Figure 413

Effects of increased arterial blood Pco2 and decreased arterial pH (increased hydrogen ion concentration) on the rate of alveolar ventilation.

Unimportance of Oxygen for Control of the Respiratory Center

Changes in oxygen concentration have virtually no direct effect on the respiratory center itself to alter respiratory drive (although oxygen changes do have an indirect effect, acting through the peripheral chemoreceptors, as explained in the next section).

We learned in Chapter 40 that the hemoglobin-oxygen buffer system delivers almost exactly normal amounts of oxygen to the tissues even when the pulmonary Po2 changes from a value as low as 60 mm Hg up to a value as high as 1000 mm Hg. Therefore, except under special conditions, adequate delivery of oxygen can occur despite changes in lung ventilation ranging from slightly below one half normal to as high as 20 or more times normal. This is not true for carbon dioxide, because both the blood and tissue Pco2 changes inversely with the rate of pulmonary ventilation; thus, the processes of animal evolution have made carbon dioxide the major controller of respiration, not oxygen.

Yet, for those special conditions in which the tissues get into trouble for lack of oxygen, the body has a special mechanism for respiratory control located in the peripheral chemoreceptors, outside the brain respiratory center; this mechanism responds when the blood oxygen falls too low, mainly below a Po2 of 70 mm Hg, as explained in the next section.

Peripheral Chemoreceptor System for Control of Respiratory Activity—Role of Oxygen in Respiratory Control

In addition to control of respiratory activity by the respiratory center itself, still another mechanism is available for controlling respiration. This is the peripheral chemoreceptor system, shown in Figure 41-4. Special nervous chemical receptors, called chemoreceptors, are located in several areas outside the brain. They are especially important for detecting changes in oxygen in the blood, although they also respond to a lesser extent to changes in carbon dioxide and hydrogen ion concentrations. The chemoreceptors transmit nervous signals to the respiratory center in the brain to help regulate respiratory activity.

Most of the chemoreceptors are in the carotid bodies. However, a few are also in the aortic bodies, shown in the lower part of Figure 41-4, and a very few are located elsewhere in association with other arteries of the thoracic and abdominal regions.

The carotid bodies are located bilaterally in the bifurcations of the common carotid arteries. Their afferent nerve fibers pass through Hering's nerves to the glossopharyngeal nerves and then to the dorsal respiratory area of the medulla. The aortic bodies are located along the arch of the aorta; their afferent nerve fibers pass through the vagi, also to the dorsal medullary respiratory area.

Each of the chemoreceptor bodies receives its own special blood supply through a minute artery directly from the adjacent arterial trunk. Further, blood flow through these bodies is extreme, 20 times the weight of the bodies themselves each minute. Therefore, the percentage of oxygen removed from the flowing blood is virtually zero. This means that the chemoreceptors are exposed at all times to arterial blood, not venous blood, and their Po2s are arterial Po2s.

Stimulation of the Chemoreceptors by Decreased Arterial Oxygen. When the oxygen concentration in the arterial blood falls below normal, the chemoreceptors become strongly stimulated. This is demonstrated in Figure 41-5, which shows the effect of different levels of arterial Po2 on the rate of nerve impulse transmission from a carotid body. Note that the impulse rate is particularly sensitive to changes in arterial Po2 in the range of 60 down to 30 mm Hg, a range in which hemoglobin saturation with oxygen decreases rapidly.

Effect of Carbon Dioxide and Hydrogen Ion Concentration on Chemoreceptor Activity. An increase in either carbon dioxide concentration or hydrogen ion concentration also excites the chemoreceptors and, in this way, indirectly increases respiratory activity. However, the direct effects of both these factors in the respiratory center itself are so much more powerful than their effects mediated through the chemoreceptors (about seven times as powerful) that, for practical purposes, the indirect effects of carbon dioxide and hydrogen ions through the chemoreceptors do not need to be considered. Yet there is one difference between the peripheral and central effects of carbon dioxide: the stimulation by way of the peripheral chemoreceptors occurs as much as five times as rapidly as central stimulation, so that the peripheral chemoreceptors might be especially important in increasing the rapidity of response to carbon dioxide at the onset of exercise.

Basic Mechanism of Stimulation of the Chemoreceptors by Oxygen Deficiency. The exact means by which low Po2 excites the nerve endings in the carotid and aortic bodies is still unknown. However, these bodies have

Respiratory control by peripheral chemoreceptors in the carotid and aortic bodies.

Effect of arterial Po2 on impulse rate from the carotid body of a cat.

Respiratory control by peripheral chemoreceptors in the carotid and aortic bodies.

Effect of arterial Po2 on impulse rate from the carotid body of a cat.

multiple highly characteristic glandular-like cells, called glomus cells, that synapse directly or indirectly with the nerve endings. Some investigators have suggested that these glomus cells might function as the chemoreceptors and then stimulate the nerve endings. But other studies suggest that the nerve endings themselves are directly sensitive to the low Po2.

Effect of Low Arterial Po2 to Stimulate Alveolar Ventilation When Arterial Carbon Dioxide and Hydrogen Ion Concentrations Remain Normal

Figure 41-6 shows the effect of low arterial Po2 on alveolar ventilation when the Pco2 and the hydrogen ion concentration are kept constant at their normal levels. In other words, in this figure, only the ventilatory drive due to the effect of low oxygen on the chemoreceptors is active. The figure shows almost no effect on ventilation as long as the arterial Po2 remains greater than 100 mm Hg. But at pressures lower than 100 mm Hg, ventilation approximately doubles when the arterial Po2 falls to 60 mm Hg and can increase as much as fivefold at very low Po2s. Under these conditions, low arterial Po2 obviously drives the ventilatory process quite strongly.

Chronic Breathing of Low Oxygen Stimulates Respiration Even More—The Phenomenon of "Acclimatization"

Mountain climbers have found that when they ascend a mountain slowly, over a period of days rather than a period of hours, they breathe much more deeply and therefore can withstand far lower atmospheric oxygen concentrations than when they ascend rapidly. This is called acclimatization.

The reason for acclimatization is that, within 2 to 3 days, the respiratory center in the brain stem loses about four fifths of its sensitivity to changes in Pco2 and hydrogen ions. Therefore, the excess ventilatory blow-off of carbon dioxide that normally would inhibit an increase in respiration fails to occur, and low oxygen can drive the respiratory system to a much higher level of alveolar ventilation than under acute conditions. Instead of the 70 per cent increase in ventilation that might occur after acute exposure to low oxygen, the alveolar ventilation often increases 400 to 500 per cent after 2 to 3 days of low oxygen; this helps immensely in supplying additional oxygen to the mountain climber.

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Essentials of Human Physiology

Essentials of Human Physiology

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