Transport of Carbon Dioxide in Blood

In a resting person, metabolism generates about 200 ml of carbon dioxide per minute. When arterial blood flows through tissue capillaries, this volume of carbon dioxide diffuses from the tissues into the blood (Figure 15-27). Carbon dioxide is much more soluble in water than is oxygen, and so more dissolved carbon dioxide than dissolved oxygen is carried in blood. Even so, only a relatively small amount of blood carbon dioxide is transported in this way; only 10 percent of the carbon dioxide entering the blood remains physically dissolved in the plasma and erythrocytes.

Another 30 percent of the carbon dioxide molecules entering the blood reacts reversibly with the amino groups of hemoglobin to form carbamino hemoglobin. For simplicity, this reaction with hemoglobin is written as:

HbCO2

In tissue capillaries

Cells

CO2 produced

Interstitial fluid

Dissolved CO2

Plasma

Some Co2 remains dissolved

Dissolved CO2

Erythrocytes

Some CO2 remains dissolved

HbCo2

hco3-

Carbonic anhydrase h2co3 *

In pulmonary capillaries

Atmosphere

Expired CO2

Alveoli co2

Plasma

Dissolved Co2

hco3

Erythrocytes

^ Carbonic anhydrase

H2CO3 *

FIGURE 15-27

Summary of CO2 movement. Expiration of CO2 is by bulk-flow, whereas all movements of CO2 across membranes are by diffusion. Arrows reflect relative proportions of the fates of the CO2. About two-thirds of the CO2 entering the blood in the tissues ultimately is converted to HCO3~ in the erythrocytes because carbonic anhydrase is located there, but most of the HCO3~ then moves out of the erythrocytes into the plasma in exchange for chloride ions (the "chloride shift"). See Figure 15-28 for the fate of the hydrogen ions generated in the erythrocytes.

Dissolved Co2 + Hb

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

III. Coordinated Body Functions

15. Respiration

Respiration CHAPTER FIFTEEN

Respiration CHAPTER FIFTEEN

This reaction is aided by the fact that deoxyhemoglo-bin, formed as blood flows through the tissue capillaries, has a greater affinity for carbon dioxide than does oxyhemoglobin.

The remaining 60 percent of the carbon dioxide molecules entering the blood in the tissues is converted to bicarbonate:

Carbonic anhydrase

H2CO3 3:

Carbonic acid

Bicarbonate

The first reaction in Equation 15-10 is rate-limiting and is very slow unless catalyzed by the enzyme carbonic anhydrase. This enzyme is present in the erythrocytes but not in the plasma; therefore, this reaction occurs mainly in the erythrocytes. In contrast, carbonic acid dissociates very rapidly into a bicarbonate ion and a hydrogen ion without any enzyme assistance. Once formed, most of the bicarbonate moves out of the erythrocytes into the plasma via a transporter that exchanges one bicarbonate for one chloride ion (this is called the "chloride shift").

The reactions shown in Equation 15-10 also explain why, as mentioned earlier, the H+ concentration in tissue capillary blood and systemic venous blood is higher than that of the arterial blood and increases as metabolic activity increases. The fate of these hydrogen ions will be discussed in the next section.

Because carbon dioxide undergoes these various fates in blood, it is customary to add up the amounts of dissolved carbon dioxide, bicarbonate, and carbon dioxide in carbamino hemoglobin and call this sum the total blood carbon dioxide.

Just the opposite events occur as systemic venous blood flows through the lung capillaries (Figure 15-27). Because the blood PCO2 is higher than alveolar PCo2, a net diffusion of CO2 from blood into alveoli occurs. This loss of CO2 from the blood lowers the blood PCO2 and drives reactions 15-10 and 15-9 to the left: HCO-f and H+ combine to give H2CO3, which then dissociates to CO2 and H2O. Similarly, HbCO2 generates Hb and free CO2. Normally, as fast as CO2 is generated from HCO3~ and H+ and from HbCO2, it diffuses into the alveoli. In this manner, all the CO2 delivered into the blood in the tissues now is delivered into the alveoli; it is eliminated from the alveoli and from the body during expiration.

Transport of Hydrogen Ions between Tissues and Lungs

To repeat, as blood flows through the tissues, a fraction of oxyhemoglobin loses its oxygen to become de-oxyhemoglobin, while simultaneously a large quantity of carbon dioxide enters the blood and undergoes the reactions that generate bicarbonate and hydrogen ions. What happens to these hydrogen ions?

Deoxyhemoglobin has a much greater affinity for H+ than does oxyhemoglobin, and so it binds (buffers) most of the hydrogen ions (Figure 15-28). Indeed, de-oxyhemoglobin is often abbreviated HbH rather than Hb to denote its binding of H+. In effect, the reaction is HbO2 + H+ HbH + O2. In this manner, only a small number of the hydrogen ions generated in the blood remains free. This explains why the acidity of venous blood (pH = 7.36) is only slightly greater than that of arterial blood (pH = 7.40).

As the venous blood passes through the lungs, all these reactions are reversed. Deoxyhemoglobin becomes converted to oxyhemoglobin and, in the process, releases the hydrogen ions it had picked up in the tissues. The hydrogen ions react with bicarbonate to give carbonic acid, which dissociates to form carbon dioxide and water, and the carbon dioxide diffuses into the alveoli to be expired. Normally all the hydrogen ions that are generated in the tissue capillaries from the reaction of carbon dioxide and water recombine with bicarbonate to form carbon dioxide and water in the pulmonary capillaries. Therefore, none of these hydrogen ions appear in the arterial blood.

But what if the person is hypoventilating or has a lung disease that prevents normal elimination of carbon dioxide? Not only would arterial PCO2 rise as a result but so would arterial H+ concentration. Increased arterial H+ concentration due to carbon dioxide retention is termed respiratory acidosis. Conversely, hyperventilation would lower the arterial values of both PCO2 and H+ concentration, producing respiratory alkalosis.

In the course of describing the transport of oxygen, carbon dioxide, and H+ in blood, we have presented multiple factors that influence the binding of these substances by hemoglobin. They are all summarized in Table 15-8.

One more aspect of the remarkable hemoglobin molecule should at least be mentioned—its ability to bind and transport nitric oxide. As described in Chapters 8, 14, and 20 respectively, nitric oxide is an important neurotransmitter and is also released by en-dothelial cells and macrophages. A present hypothesis is that as blood passes through the lungs, hemoglobin picks up and binds not only oxygen but nitric oxide synthesized there, carries it to the peripheral tissues, and releases it along with oxygen. Simultaneously, via a different binding site hemoglobin picks up and ca-tabolizes nitric oxide produced in the peripheral tissues. Theoretically this cycle could play an important role in determining the peripheral concentration of nitric oxide and, thereby, the overall effect of this vasodilator agent. For example, by supplying net nitric

Vander et al.: Human I III. Coordinated Body I 15. Respiration I I © The McGraw-Hill

Physiology: The Functions Companies, 2001 Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

Cells

Interstitial fluid

Plasma

Erythrocytes

HbO2

O2 Hb

FIGURE 15-28

Binding of hydrogen ions by hemoglobin as blood flows through tissue capillaries. This reaction is facilitated because deoxyhemoglobin, formed as oxygen dissociates from hemoglobin, has a greater affinity for hydrogen ions than does oxyhemoglobin. For this reason, Hb and HbH are both abbreviations for deoxyhemoglobin.

oxide to the periphery, the process could cause additional vasodilation by systemic blood vessels; this would have effects on both local blood flow and systemic arterial blood pressure.

Control of Respiration

Neural Generation of Rhythmical Breathing

The diaphragm and intercostal muscles are skeletal muscles and therefore do not contract unless stimulated to do so by nerves. Thus, breathing depends entirely upon cyclical respiratory muscle excitation of the diaphragm and the intercostal muscles by their motor nerves. Destruction of these nerves (as in the viral disease poliomyelitis, for example) results in paralysis of the respiratory muscles and death, unless some form of artificial respiration can be instituted.

Inspiration is initiated by a burst of action potentials in the nerves to the inspiratory muscles. Then the action potentials cease, the inspiratory muscles relax, and expiration occurs as the elastic lungs recoil. In situations when expiration is facilitated by contraction of expiratory muscles, the nerves to these muscles, which were quiescent during inspiration, begin firing during expiration.

By what mechanism are nerve impulses to the respiratory muscles alternately increased and decreased? Control of this neural activity resides primarily in neurons in the medulla oblongata, the same area of brain that contains the major cardiovascular control centers. (For the rest of this chapter we shall refer to the medulla oblongata simply as the medulla.) In several nuclei of the medulla, neurons called medullary inspiratory neurons discharge in synchrony with inspiration and cease discharging during expiration. They provide, through either direct or interneuronal connections, the rhythmic input to the motor neurons innervating the inspiratory muscles. The alternating cycles of firing and quiescence in the medullary inspi-ratory neurons are generated by a cooperative interaction between synaptic input from other medullary neurons and intrinsic pacemaker potentials in the in-spiratory neurons themselves.

The medullary inspiratory neurons receive a rich synaptic input from neurons in various areas of the pons, the part of the brainstem just above the medulla. This input modulates the output of the medullary in-spiratory neurons and may help terminate inspiration by inhibiting them. It is likely that an area of the lower pons called the apneustic center is the major source of this output, whereas an area of the upper pons called the pneumotaxic center modulates the activity of the apneustic center.

TABLE 15-8 Effects of Various Factors on Hemoglobin

The affinity of hemoglobin for oxygen is decreased by:

1. Increased hydrogen-ion concentration

2. Increased PCO2

3. Increased temperature

4. Increased DPG concentration

The affinity of hemoglobin for both hydrogen ions and carbon dioxide is decreased by increased POj that is, deoxyhemoglobin has a greater affinity for hydrogen ions and carbon dioxide than does oxyhemoglobin.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Respiration CHAPTER FIFTEEN

Respiration CHAPTER FIFTEEN

Another cutoff signal for inspiration comes from pulmonary stretch receptors, which lie in the airway smooth-muscle layer and are activated by a large lung inflation. Action potentials in the afferent nerve fibers from the stretch receptors travel to the brain and inhibit the medullary inspiratory neurons. (This is known as the Hering-Breur inflation reflex.) Thus, feedback from the lungs helps to terminate inspiration. However, this pulmonary stretch-receptor reflex plays a role in setting respiratory rhythm only under conditions of very large tidal volumes, as in rigorous exercise.

One last point about the medullary inspiratory neurons should be made: They are quite sensitive to depression by drugs such as barbiturates and morphine, and death from an overdose of these drugs is often due directly to a cessation of ventilation.

Control of Ventilation by PO2, PCo2/ and H+ Concentration

Respiratory rate and tidal volume are not fixed but can be increased or decreased over a wide range. For simplicity, we shall describe the control of ventilation without discussing whether rate or depth makes the greater contribution to the change.

There are many inputs to the medullary inspira-tory neurons, but the most important for the automatic control of ventilation at rest are from peripheral chemoreceptors and central chemoreceptors.

The peripheral chemoreceptors, located high in the neck at the bifurcation of the common carotid arteries and in the thorax on the arch of the aorta (Figure 15-29), are called the carotid bodies and aortic bodies. In both locations they are quite close to, but distinct from, the arterial baroreceptors described in Chapter 14 and are in intimate contact with the arterial blood. The peripheral chemoreceptors are composed of specialized receptor cells that are stimulated mainly by a decrease in the arterial PO2 and an increase in the arterial H+ concentration (Table 15-9). These cells communicate synaptically with neuron terminals from which afferent nerve fibers pass to the brainstem. There they provide excitatory synaptic input to the medullary inspiratory neurons.

The central chemoreceptors are located in the medulla and, like the peripheral chemoreceptors, provide excitatory synaptic input to the medullary inspi-ratory neurons. They are stimulated by an increase in the H+ concentration of the brain's extracellular fluid. As we shall see, such changes result mainly from changes in blood PCO2.

Control by PO2 Figure 15-30 illustrates an experiment in which healthy subjects breathe low PO2 gas mixtures for several minutes. (The experiment is per-

Carotid bodies

Carotid bodies

Right common carotid artery

Aorta

Aorta

Peripheral Chemoreceptors

Aortic bodies

FIGURE 15-29

Location of the carotid and aortic bodies. Note that each carotid body is quite close to a carotid sinus, the major arterial baroreceptor. Both right and left common carotid bifurcations contain a carotid sinus and a carotid body.

Carotid sinus

Left common carotid artery

Aortic bodies

FIGURE 15-29

Location of the carotid and aortic bodies. Note that each carotid body is quite close to a carotid sinus, the major arterial baroreceptor. Both right and left common carotid bifurcations contain a carotid sinus and a carotid body.

formed in a way that keeps arterial PCO2 constant so that the pure effects of changing only PO2 can be studied.) Little increase in ventilation is observed until the oxygen content of the inspired air is reduced enough to lower arterial PO2 to 60 mmHg. Beyond this point, any further reduction in arterial PO2 causes a marked reflex increase in ventilation.

TABLE 15-9 Major Stimuli for the Central and Peripheral Chemoreceptors

Peripheral chemoreceptors—that is, carotid bodies and aortic bodies—respond to changes in the arterial blood. They are stimulated by:

1. Decreased POi

2. Increased hydrogen-ion concentration

Central chemoreceptors—that is, located in the medulla oblongata—respond to changes in the brain extracellular fluid. They are stimulated by increased PCO , via associated changes in hydrogen-ion concentration. (See Equation 15-10.)

Vander et al.: Human I III. Coordinated Body I 15. Respiration I I © The McGraw-Hill

Physiology: The Functions Companies, 2001 Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

Chemoreceptors Stimulate Mmhg

0 20 40 60 80 100 120

Arterial POj (mmHg)

FIGURE 15-30

The effect on ventilation of breathing low-oxygen mixtures. The arterial PCO2 was maintained at 40 mmHg throughout the experiment.

0 20 40 60 80 100 120

Arterial POj (mmHg)

FIGURE 15-30

The effect on ventilation of breathing low-oxygen mixtures. The arterial PCO2 was maintained at 40 mmHg throughout the experiment.

Control by PCO2 Figure 15-32 illustrates an experiment in which subjects breathe air to which variable quantities of carbon dioxide have been added. The presence of carbon dioxide in the inspired air causes an elevation of alveolar PCO2 and thereby an elevation of arterial PCO2. Note that even a very small increase in arterial PCO2 causes a marked reflex increase in ventilation. Experiments like this have documented that small increases in arterial PCO2 are resisted by the reflex mechanisms controlling ventilation to a much greater degree than are equivalent decreases in arterial PO2.

Of course we don't usually breathe bags of gas containing carbon dioxide. What is the physiological role of this reflex? If a defect in the respiratory system (emphysema, for example) causes a retention of carbon dioxide in the body, the increase in arterial PCO2

Retention Carbon Dioxide

This reflex is mediated by the peripheral chemo-receptors (Figure 15-31). The low arterial PO2 increases the rate at which the receptors discharge, resulting in an increased number of action potentials traveling up the afferent nerve fibers and stimulating the medullary inspiratory neurons. The resulting increase in ventilation provides more oxygen to the alveoli and minimizes the drop in alveolar and arterial PO2 produced by the low PO2 gas mixture.

It may seem surprising that we are so insensitive to smaller reductions of arterial PO2, but look again at the oxygen-hemoglobin dissociation curve (see Figure 15-23). Total oxygen transport by the blood is not really reduced very much until the arterial PO2 falls below about 60 mmHg. Therefore, increased ventilation would not result in very much more oxygen being added to the blood until that point is reached.

To reiterate, the peripheral chemoreceptors respond to decreases in arterial PO2, as occurs in lung disease or exposure to high altitude. However, the peripheral chemoreceptors are not stimulated in situations in which there are modest reductions in the oxygen content of the blood but no change in arterial PO2. An example of this is anemia, where there is a decrease in the amount of hemoglobin present in the blood (Chapter 14) but no decrease in arterial PO2, because the concentration of dissolved oxygen in the blood is normal.

This same analysis holds true when oxygen content is reduced moderately by the presence of carbon monoxide, which as described earlier reduces the amount of oxygen combined with hemoglobin by competing for these sites. Since carbon monoxide does not affect the amount of oxygen that can dissolve in blood, the arterial PO2 is unaltered, and no increase in peripheral chemoreceptor output occurs.

FIGURE 15-31

Sequence of events by which a low arterial PO2 causes hyperventilation, which maintains alveolar (and, hence, arterial) PO2 at a value higher than would exist if the ventilation had remained unchanged.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Respiration CHAPTER FIFTEEN

Respiration CHAPTER FIFTEEN

Minute Ventilation Pco2

nrierial PCO2 \mmng;

FIGURE 15-32

Effects on respiration of increasing arterial PCO2 achieved by adding carbon dioxide to inspired air.

nrierial PCO2 \mmng;

FIGURE 15-32

Effects on respiration of increasing arterial PCO2 achieved by adding carbon dioxide to inspired air.

stimulates ventilation, which promotes the elimination of carbon dioxide. Conversely, if arterial PCO2 decreases below normal levels for whatever reason, this removes some of the stimulus for ventilation, thereby reducing ventilation and allowing metabolically produced carbon dioxide to accumulate and return the Pco to normal. In this manner, the arterial PCO2 is stabilized near the normal value of 40 mmHg.

The ability of changes in arterial PCO2 to control ventilation reflexly is largely due to associated changes in H+ concentration (Equation 15-10). As summarized in Figure 15-33, the pathways that mediate these reflexes are initiated by both the peripheral and central chemoreceptors. The peripheral chemoreceptors are stimulated by the increased arterial H+ concentration resulting from the increased PCO2. At the same time, because carbon dioxide diffuses rapidly across the membranes separating capillary blood and brain tissue, the increase in arterial PCO2 causes a rapid increase in brain extracellular fluid PCO2. This increased PCO2 increases brain extracellular-fluid H+ concentration, which stimulates the central chemoreceptors. Inputs from both the peripheral and central chemoreceptors stimulate the medullary inspiratory neurons to increase ventilation. The end result is a return of arterial and brain extracellular fluid PCO2 and H+ concentration toward normal. Of the two sets of receptors involved in this reflex response to elevated PCO2, the central chemoreceptors are the more important, accounting for about 70 percent of the increased ventilation.

It should also be noted that the effects of increased PCO2 and decreased PO2 not only exist as independent inputs to the medulla but manifest synergistic interactions as well. Acute ventilatory response to combined low PO2 and high PCO2 is considerably greater than the sum of the individual responses.

Throughout this section, we have described the stimulatory effects of carbon dioxide on ventilation via reflex input to the medulla, but very high levels of carbon dioxide actually inhibit ventilation and may be lethal. This is because such concentrations of carbon dioxide act directly on the medulla to inhibit the respiratory neurons by an anesthesia-like effect. Other symptoms caused by very high blood PCO2 include severe headaches, restlessness, and dulling or loss of consciousness.

Control by Changes in Arterial H+ Concentration That Are Not Due to Altered Carbon Dioxide We have seen that retention or excessive elimination of carbon dioxide causes respiratory acidosis and respiratory alkalosis, respectively. There are, however, many normal and pathological situations in which a change in arterial H+ concentration is due to some cause other than a primary change in PCO2. These are termed metabolic acidosis when H+ concentration is increased and metabolic alkalosis when it is decreased. In such cases, the peripheral chemoreceptors play the major role in altering ventilation.

For example, addition of lactic acid to the blood, as in strenuous exercise, causes hyperventilation almost entirely by stimulation of the peripheral chemoreceptors (Figures 15-34 and 15-35). The central chemoreceptors are only minimally stimulated in this case because brain H+ concentration is increased to only a small extent, at least early on, by the hydrogen ions generated from the lactic acid. This is because hydrogen ions penetrate the blood-brain barrier very slowly. In contrast, as described earlier, carbon dioxide penetrates the blood-brain barrier easily and changes brain H+ concentration.

The converse of the above situation is also true: When arterial H+ concentration is lowered by any means other than by a reduction in PCO2 (for example, by loss of hydrogen ions from the stomach in vomiting), ventilation is reflexly depressed because of decreased peripheral chemoreceptor output.

The adaptive value such reflexes have in regulating arterial H+ concentration is shown in Figure 15-35. The hyperventilation induced by a metabolic acidosis reduces arterial PCO2, which lowers arterial H+ concentration back toward normal. Similarly, hypoventilation induced by a metabolic alkalosis results in an elevated arterial PCO2 and a restoration of H+ concentration toward normal.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

Breathing gas mixture containing CO2

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Responses

  • cettina
    Where is more than 70 percent of the carbon dioxide carried in the blood?
    7 years ago
  • milen
    What are specialized cells that respond to changes in carbon dioxide, oxygen, and h concentrations?
    7 years ago
  • andi
    When carbon dioxide enters the blood from tissue cells it is converted to?
    7 years ago
  • Prisca
    What are the steps for carbon dioxide transportation in the body.?
    7 years ago
  • katie
    How is carbon dioxide transport in the body?
    7 years ago
  • hilda
    Does person's pCO2 increase at point of death?
    7 years ago
  • Semere
    How carbon dioxide concentration tissue fluid effects the rate of breathing?
    7 years ago
  • AMANDA
    When carbon dioxide enters the bloodfrom tissu cells it is convete to?
    7 years ago
  • vilho
    What percentage of the carbon dioxide produced is transported via hemoglobin?
    7 years ago
  • amina
    How does an increase in the carbon dioxide in the blood and interstitial fluid effects?
    7 years ago
  • fioretta pirozzi
    How is bulk of carbon dioxide carried in blood?
    6 years ago
  • daniel
    How is carbon dioxide carried from the body tissues to lungs hemoglobin?
    6 years ago
  • bosco
    How is carbon dioxide generated in the human body?
    6 years ago
  • deodata marino
    What are the steps of transport of carbon dioxide?
    6 years ago
  • ilmari pappila
    When the amount of carbon dioxide pco2 increases what occurs?
    6 years ago
  • luce
    How is carbon dioxide transported in the blood and discharged at the lung capillaries?
    6 years ago
  • genet
    What problem could be a result if the capillaries only carried blood with carbon dioxide?
    6 years ago
  • ANNA
    What percentage of co2 passes the blood brain barrier?
    6 years ago
  • Lino
    What reactions enhance the transport of carvone deoxide throughout the body?
    6 years ago
  • Faizan
    Does the increase of Carbon Dioxide, inhibit the medulla?
    6 years ago
  • william
    What funtion can transport carbon dioxide?
    5 years ago
  • MEBRAT
    Why does co2 form HCO3 H in the sytemic capillires?
    5 years ago
  • troy tellez
    What reactions enhance the transport of carbon dioxide throughout the body?
    5 years ago
  • anna-liisa larnia
    How is the inflation reflex occurs in the lung tissues?
    4 years ago
  • jay
    What is the function of chloride ions in CO2?
    3 years ago
  • lyyli
    When CO2 enters the blood in tissues?
    3 years ago
  • eerik larnia
    How does carbon iv oxide is carried in the arterial and venous blood?
    3 years ago
  • tero kononen
    Does transport of carbon dioxide increase pco2?
    2 years ago
  • fesahaye
    What happen when carbon dioxide enters tje blood stream?
    2 years ago
  • krystal
    How co2 is transported from pheriphery to lungs for expiration?
    2 years ago
  • Marcel
    Which form is carbon iv oxide transportrd in blood?
    2 years ago
  • makda
    What occurs in venous look during transportation of CO2?
    2 years ago
  • krystian
    Does hydrogen ion and bicarbonate penetrate blood brain barrier slowly?
    2 years ago
  • PENNY
    What happens to remaining 7% of the carbon dioxide in the plasma during CO2 transportation?
    2 years ago
  • Eero
    What is the % of CO2 is transported as HBCO2?
    2 years ago
  • dennis
    What happen to the carbon(iv)oxide that dissolve in the plasma?
    2 years ago
  • kerttu fr
    What does the carbon dioxide react with, the moment it diffuse from the tissues?
    2 years ago
  • pearl brandybuck
    What Carbon Dioxide from the cells in the tissues diffuses into the capillaries what forms?
    2 years ago
  • CHRISTIAN
    What is the function of the blood plasma in carbon dioxide transport?
    2 years ago
  • hobson
    Why co2 transport is 200ml?
    2 years ago
  • Tombur
    How is carbon (IV) oxide be transported out of the body cells?
    2 years ago
  • kisanet samuel
    How is carbondioxide taken up from the tissue and transported to lungs?
    2 years ago
  • Esa
    Why volume of carbondioxide is 200mililiter per minute metabolic biochemistry?
    1 year ago
  • saare omar
    What happens to carbondioxide when it enters the blood?
    1 year ago
  • genet
    How carbon dioxide is picked up by tissue capillary blood and then discharged in alveoli?
    1 year ago
  • eglantine
    How does Carbon dioxide is transported in the blood of alveolus?
    1 year ago
  • asmait
    How caebondioxide is transported from the body?
    12 months ago
  • Markus
    What are 3 ways that carbon dioxide is carried in the blood back to the alveolar capillaries?
    6 days ago

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