Measuring arterial oxygen saturation from an intraosseous photoplethysmographic signal derived from the sternum.

Photoplethysmography performed on the peripheral extremities or the earlobes cannot always provide sufficiently rapid and accurate calculation of arterial oxygen saturation. The purpose of this study was to evaluate a novel photoplethysmography prototype to be fixed over the sternum. Our hypotheses were that arterial oxygen saturation can be determined from an intraosseous photoplethysmography signal from the sternum and that such monitoring detects hypoxemia faster than pulse oximetry at standard sites. Sixteen healthy male volunteers were subjected to incremental hypoxemia using different gas mixtures with decreasing oxygen content. The sternal probe was calibrated using arterial haemoglobin CO-oximetry (SaO2%). Sternal probe readings (SRHO2%) were then compared to SaO2% at various degrees of hypoxia. The time to detect hypoxemia was compared to measurements from standard finger and ear pulse oximeters. A significant association from individual regression between SRHO2% and SaO2% was found (r2 0.97), Spearman R ranged between 0.71 and 0.92 for the different inhaled gas mixtures. Limits of agreement according to Bland-Altman plots had a increased interval with decreasing arterial oxygen saturation. The sternal probe detected hypoxemia 28.7 s faster than a finger probe (95% CI 20.0-37.4 s, p < 0.001) and 6.6 s faster than an ear probe (95% CI 5.3-8.7 s, p < 0.001). In an experimental setting, arterial oxygen saturation could be determined using the photoplethysmography signal obtained from sternal blood flow after calibration with CO-oximetry. This method detected hypoxemia significantly faster than pulse oximetry performed on the finger or the ear.

Chemical denervation using botulinum toxin increases Akt expression and reduces submaximal insulin-stimulated glucose transport in mouse muscle.

Botulinum toxin A (botox) is a toxin used for spasticity treatment and cosmetic purposes. Botox blocks the excitation of skeletal muscle fibers by preventing the release of acetylcholine from motor nerves, a process termed chemical denervation. Surgical denervation is associated with increased expression of the canonical insulin-activated kinase Akt, lower expression of glucose handling proteins GLUT4 and hexokinase II (HKII) and insulin resistant glucose uptake, but it is not known if botox has a similar effect. To test this, we performed a time-course study using supra-maximal insulin-stimulation in mouse soleus ex vivo. No effect was observed in the glucose transport responsiveness at day 1, 7 and 21 after intramuscular botox injection, despite lower expression of GLUT4, HKII and expression and phosphorylation of TBC1D4. Akt protein expression and phosphorylation of the upstream kinase Akt were increased by botox treatment at day 21. In a follow-up study, botox decreased submaximal insulin-stimulated glucose transport. The marked alterations of insulin signaling, GLUT4 and HKII and submaximal insulin-stimulated glucose transport are a potential concern with botox treatment which merit further investigation in human muscle. Furthermore, the botox-induced chemical denervation model may be a less invasive alternative to surgical denervation.

Muscle disuse caused by botulinum toxin injection leads to increased central gain of the stretch reflex in the rat.

Botulinum toxin (Btx) is used in children with cerebral palsy and in other neurological patients to diminish spasticity and reduce the risk of development of contractures. We investigated changes in the central gain of the stretch reflex circuitry in response to Btx injection in the triceps surae muscle in rats. Experiments were performed in 21 rats. Eight rats were a control group, and 13 rats were injected with 6 IU of Btx in the left triceps surae muscle. Two weeks after Btx injection, larger monosynaptic reflexes (MSR) were recorded from the left (injected) than the right (noninjected) L4 + L5 ventral roots following stimulation of the corresponding dorsal roots. A similar increase on the left side was observed in response to stimulation of descending motor tracts, suggesting that increased excitability of spinal motor neurons may at least partly explain the increased reflexes. However, significant changes were also observed in postactivation depression of the MSR, suggesting that plastic changes in transmission from Ia afferent to the motor neurons also may be involved. The data demonstrate that muscle paralysis induced by Btx injection is accompanied by plastic adaptations in the central stretch reflex circuitry, which counteract the antispastic effect of Btx.NEW & NOTEWORTHY Injection of botulinum toxin into ankle muscles causes increased gain of stretch reflex. This is caused by adaptive changes in regulation of transmitter release from Ia afferents and increased excitability of spinal motor neurons.