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• W2289049938 abstract "The peripheral chemoreceptors are located primarily in the carotid bodies at the junction of the internal and external carotid arteries, with a lesser presence in the aortic bodies. They monitor arterial and and transmit information within seconds via neural afferent pathways to the medullary central respiratory control centre on the status of alveolar ventilation and blood oxygenation (Dempsey & Smith, 2014). In their role as rapid sensors of arterial they influence the central chemoreceptors, whose response time to CO2 changes is a bit slower. Positioning of the peripheral chemoreceptors at a point only several seconds downstream of the creation of arterial blood in the pulmonary capillaries gives the CNS an immediate gauge of the adequacy of ventilation. How best to isolate the input and ventilatory response arising from the carotid body chemoreceptors to judge their function in vivo has been the subject of much methodological and analytical work using brief hypoxic ventilatory response (HVR) and hypercapnic ventilatory response testing. Largely, it has come down to quasi-steady-state tests that vary the inspiration of one gas while holding the alveolar (and thus arterial) partial pressure of the other gas constant (and usually at pre-test values) by means such as dynamic end-tidal forcing. In addition, with HVR testing, allowing the to vary and decrease as a result of the subject's ventilatory response to the hypoxia (poikilocapnic) better to mimic the reality of breathing in response to lower inspired O2 concentrations is of separate interest to questions of adaptation to high altitude. Steady-state tests require 10–20 min to complete, during which there will be cardiovascular, pulmonary, renal and cerebrovascular responses to the developing systemic hypoxaemia or hypercapnia and/or hypocapnia that might add to or subtract from the change in ventilation driven solely by the peripheral chemoreceptors. The other approach to avoid or minimize these non-chemoreceptor contributions to the ventilatory response (changes in blood pressure, cerebral blood flow, sympathetic activation and the interaction of peripheral and central chemoreceptor inputs) is to take advantage of the extreme rapidity of the peripheral chemoreflex and perform very brief transient tests that entail no more than one to three breaths of a new O2 or CO2 content in the inspired gas, a short enough duration of exposure that the CNS and elsewhere in the body experience very little significant hypoxia or acid–base changes. Transient tests, while not carried out as commonly, can be performed easily and used in field studies with much less equipment, especially that involved with ‘state-of-the-art’ dynamic end-tidal forcing for optimal steady-state testing. In this issue of Experimental Physiology, Pfoh and colleagues (2016) have performed a valuable and interesting study. They have undertaken the first comprehensive head-to-head study of steady-state ventilatory response testing with transient testing in healthy subjects to assess both hypoxic and hypercapnic peripheral chemoreceptor responsiveness. In response to the transient testing, heart rate, mean arterial blood pressure and middle and posterior cerebral artery blood flow velocity (measured by pulsed Doppler ultrasound) all increased no more than 10%, thus minimizing but not wholly eliminating some extra-chemoreceptor contributions to the ventilatory responses. To deal with the inability to gauge the true oxygen stimulus arriving at the chemoreceptors in the very brief transient testing because of the lag time inherent in pulse oximetry (circulatory delay), they also calculated instantaneous breath-by-breath saturation () from changes in end-tidal O2 using a previously published method of generating arterial saturation values from end-tidal oxygen values. The authors show that while the use of arterial O2 saturation by pulse oximetry () rather than a more real-time yielded roughly twofold higher HVR values in the transient testing, there was a good correlation (r = 0.8) within individuals. What they determined using measured pulse oximetry () values was that the transient test HVR values matched the magnitude of the isocapnic steady-state hypoxic testing but had little correlation among individuals (r = 0.06, P = 0.8). In contrast, the transient test values were better correlated with the poikilocapnic steady-state values (r = 0.57, P < 0.01). For reasons not given, the transient hypercapnic tests were not compared in the same individuals with the conventional hyperoxic hypercapnic ventilatory response to determine how these two forms of testing might isolate the sensing of CO2 from the peripheral chemoreceptors. In their attempt to minimize any non-peripheral chemoreceptor input into the ventilatory response, Pfoh and colleagues (2016) have shown that transient testing moves closer to that ideal. However, it may be something of a holy grail, apart from a very invasive isolated perfusion of the carotid bodies as can be performed in animals (Dempsey & Smith, 2014). Furthermore, it must be realized that the peripheral chemoreceptors themselves when stimulated by hypoxia or CO2 directly alter cerebral blood flow and other systemic blood flows (Ponte & Purves, 1974) via their afferent output. This direct neural output from the peripheral chemoreceptors may account for the measured haemodynamic and cerebral vascular changes that the authors note. Additionally, there exists another site of chemoreception for both O2 and CO2 in specialized cells of the airways termed neuroepithelial bodies (Livermore et al. 2015) that could potentially contribute to changes in ventilation in transient testing because they will be exposed to any changes in inspired oxygen or carbon dioxide even sooner than the peripheral chemoreceptors. These chemoreceptors are proposed to possibly function in hypoxic (and hypercapnic) pulmonary vasoconstriction (HPV), in hypercapnic bronchodilatation and in newborn ventilatory control before maturation of carotid body innervation and function occurs (Livermore et al. 2015). Although impossible to perform in humans, studies in animals with acute lung denervation would be very informative regarding their contribution to ventilatory control. Another use of well-performed transient testing and more accurate assessment of ‘pure’ peripheral chemoreceptor responsiveness would be to explore further two phenomena in humans that appear to be non-ventilatory consequences of peripheral chemoreceptor stimulation, namely acute hypoxic diuresis (Swenson et al. 1995) and HPV moderation (Albert & Swenson, 2014). Studies in animals reveal that hypoxic diuresis is abolished (Swenson et al. 1995) and that HPV is stronger with carotid body denervation (Albert & Swenson, 2014). Overally, the study by Pfoh and colleagues (2016) sets down a good foundation for exploration of the utility of transient testing in the measurement of peripheral chemoreceptor function and adaptation with environmental stresses, such as high altitude, and with drug therapies in disorders of ventilatory control and in cardiovascular disease. This last aspect is clinically relevant given the emerging evidence of heightened peripheral chemoreceptor sensitivity in both right- and left-sided heart failure, which may negatively affect quality of life and outcomes (Dempsey & Smith, 2014)." @default.
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• W2289049938 title "How and why transient testing may better reveal peripheral chemoreceptor function in humans" @default.
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