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muscles, is similar to the internal intercostal activity shown in Fig. 3. Inspiratory and expiratory activity in the vagus and hypoglossal (XII cranial) nerves, which innervate the upper airway muscles in the larynx and pharynx, is also similar to the patterns shown in Fig. 3.

The patterns of motor neuron discharge, which determine ventilatory flow profiles and tidal volume, are shaped by central integration of respiratory reflexes in the brain stem. However, some central integration does occur in the spinal cord through y-efferent control of muscle spindles, as described in Chapter 55. Afferent feedback from muscle spindles, and the modulation of this feedback by the y-efferent system, is more important for the intercostal muscles than the diaphragm. This reflex may stabilize ventilation when mechanical loads are applied to the chest wall, and act in concert with reflexes from the lungs that fine-tune the pattern of ventilation to minimize the work of breathing under different conditions.

In addition to the ventilatory muscle pathways described, respiratory reflexes can stimulate responses from the autonomic nervous system, which are described separately in the Reflexes from the Lungs and Airways section.

VENTILATORY RESPONSE TO ARTERIAL Po2, Pco2, AND pH

The chemical control of ventilation is a negative feedback system that monitors arterial blood gases as the output from gas exchange in the lungs and causes reflex changes in ventilation that tend to keep arterial blood gases at a normal level. Arterial Po2, Pco2, and pH are sensed directly by arterial chemoreceptors, and Paco2 is also sensed indirectly by chemoreceptors in the CNS. There is no strong evidence for mixed-venous or alveolar chemoreceptors that can affect breathing. Normally, the overall level of ventilation is determined by arterial blood gases, with Paco2 being the most important stimulus. Differences in the ventilatory response to Pao2, Paco2, and pH can be explained by differences in the sensory mechanisms for each stimulus, which are described next.

Central Chemoreceptors

A ventilatory response to increases in Paco2 can be observed in experimental animals that have no afferent input to the cNS from any peripheral sensory nerves. This response to Paco2 is mediated by central chemo-sensitive areas of the medulla, including the retrotrape-zoid nucleus, raphe;, nucleus of the solitary tract, and the ventral surface of the medulla at the fourth ventricle.

Chemosensitive Neurons

FIGURE 4 Central chemoreceptor cells sense changes in Paco2 by a H+ mechanism, but central chemoreceptors are not affected by changes in arterial pH because the blood-brain barrier prevents H+ ion movement across capillaries in the brain. In contrast, PCO2 easily crosses brain capillaries and changes pH in the chemoreceptor cells, in the interstitial fluid surrounding the cells, and in the CSF between the surface of the brain and the pia mater.

FIGURE 4 Central chemoreceptor cells sense changes in Paco2 by a H+ mechanism, but central chemoreceptors are not affected by changes in arterial pH because the blood-brain barrier prevents H+ ion movement across capillaries in the brain. In contrast, PCO2 easily crosses brain capillaries and changes pH in the chemoreceptor cells, in the interstitial fluid surrounding the cells, and in the CSF between the surface of the brain and the pia mater.

Many of the sites are near the respiratory centers described earlier (see the Respiratory Rhythm Generation section). Clearly delineated chemosensory organs, analogous to the arterial chemoreceptors described later, have not been identified in the CNS but experiments show certain neurons in these central chemosen-sitive areas are sensitive to changes in PCO2 and pH.

A common feature of central chemosensitive neurons is that they have dendrites with endings near cerebral blood vessels. As shown in Fig. 4, these vessels and nerve endings are also frequently near the surface of the brain, which is bathed in cerebral spinal fluid (CSF). Specialized chemosensitive nerve endings depolarize in response to decreased intracellular pH, which occurs when arterial PCO2 increases. CO2 is very soluble in lipids so it moves easily across the capillaries and membranes in the brain and generates H+ inside central chemosensitive neurons, as well as in the extracellular space and CSF around these neurons. In contrast, the so-called blood-brain barrier prevents polar molecules like H+ (and certain drugs) from moving across the capillaries, or through tight junctions between capillary endothelial cells, in the brain. Hence, changes in arterial pH are not sensed by central chemosensitive neurons because the H+ stimulus cannot reach the chemosensi-tive dendrites. This means that the ventilatory response to changes in arterial pH requires other chemoreceptors, i.e., the arterial chemoreceptors described later.

Although the mechanism is unknown, central chemo-sensitive neurons may decrease CO2 sensitivity in response to long-term increases in arterial PCO2 (e.g., in patients with chronic lung disease) and increase CO2

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