Oud L, Kruse J A
Division of Pulmonary/Critical Care Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Shock. 1996 Jul;6(1):61-5. doi: 10.1097/00024382-199607000-00013.
The time course of gastric intramucosal pH (pHi) during the early phase of resuscitation of hemorrhagic shock has not been adequately characterized. We examined pHi using gastric tonometry catheters in an anesthetized dog model of hemorrhagic shock. Shock was induced in 10 animals to maintain mean arterial blood pressure (MAP) at 40-45 mmHg for 30 min, followed by transfusion of shed blood plus additional saline as needed to maintain MAP at pre-shock values. Five animals served as controls. Baseline pHi values were nearly identical in both groups. Resuscitation promptly restored MAP. Following a precipitous drop of pHi during shock, there was only partial recovery 60 min post-shock, followed by progressive worsening of intramucosal acidosis (7.02 +/- .10 vs. 6.82 +/- .24 at 60 and 210 min post-shock, respectively; p < .002). MAP, heart rate, and pHi did not change significantly during the experiment in the control group. These results indicate that prompt and adequate MAP response to resuscitation failed to prevent significant decreases of pHi in the first few hours post-resuscitation. This finding may be related to persistent splanchnic hypoperfusion or reperfusion injury.
失血性休克复苏早期胃黏膜内pH值（pHi）的时间进程尚未得到充分描述。我们在失血性休克的麻醉犬模型中使用胃张力测定导管检测pHi。对10只动物诱导休克，将平均动脉血压（MAP）维持在40 - 45 mmHg 30分钟，然后根据需要输注 shed blood 加额外的生理盐水，以将MAP维持在休克前值。5只动物作为对照。两组的基线pHi值几乎相同。复苏迅速恢复了MAP。休克期间pHi急剧下降后，休克后60分钟仅部分恢复，随后黏膜内酸中毒逐渐加重（休克后60分钟和210分钟时分别为7.02±.10和6.82±.24；p <.002）。对照组实验期间MAP、心率和pHi无显著变化。这些结果表明，复苏后迅速且充分的MAP反应未能防止复苏后最初几小时内pHi的显著下降。这一发现可能与持续性内脏低灌注或再灌注损伤有关。
