Ventilatory Response to Arterial Po2, Pco2, and pH
sensitivity in response to chronic decreases in arterial Pco2 (e.g., in normal subjects experiencing chronic hypoxia at altitude). Previously, it was thought that changes in central CO2 sensitivity could be explained by metabolic compensations for respiratory disturbances in CSF pH. However, the pH of CSF does not show complete compensation to its normal value (7.3) during chronic respiratory acidosis or alkalosis, but remains acidotic or alkalotic. Renal compensation of respiratory changes in arterial pH could not correct CSF pH because metabolic acids do not cross the blood-brain barrier (see Fig. 4). Nevertheless, ventilatory reflexes from central chemoreceptors can adapt to chronic changes in Pco2 "as if'' the H+ stimulus at central chemoreceptors changed in parallel with metabolic compensations of arterial pH, at least under some conditions (see Ventilatory Responses to Paco2 section later).
Arterial chemoreceptors is a generic term for both the carotid body chemoreceptors and aortic body chemo-receptors. The carotid bodies are small (diameter « 2 mm) sensory organs located near the carotid sinus at the bifurcation of the common carotid artery at the base of the skull. The aortic bodies are on the aortic arch near the aortic arch baroreceptors. Afferent nerves travel to the CNS from the carotid bodies in the glossopharyngeal (IX cranial) nerve, and from the aortic bodies in the vagus (X cranial) nerve. Most of our knowledge about arterial chemoreceptors is based on studies of the carotid body, and the aortic bodies will be considered similar throughout this chapter unless noted otherwise.
Carotid body chemoreceptors respond to changes in arterial Po2, Pco2, and pH. These organs have the highest blood flow per unit mass, and this rich blood supply makes them efficient at sensing changes in arterial blood gases. Carotid bodies are the most important chemoreceptors for ventilatory sensitivity to Pao2 and they respond to changes in o2 partial pressure, but not changes in o2 content or hemoglobin saturation. This is critical to understanding clinical problems such as anemia or carbon monoxide poisoning. In these cases, ventilation will not be stimulated because Pao2 is normal, or even elevated, and there is no sensory system for decreases in o2 content of hemoglobin saturation.
The mechanism of Po2 sensing in the carotid bodies is not completely understood but it depends on specialized neurosecretory cells, called glomus (or chief) cells. The carotid body is a complex organ, consisting of glomus cells, glial-like sustentacular (or sheath) cells, capillary endothelial cells, afferent nerve endings from the glossopharyngeal nerve, and even sympathetic efferent nerve endings. Candidates for molecular O2 sensors are specialized NADP(H) oxidases or cytochromes, or o2-sensitive potassium channels, and o2-sensing appears to involve signaling by reactive oxygen species. The glomus cells contain several types of neurotransmitters and neuropeptides. Hypoxia depolarizes these cells, causing release of an (unknown) excitatory neurotransmitter and excitation of the afferent nerve ending that sends action potentials to respiratory centers in the brain.
Changes in Pao2 are coded as changes in the frequency of action potentials in the afferent nerves from the arterial chemoreceptors. Figure 5 shows that carotid body afferent nerve activity has a low level of tonic activity with normal Pao2 (100 mm Hg) and Paco2 (40 mm Hg). Arterial chemoreceptor activity does not increase until Pao2 falls below normal levels if Paco2 is normal. However, carotid body chemoreceptors are also sensitive to Paco2. If Paco2 is below normal levels, then Pao2 must decrease even further below normal to excite
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