Evaluation of microfluidic blood gas sensors that combine microdialysis and optical monitoring.

It is shown that microdialysis-based blood gas (pH, pCO2 and pO2) optical sensors are stable for durations of several hours in blood. This performance is uncommon with many types of membrane sensor. Microdialysis techniques can be designed to ensure that the sweep microflow samples are in biochemical equilibrium with the bulk media, even after hours of exposure to the complex composition of blood. The rate of diffusion through the membrane is not the determining factor in sensor reading, as it is with other sensor techniques that consume the analyte. The sweep fluid 95% equilibration times for microdialysis fibres were approximately double in blood compared with buffer, reflecting slower diffusion of ions. This is in contrast to the equilibration of gases through silicone hollow-fibre membranes in blood, which showed unchanged equilibration times between blood and buffer. Sensor measurements correlate well with a blood gas analyser for up to 9 h in blood, with correlation coefficients of 0.973 for the pO2 sensor 0.974 for the pCO2 sensor and 0.947 for the pH sensor. In blood, the sensors have precisions of 1.7 mmHg, 3.7 mmHg and 0.019 pH units and bias levels of -0.7 mmHg, 1.2 mmHg and 0.002 pH units, for pO2, pCO2 and pH, respectively.

Intravascular carbon dioxide monitoring using micro-flow colorimetry.

An intravascular carbon dioxide sensor is investigated which employs continuous perfusion of micro-quantities of reagent through silicone membrane tubing in contact with blood. Blood is sampled from a vessel by periodic withdrawal-reinfusion through a catheter and passes by the sensor membrane tubing integrated into the catheter system. Blood CO2 equilibrates across the silicone membrane causing a color change in the reagent micro-flow stream that is detected by an optical cell external to the vessel. In vivo trials on pigs demonstrate a stable sensor response, a fast response time, and high signal-to-noise ratios. The sensor also exhibits an immunity to temperature changes, reduced intravascular blood flow, photobleaching, and leaching. It has a 2 min response time, a +/-2 mmHg resolution, and minimal drift over a 12 h duration. Using a pig model, measured values compared with true values indicate a 0.998 correlation coefficient, a 1.3 mmHg precision, and a 1.7 mmHg bias.

Hydrogen peroxide-induced alterations in prostaglandin secretion in the rat colon in vitro.

Although the specific cause(s) of inflammatory bowel diseases (IBD) has not been identified, one theory suggests ischemia as the early event that occurs in IBD and reperfusion causes sustained release of oxyradicals, leading to inflammation and ulceration. In this study, we have confirmed that H2O2 in the concentration seen during ischemia/reperfusion is primarily responsible for cellular membrane damage in the rat colonic fragments in vitro. Hydrogen peroxide caused a time and dose-dependent increase in 6-keto-PGF1 alpha and TXB2 release. Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was blocked (50%) by phospholipase A2 (PLA2) inhibitors quinacrine and dimethyleicosadienoic acid at 5 min. Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was completely blocked by indomethacin, significantly blocked (69%) by nordihydroguiaretic acid, and completely blocked by catalase. Superoxide dismutase and uric acid failed to inhibit H2O2-stimulated 6-keto-PGF1 alpha release. Endogenous catalase inhibitors 3-aminotriazole and sodium azide further enhanced the release of 6-keto-PGF1 alpha stimulated by H2O2 by 29% and 73%, respectively. Xanthine-xanthine oxidase also increased 6-keto-PGF1 alpha release from the fragments by 110%. This release was not inhibited by superoxide dismutase and uric acid, but was completely inhibited by catalase. These studies suggest a direct effect of H2O2 on colonic fragments leading to submicroscopic cellular membrane damage and excess prostanoid production utilizing a PLA2/cyclooxygenase and catalase-sensitive pathway without the formation of toxic hydroxyl ions. The quick release of 6-keto-PGF1 alpha also suggests an early manifestation of H2O2-induced damage in rat colonic fragments.