Distribution of intracapillary hemoglobin O₂ saturations in gastric mucosa, gastric outer wall and skeletal muscle in septic shock

Introduction

Alterations in capillary density associated with a heterogeneity in microcirculatory blood flow in the intestine and skeletal muscle are found after both endotoxin infusion and cecal ligation and perforation leading to areas of hypoxia.

Objectives

To investigate the effects of septic shock on spatial distribution of intracapillary hemoglobin O₂-saturations (cHbO₂) and relative hemoglobin concentrations [rel(Hb)] in gastric rnucosa, gastric outer wall and skeletal muscle tissue.

Methods

Eight domestic pigs of either sex were studied. After surgery and a 90 min recovery period baseline data sets were collected. Septic shock was then induced by a bolus infusion of E coli-endotoxin followed by a continuous infusion. All measurements were repeated at 60 min intervals over a time frame of 8 h.

Empho (Erlanger Microlightguide Spectrophotometer): Gastric mucosal cHbO₂ spectra were recorded via a fibreoptic probe at the greater curvature at five sites. Gastric outer wall cHbO₂ values were collected from the stomach surface through a ventral recloseable laparotomy, and skeletal muscle cHbO₂ values were assessed in a foreleg muscle preparation. cHbO₂ values obtained were classified into three ranges: critical (0–10%), reserve (11–50%) and normal (51–100%).

Results

At baseline the cHbO₂ gradients exhibit a homogeneous oxygenation profile at the five measuring sites within the organs. Between organs, however, cHbO₂ distributions were different. In the mucosa 20, 75 and 5% of the recorded cHbO₂ values were found in the critical, reserve and normal range, whereas the gastric outer wall distributions were 2, 30 and 67%. In skeletal muscle 0.34% of the cHbO₂ were in the critical, 25 and 74% were in the reserve and normal range. In septic shock (1 h), the incidence of cHbO₂ values below 10% increased from 20 to 47% in the mucosa and from 2 to 4% in the outer wall, whereas no change could be detected in the skeletal muscle in this range. The incidence of cHbO₂values between 11 to 50% dropped from 75 to 52% in the mucosa, but increased from 30 and 25% to 67 and 46% in the outer wall and skeletal muscle, respectively. The incidence of the normal range values decreased from 6, 67 and 74% to 0.5, 28 and 53% in mucosa, outer wall and skeletal muscle. After 4 h of septic shock distributions of cHbO₂ were unchanged in all organs compared to 1 h values, but as septic shock continued the oxygenation profile progressively shifted to lower values primarily in the mucosa whereas in the skeletal muscle values below 10% cHbO₂ only appeared after 8 h of shock. The relative hemoglobin concentrations changed from 0.79, 0.72, 0.72 at baseline to 0.57, 0.43, 0.52 after induction of shock and 0.37, 0.23, 0.53 at 8 h of shock (mucosa-outerwall-muscle).

Conclusion

In septic shock the shift of HbO₂ distribution to critical values is mainly found in the gastric mucosa and to a lower extent in the gastric outer wall. In skeletal muscle, however, cHbO₂, although also shifted to lower values, were always maintained within the normal or reserve range for 7 h of shock. Only after 8 h did critical values appear. These findings are supported by the changes in the rel(Hb). Thus, it appears that septic shock causes critical cHbO₂ in the gut, a non-vital organ suffering from redistribution of flow, but barely in the skeletal muscle, an organ of locomotion.