Progressive gastric intramucosal acidosis follows resuscitation from hemorrhagic shock.

Abstract

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.