Abstract
The defining characteristic of sepsis is a progressive microvascular dysfunction remote to the locus of infection. Our objective was to quantify the time course of changing tissue PO2 due to microvascular injury in early sepsis using an established mathematical model. Experimental data obtained from a rat cecal‐ligation and perforation (CLP) model of sepsis has demonstrated a progressive FCD loss at 2, 3 and 4 hours (11±4%, 15±1%, 21±5% SHAM vs 18±3%, 32±5%, 48±7% CLP respectively). Microvascular blood flow was recorded in skeletal muscle using dual wavelength intra‐vital video microscopy. Capillaries were analyzed at baseline in vivo for O2 saturations and hemodynamics. Custom vascular mapping software was used to reconstruct the real geometry (length, diameter, tissue depth and connections between vessels) of the experimental network (Volume 420 × 420 × 60 μm). A constant consumption computational model applied to the FCD conditions at each time point found mean tissue PO2 was not different between SHAM and CLP at 2 hours (34.2±4.3 vs 33.3±4.2 mmHg) or 3 hours (33.0±4.3 vs 31.2±4.5 mmHg) post. At 4 hours tissue PO2 was significantly different between SHAM and CLP (32.7±4.3 vs 25.9±6.5 mmHg, p < 0.01). This simulation suggests that a substantial FCD loss precedes a significant decrease in tissue oxygenation due to diffusional exchange between adjacent capillaries.Supported by CIHR grant to DG and CGE.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call