Wilhelms-Universität Münster, Germany.
Crit Care Med. 1998 Sep;26(9):1550-7. doi: 10.1097/00003246-199809000-00023.
The intestinal metabolic and histologic changes that occur in the gastrointestinal tract with ischemia and that form the basis of intramucosal pH and PCO2 alterations have not been well established. Recent evidence suggests that apart from technical problems with gastric tonometry, some methodologic misconceptions in the interpretation of intramucosal pH and PCO2 exist. The present study was designed to demonstrate the effects of impaired mesenteric perfusion with specific consideration to the induced intramucosal PCO2 changes using a new technique, the continuous fiberoptic CO2 sensor, and a new concept of interpretation.
Randomized, controlled intervention trial.
University animal laboratory.
Twelve anesthetized female pigs, weighing 67+/-6 kg.
The pigs were assigned to control and stenosis groups. In the stenosis group, blood flow in the superior mesenteric artery was reduced by 70% from baseline for 180 mins, followed by 120 mins of reperfusion. Serum lactate concentration, pH, PCO2, PO2, and bicarbonate concentration (cHCO3-) were determined in arterial, superior mesenteric venous, portal venous, hepatic venous, and pulmonary arterial blood. In the lumen of the ileum, intramucosal PCO2 was continuously determined by a fiberoptic CO2 sensor. At the end of the experiment, the gut was examined for histologic changes.
During mesenterial hypoperfusion, a sudden and significant increase in intramucosal PCO2 was observed. This increase was paralleled by increases in superior mesenteric venous PCO2 and portal venous PCO2 (p < .05) and a concomitant decrease in intramucosal pH, superior mesenteric venous pH, and portal venous pH. Arterial and mixed venous PCO2 and pH did not change. cHCO3- did not change in local or systemic blood samples.
Compromised mesenteric blood flow causes significant metabolic and histologic changes. These local changes could not be detected by arterial or mixed venous lactate concentrations, pH, and PCO2 determinations. Under closed-system conditions, mesenteric CO2 accumulation causes an impairment of the CO2-HCO3- buffer, resulting in an unchanged cHCO3-. With impaired mesenteric perfusion, only intramucosal PCO2 alterations occur and an intramucosal pH calculation based on systemic cHCO3-changes is not necessarily correct. Therefore, the only parameter of importance is the intraluminal measurement of intramucosal PCO2 that can reflect isolated mesenteric changes. Thus, we recommended abolishing the terms "intramucosal pH measurement" and "gastric tonometry" and propose using the definition "intramucosal PCO2 measurement."
胃肠道缺血时发生的肠道代谢和组织学变化，是黏膜内pH值和PCO₂改变的基础，但尚未完全明确。最近的证据表明，除了胃张力测定法存在技术问题外，在解释黏膜内pH值和PCO₂时还存在一些方法学上的误解。本研究旨在通过一种新技术——连续光纤CO₂传感器和一种新的解释概念，特别考虑诱导的黏膜内PCO₂变化，来证明肠系膜灌注受损的影响。
随机对照干预试验。
大学动物实验室。
12只麻醉的雌性猪，体重67±6千克。
将猪分为对照组和狭窄组。在狭窄组中，肠系膜上动脉的血流从基线减少70%，持续180分钟，随后再灌注120分钟。测定动脉血、肠系膜上静脉血、门静脉血、肝静脉血和肺动脉血中的血清乳酸浓度、pH值、PCO₂、PO₂和碳酸氢盐浓度（cHCO₃⁻）。在回肠腔内，用光纤CO₂传感器连续测定黏膜内PCO₂。实验结束时，检查肠道的组织学变化。
在肠系膜灌注不足期间，观察到黏膜内PCO₂突然显著升高。这种升高与肠系膜上静脉PCO₂和门静脉PCO₂的升高平行（p < 0.05），同时黏膜内pH值、肠系膜上静脉pH值和门静脉pH值下降。动脉血和混合静脉血的PCO₂和pH值没有变化。局部或全身血样中的cHCO₃⁻没有变化。
肠系膜血流受损会导致显著的代谢和组织学变化。这些局部变化无法通过动脉血或混合静脉血中的乳酸浓度、pH值和PCO₂测定来检测。在封闭系统条件下，肠系膜CO₂蓄积会导致CO₂-HCO₃⁻缓冲系统受损，导致cHCO₃⁻不变。随着肠系膜灌注受损，仅发生黏膜内PCO₂改变，基于全身cHCO₃⁻变化计算黏膜内pH值不一定正确。因此，唯一重要的参数是能够反映孤立肠系膜变化的腔内黏膜内PCO₂测量值。因此，我们建议废除“黏膜内pH值测量”和“胃张力测定法”这两个术语，并建议使用“黏膜内PCO₂测量”这一定义。
