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This article is part of the supplement: 24th International Symposium on Intensive Care and Emergency Medicine

Poster presentation

Microvascular oxygen transport abnormalities in experimental sepsis interpreted using a computational model

C Ellis1, D Goldman2, R Bateman3 and M Sharpe4

Author Affiliations

1 University of Western Ontario, London, Canada

2 New Jersey Institute of Technology, Newark, Delaware, USA

3 St Paul's Hospital, Vancouver, Canada

4 London Health Sciences Centre, London, Canada

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Critical Care 2004, 8(Suppl 1):P67  doi:10.1186/cc2534


The electronic version of this article is the complete one and can be found online at:


Published:15 March 2004

©

Poster presentation

Experimental studies using a peritonitis model of sepsis in rats have reported abnormalities in microvascular perfusion including increased stopped flow capillaries, increased fast flow capillaries and impaired regulation of blood flow. We have used a spectrophotometric functional microvascular imaging system to quantify capillary geometry, red blood cell flow and red blood cell hemoglobin oxygen saturation during sepsis. We found that while oxygen saturation at the entrance of the capillary bed was unaffected in sepsis, there was a significant drop in saturation at the venous end of capillaries with normal velocities. Although the fall in oxygen saturation correlated with the number of stopped flow capillaries, we could not determine from this data whether tissue oxygen consumption changed with sepsis, whether fast flow capillaries acted as functional oxygen shunts or whether any regions of the tissue were anoxic. To address these questions we constructed a computational model that simulated O2 transport in a three-dimensional volume of tissue supplied by heterogeneously spaced capillaries with fast, normal and stopped flow. The model was based on our experimental oxygen transport data (capillary density, number of stopped flow capillaries, capillary red blood cell velocity and supply rate, and entrance oxygen saturation levels) and the model predicted oxygen consumption, tissue oxygen levels and oxygen transport in fast flow capillaries; data that could not be measured experimentally with current technology. Tissue oxygen consumption in the model was adjusted to yield the same venous end oxygen saturation values as measured experimentally. Two cases were modeled; average sepsis (AS) with 33% stopped, 33% normal and 33% fast flow, and extreme sepsis (ES) with 50% stopped, 25% normal and 25% fast flow. Simulations found approximately twofold and fourfold increases in tissue oxygen consumption for AS and ES, respectively. Average (minimum) tissue PO2 decreased from 43(40) mmHg in control to 34 (27) and 26 (15) mmHg in AS and ES, respectively. Clustering fast flow capillaries to increase flow heterogeneity resulted in only a slight decrease in minimum tissue PO2, to 14.5 mmHg. Although fast flow capillaries did appear to be oxygen shunts with higher venous oxygen saturations, they were a significant factor in preventing tissue anoxia during sepsis. Despite the contribution of fast flow capillaries, simulated tissue PO2 values continued to fall as the degree of microvascular injury increased. The model predicts that microvascular oxygen transport abnormalities associated with sepsis expose the tissue to local regions of a hypoxic environment that may lead ultimately to significant changes in cellular function.

Acknowledgement

Supported by CIHR grant MOP-49416 to CE.