Antonsson J B, Engström L, Rasmussen I, Wollert S, Haglund U H
Department of Surgery, University Hospital, Uppsala, Sweden.
Crit Care Med. 1995 Nov;23(11):1872-81. doi: 10.1097/00003246-199511000-00014.
To establish the relationship between gut intramucosal pH and blood flow to the gut, gut oxygen delivery, and gut oxygen extraction ratio in a porcine model of peritonitis and hemorrhage.
Prospective, controlled study.
Experimental laboratory in a university teaching hospital.
Thirty pigs of both sexes, weighing 15 to 22 kg.
Animals were anesthetized, intubated, and mechanically ventilated. A flow probe was placed around the superior mesenteric artery for registration of blood flow. A tonometer was placed in the lumen of midileum for calculation of gut intramucosal pH. Hourly, for 5 hrs, blood samples were taken from mixed venous, mesenteric venous, and arterial blood. Five animals served as controls, ten animals had peritonitis induced by fecal instillation in the abdominal cavity, five were bled stepwise, five were bled rapidly (to a mean arterial pressure of 30 mm Hg), and five were bled rapidly and reinfused after 3 hrs.
Both peritonitis and hemorrhage caused decreases in gut blood flow and intramucosal pH. In mild peritonitis, the intramucosal pH decrease preceded that of blood flow. In all experimental groups, oxygen delivery decreased over time; in both mild and severe peritonitis, this decrease was preceded by a decrease of intramucosal pH. Intramucosal pH correlated well with gut oxygen extraction ratio in peritonitis (r2 = .86). In hemorrhage, there was a correlation of r2 = .66, but in intramucosal pH of < 7.12, a further decrease was accompanied only by minor changes in extraction ratio.
Since a reduction in blood flow was preceded by a decrease in intramucosal pH, low intramucosal pH in peritonitis cannot be explained by low flow alone. Gut oxygen delivery proved to be a poor indicator of gut acidosis (i.e., low intramucosal pH). In peritonitis, a decreasing intramucosal pH was associated with an increasing oxygen extraction ratio. In hemorrhage, this association had a sharp deflection point below which a further decrease in intramucosal pH occurred concomitantly with an unchanged gut oxygen extraction ratio. Increased extraction ratio was not sufficient, not even initially, to maintain aerobic metabolism (i.e., unchanged intramucosal pH).
在猪腹膜炎和出血模型中建立肠道黏膜内pH值与肠道血流量、肠道氧输送及肠道氧摄取率之间的关系。
前瞻性对照研究。
大学教学医院的实验实验室。
30头体重15至22千克的雌雄猪。
动物麻醉、插管并机械通气。在肠系膜上动脉周围放置流量探头记录血流量。在回肠中段肠腔内放置张力计计算肠道黏膜内pH值。每小时采集混合静脉血、肠系膜静脉血和动脉血样本,共采集5小时。5只动物作为对照,10只动物通过腹腔内注入粪便诱导腹膜炎,5只动物逐步放血,5只动物快速放血(至平均动脉压30毫米汞柱),5只动物快速放血并在3小时后再输注。
腹膜炎和出血均导致肠道血流量和黏膜内pH值下降。在轻度腹膜炎中,黏膜内pH值下降先于血流量下降。在所有实验组中,氧输送随时间下降;在轻度和重度腹膜炎中,这种下降之前黏膜内pH值先下降。在腹膜炎中,黏膜内pH值与肠道氧摄取率相关性良好(r2 = 0.86)。在出血时,相关性r2 = 0.66,但在黏膜内pH值<7.12时,进一步下降仅伴有摄取率的微小变化。
由于血流量减少之前黏膜内pH值已下降,腹膜炎时低黏膜内pH值不能仅用低血流量来解释。肠道氧输送被证明是肠道酸中毒(即低黏膜内pH值)的不良指标。在腹膜炎中,黏膜内pH值下降与氧摄取率增加相关。在出血时,这种关联有一个明显的转折点,低于该点黏膜内pH值进一步下降时肠道氧摄取率不变。氧摄取率增加并不足以维持有氧代谢(即黏膜内pH值不变),甚至最初也不行。