Keeping Metabolic Warning Signals Close to the Organ: Bioresorbable Sensor Tracks Lactate in Animals for More Than 10 Days

A critically ill patient’s condition can deteriorate rapidly between two blood draws. Lactate can reflect tissue oxygen supply, cellular demand, and mitochondrial function, but it is usually monitored only through intermittent blood tests. Metabolic abnormalities that emerge earlier around a single organ may therefore be obscured by systemic measurements. A research team has now demonstrated in animals a flexible sensor that can be gradually absorbed, seeking to move lactate monitoring closer to the site of disease and continuously cover this gap.

The device uses a hydrogel that can adhere to wet tissue as its substrate, combined with molybdenum/molybdenum oxide electrodes and lactate dehydrogenase. After lactate produces protons through an enzymatic reaction, the protons intercalate into the molybdenum oxide and are converted into a readable current signal. The sensing range is 0 to 30 millimolar, with a detection limit of 0.1 millimolar. Within the 0-to-8-millimolar range, the researchers measured a sensitivity of 0.78 microamperes per millimolar.

The study included pigs, rabbits, and rats, with sensors placed in the brain, heart, or limb tissue to observe lactate fluctuations during systemic and local hypoxia, cerebral and myocardial ischemia, seizures, and septic shock. Long-term experiments showed that the device could operate in the body for more than 10 days. Signals were carried by wires passing through the skin to an external circuit and then transmitted via Bluetooth for recording.

The result with the greatest potential clinical implications came from the rabbit septic shock model. Lactate in the pericardial cavity rose before a marked decline in mean arterial pressure. Researchers administered fluids early in response to a signal showing lactate more than 25% above baseline, and the animals maintained better hemodynamic status during the experimental observation period than the group treated only after blood pressure had fallen. However, each comparison involved only a small number of animals, and shock was artificially induced with lipopolysaccharide, so these findings cannot establish that the strategy can improve outcomes in human sepsis.

“Bioresorbable” addresses the possibility that the sensor itself might otherwise need to be removed later; it does not mean that the entire system disappears inside the body. In rat experiments, the hydrogel degraded within 16 weeks, while the molybdenum/molybdenum oxide electrodes gradually shrank over the 32-week follow-up period. No obvious inflammation or molybdenum accumulation was observed in the tested tissues. In a separate accelerated test conducted in buffer at 55 degrees Celsius, the device fully decomposed within 170 days, but this in vitro result cannot be directly converted into its degradation rate or long-term safety in the human body.

Before the technology can reach intensive care units, the research team must still demonstrate that differences among patients, organ locations, and complex disease courses will not compromise measurement accuracy, while also addressing calibration, sterilization, implantation procedures, and the infection risk posed by transcutaneous wires. The external battery and readout circuit are also currently not bioresorbable and would still need to be removed or redesigned. The study is therefore best viewed as a comprehensive animal proof of concept: it shows that metabolic warning signals in deep tissue can be captured continuously, but whether they can change clinical decisions earlier and more reliably than blood tests remains to be answered by human studies.