Task2 K + channel expression in the central nervous system is surprisingly restricted to a few brainstem nuclei, including the retrotrapezoid (RTN) region. All Task2-positive RTN neurons were lost in mice bearing a Phox2b mutation that causes the human congenital central hypoventilation syndrome. In plethysmography, Task2 −/− mice showed disturbed chemosensory function with hypersensitivity to low CO 2 concentrations, leading to hyperventilation. Task2 probably is needed to stabilize the membrane potential of chemoreceptive cells. In addition, Task2 −/− mice lost the long-term hypoxia-induced respiratory decrease whereas the acute carotid-body-mediated increase was maintained. The lack of anoxia-induced respiratory depression in the isolated brainstemspinal cord preparation suggested a central origin of the phenotype. Task2 activation by reactive oxygen species generated during hypoxia could silence RTN neurons, thus contributing to respiratory depression. These data identify Task2 as a determinant of central O 2 chemoreception and demonstrate that this phenomenon is due to the activity of a small number of neurons located at the ventral medullary surface.breathing | central chemoreceptors | K2P | KCNK5 | ventral medullary surface S pontaneous breathing requires feedback controls in which detection of blood gases and pH is critical. At present, there is good understanding of the brainstem topology of respiratory centers, and functional measurements in vitro and in vivo have revealed the basic principles of the neuronal network required for respiratory rhythmogenesis and pattern generation. This network comprises several groups of respiratory neurons forming columns extending from the caudal ventrolateral medulla to the dorsolateral pons (1, 2). The activity of this network must be stable yet permanently adjusted to variations of O 2 , CO 2 , and pH during diverse physiological conditions, e.g., sleep, exercise, or high altitude (3). The precise physiological processes by which pH, CO 2 , and O 2 changes are sensed and translated into the appropriate respiratory neural output are important mechanisms that are still a matter of debate (4, 5). Changes in arterial CO 2 / pH are detected by peripheral chemoreceptors, mainly carotid bodies, and multiple chemoreceptive areas within the brainstem. Among the central chemoreceptive areas, two have attracted most attention: the raphe nuclei and the retrotrapezoid nucleus (RTN) (6, 7). The carotid bodies are the major sensors for acute O 2 changes. However, for longer periods of hypoxia, respiratory adaptation is substantially mediated by central mechanisms (8). The ventrolateral medullary surface comprising the RTN and the parafacial respiratory group (pFRG) has been proposed to contain intrinsically CO 2 -and O 2 -sensing neurons (9-12). Recently, a mouse model that carries a mutation of the transcription factor Phox2b, which causes congenital central hypoventilation syndrome in humans, was engineered. A specific loss of a population of Phox2b-expressing RTN/pFRG neurons ...

Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

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Study objective: The Broselow ® tape (BT) is a pediatric emergency tape (PET) supporting medical teams during pediatric emergencies in estimating body weight, recommending drug dosage and medical equipment. Publications have reported the risk of incorrect use and low accuracy. A recently published digital algorithm for length-based body weight estimation showed higher accuracy for weight estimation. A prototype for an electronic Pediatric Emergency Ruler (ePER) utilizing this algorithm was developed for further testing. The aim of this study was to compare the BT with the ePER in terms of time and correctness of identifying medical information required during pediatric emergency treatment. Methods: Voluntary participants were randomly assigned to use the BT or the ePER in a simulated low-fidelity pediatric emergency manikin scenario and instructed to identify four parameters. Outcomes were time required for identification of all parameters, correct determination of lengthbased weight and erroneous reading of parameters for the selected weight category. Data are mean or percent. T-test for statistical significance (p < 0.05) and standardized mean difference (SMD > 0.8) were calculated. Results: Identifying medical information was significantly faster with the ePER than with the BT (24.5 vs 36.7 sec, p<0.001; SMD 1.53). Both devices were used correctly in 77.8% of the cases. Overall erroneous readings occurred in 1.9%. Conclusion: The ePER represents a modern and comprehensive solution to support medical staff during pediatric emergencies. This digital solution could be considered as an alternative to the BT.