Desai V S, Weil M H, Tang W, Yang G, Bisera J
Department of Pediatrics, University of health Sciences, Chicago Medical School, North Chicago, IL 60064-3095.
Chest. 1993 Oct;104(4):1254-8. doi: 10.1378/chest.104.4.1254.
To define whether increases in gastric intramural tissue CO2 and H+ increase during experimentally induced peritonitis with circulatory shock as they do under conditions of hemorrhagic shock and cardiac arrest.
Peritonitis was induced in Sprague-Dawley rats by cecal ligation and fecal spillage.
Over an interval of 260 +/- 20 min in 5 animals, there was a progressive reduction in mean aortic pressure from 153 +/- 12 to 40 +/- 20 mm Hg and a decline in cardiac index from 429 +/- 135 to 178 +/- 7 ml/min. This was associated with increases in gastric intramural [H+] from 34 +/- 5 to 217 +/- 93 mmol/L (p = 0.001). Arterial blood lactate content concurrently increased from 0.9 +/- 0.1 to 4.6 +/- 0.7 mmol/L (p = 0.001). Only a late increase in gastric intramural PCO2 from 45 +/- 5 to 128 +/- 38 mm Hg (p = 0.01) was observed.
In contrast to the gastric acid base changes that accompany hemorrhagic shock, in which there is an early and prominent increase in both PCO2 and [H+] in close relationship to decreases in cardiac output and arterial pressure, there was a prominent increase in gastric [H+] but only a delayed rise in gastric intramural PCO2. Arterial blood lactate and central venous oxygen saturation were earlier indicators of perfusion failure. Since the bicarbonate concentration in the stomach wall was substantially greater than that of simultaneously measured arterial blood, this has bearing on the current clinical method of gastric tonometry which assumes that arterial blood bicarbonate is equivalent to gastric wall bicarbonate.
确定在实验性诱导的伴有循环性休克的腹膜炎期间，胃壁内组织二氧化碳（CO₂）和氢离子（H⁺）浓度是否如在失血性休克和心脏骤停情况下那样升高。
通过盲肠结扎和粪便溢出在斯普拉格-道利大鼠中诱导腹膜炎。
在5只动物的260±20分钟时间段内，平均主动脉压从153±12毫米汞柱逐渐降至40±20毫米汞柱，心脏指数从429±135降至178±7毫升/分钟。这与胃壁内[H⁺]从34±5毫摩尔/升增加到217±93毫摩尔/升相关（p = 0.001）。动脉血乳酸含量同时从0.9±0.1毫摩尔/升增加到4.6±0.7毫摩尔/升（p = 0.001）。仅观察到胃壁内PCO₂较晚从45±5毫米汞柱增加到128±38毫米汞柱（p = 0.01）。
与失血性休克时伴随的胃酸碱变化不同，在失血性休克中，PCO₂和[H⁺]会随着心输出量和动脉压的降低而早期显著升高，而在本研究中，胃内[H⁺]显著升高，但胃壁内PCO₂仅延迟升高。动脉血乳酸和中心静脉血氧饱和度是灌注衰竭的较早指标。由于胃壁中的碳酸氢盐浓度明显高于同时测量的动脉血中的浓度，这与当前假设动脉血碳酸氢盐等同于胃壁碳酸氢盐的胃张力测定临床方法有关。
