- Meeting abstract
- Open Access
Distribution of intracapillary hemoglobin O2 saturations in gastric mucosa, gastric outer wall and skeletal muscle in septic shock
© BioMed Central Ltd 2001
- Published: 1 March 1997
- Skeletal Muscle
- Septic Shock
- Gastric Mucosa
- Outer Wall
- Skeletal Muscle Tissue
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.
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.
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%).
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).
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.