Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange?

Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange?

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From my understanding, the process that displaces the carbon dioxide and oxygen in our erythrocytes and lungs is diffusion. I've been taught that diffusion is the net movement of particles from a region of higher concentration to a region of lower concentration, until an equillibrium is reached.

For there to be an equillibrium in carbon dioxide and oxygen, doesn't that mean that there should be equal portions of those elements present at all times? So therefore, erythrocytes should contain both of those chemicals simultaneously. Am I correct in assuming this? If I am, then I have a follow-up question: wouldn't carbon dioxide floating about in our blood indefinitely cause some unhealthy side effects, and is there something that prevents it from doing so?

I'm currently only in GCSEs, so apologies if this question might actually have a very simple answer.


For diffusion to occur there must be a "concentration gradient", that is one area where the substance that is diffusing from, to where it is diffusing to. Where the substance is diffusing from, the concentration is high and where it is going to, the concentration is low. Our bodies continually use up oxygen and produces carbon dioxide. Carbon dioxide is generally carried in the blood plasma, and oxygen is generally carried by the red blood cell (erythrocytes). Whereas, it is true that in diffusion an equilibrium is usually achieved, in this case you mention there is no equilibrium. Our physiological processes (respiration) continually maintains that concentration gradient and so carbon dioxide always flows out and oxygen always comes in. Too much carbon dioxide in the blood will raise the pH and cause serious metabolic problems with enzymes and their efficient function.

There in fact typically is an equilibrium of diffusion for both oxygen and for carbon dioxide by the time the blood finishes gas exchange in the alveoli of the lung. One confusion in the OP is that there is no real meaning for a chemical equilibrium between carbon dioxide and oxygen, as they are separate chemical entities. Carbon dioxide in the lung capillary blood equilibrates with carbon dioxide in the lung alveolar gas; oxygen similarly equilibrates between blood and gas. Each effectively on its own.

Yes, oxygen is continually being consumed and carbon dioxide being produced by the body, so from that perspective we have a whole body steady state. At overall equilibrium we are dead. But at the site of gas exchange in the lung, there is generally no difference in the chemical activity of either gas between the alveolar air and the capillary blood leaving the alveolus. So from a chemical perspective there is generally local equilibrium of both gases at that point.

In some circumstances this local equilibrium is not reached. The transport of carbon dioxide is very complicated, as it exists in several inter-convertible forms: dissolved carbon dioxide gas, a form called carbonic acid where it has chemically reacted with water, the bicarbonate and carbonate ions that come from dissociation of carbonic acid, and a carbamate form that is a reversible chemical bond with amino groups on proteins. The reaction with water is slow on its own; it is catalyzed by the enzyme carbonic anhydrase in red cells. If that enzyme is inhibited (for example, by the drug acetazolamide) then there might not be chemical equilibrium of total carbon dioxide between alveolar air and capillary blood as there might not be enough time, as blood flows through the alveolus, for all the other forms to convert to the dissolved gas that can diffuse from blood into alveolar air.

Another complication is that transport of oxygen and carbon dioxide in the blood are somewhat interdependent. Acidification by carbon dioxide (lower pH is more acid) affects the ability of hemoglobin to bind oxygen, tending to release more oxygen. Nevertheless, in most circumstances in humans, both gases are individually at equilibrium between alveolar air and the blood that leaves the alveolus.

Finally, the continued presence of carbon dioxide in the body is a normal, healthy part of physiologic functioning. It does have to be kept in balance, but it does have to be there.

Exchanging Oxygen and Carbon Dioxide

The primary function of the respiratory system is to take in oxygen and eliminate carbon dioxide. Inhaled oxygen enters the lungs and reaches the alveoli. The layers of cells lining the alveoli and the surrounding capillaries are each only one cell thick and are in very close contact with each other. This barrier between air and blood averages about 1 micron ( 1 /10,000 of a centimeter, or 0.000039 inch) in thickness. Oxygen passes quickly through this air-blood barrier into the blood in the capillaries. Similarly, carbon dioxide passes from the blood into the alveoli and is then exhaled.

Oxygenated blood travels from the lungs through the pulmonary veins and into the left side of the heart, which pumps the blood to the rest of the body (see Function of the Heart). Oxygen-deficient, carbon dioxide-rich blood returns to the right side of the heart through two large veins, the superior vena cava and the inferior vena cava. Then the blood is pumped through the pulmonary artery to the lungs, where it picks up oxygen and releases carbon dioxide.

The function of the respiratory system is to add oxygen to the blood and remove carbon dioxide. The microscopically thin walls of the alveoli allow inhaled oxygen to move quickly and easily from the lungs to the red blood cells in the surrounding capillaries. At the same time, carbon dioxide moves from the blood in the capillaries into the alveoli.

To support the absorption of oxygen and release of carbon dioxide, about 5 to 8 liters (about 1.3 to 2.1 gallons) of air per minute are brought in and out of the lungs, and about three tenths of a liter (about three tenths of a quart) of oxygen is transferred from the alveoli to the blood each minute, even when the person is at rest. At the same time, a similar volume of carbon dioxide moves from the blood to the alveoli and is exhaled. During exercise, it is possible to breathe in and out more than 100 liters (about 26 gallons) of air per minute and extract 3 liters (a little less than 1 gallon) of oxygen from this air per minute. The rate at which oxygen is used by the body is one measure of the rate of energy expended by the body. Breathing in and out is accomplished by respiratory muscles.

Gas Exchange Between Alveolar Spaces and Capillaries

The function of the respiratory system is to move two gases: oxygen and carbon dioxide. Gas exchange takes place in the millions of alveoli in the lungs and the capillaries that envelop them. As shown below, inhaled oxygen moves from the alveoli to the blood in the capillaries, and carbon dioxide moves from the blood in the capillaries to the air in the alveoli.

Transport of Oxygen and Carbon Dioxide in the Blood

The reader understands how oxygen and carbon dioxide are transported to and from the tissues in the blood .

  • States the relationship between the partial pressure of oxygen in the blood and the amount of oxygen physically dissolved in the blood .
  • Describes the chemical combination of oxygen with hemoglobin and the “oxyhemoglobin dissociation curve.”
  • Defines hemoglobin saturation, the oxygen-carrying capacity, and the oxygen content of blood .
  • States the physiologic consequences of the shape of the oxyhemoglobin dissociation curve .
  • Lists the physiologic factors that can influence the oxyhemoglobin dissociation curve, and predicts their effects on oxygen transport by the blood .
  • States the relationship between the partial pressure of carbon dioxide in the blood and the amount of carbon dioxide physically dissolved in the blood .
  • Describes the transport of carbon dioxide as carbamino compounds with blood proteins .
  • Explains how most of the carbon dioxide in the blood is transported as bicarbonate .
  • Describes the carbon dioxide dissociation curve for whole blood .
  • Explains the Bohr and Haldane effects .

Transport of Oxygen and Carbon Dioxide in the Blood: Introduction

The final step in the exchange of gases between the external environment and the tissues is the transport of oxygen and carbon dioxide to and from the lung by the blood. Oxygen is carried both physically dissolved in the blood and chemically combined to hemoglobin. Carbon dioxide is carried physically dissolved in the blood, chemically combined to blood proteins as carbamino compounds, and as bicarbonate.

Transport of Oxygen by the Blood

Oxygen is transported both physically dissolved in blood and chemically combined to the hemoglobin in the erythrocytes. Much more oxygen is normally transported combined with hemoglobin than is physically dissolved in the blood. Without hemoglobin, the cardiovascular system could not supply sufficient oxygen to meet tissue demands.

Physically Dissolved

At a temperature of 37°C, 1 mL of plasma contains 0.00003 mL O 2 /mm Hg . This corresponds to Henry’s law, as discussed in Chapter 6. Whole blood contains a similar amount of dissolved oxygen per milliliter because oxygen dissolves in the fluid of the erythrocytes in about the same amount. Therefore, normal arterial blood with a of approximately 100 mm Hg contains only about 0.003 mL O 2 /mL of blood, or 0.3 mL O 2 /100 mL of blood. (Blood oxygen content is conventionally expressed in milliliters of oxygen per 100 mL of blood, or volumes percent .)

A few simple calculations can demonstrate that the oxygen physically dissolved in the blood is not sufficient to fulfill the body’s oxygen demand (at normal F i o 2 and barometric pressure). The resting oxygen consumption of an adult is approximately 250 to 300 mL O 2 /min. If the tissues were able to remove the entire 0.3 mL O 2 /100 mL of blood flow they receive, the cardiac output would have to be about 83.3 L/min to meet the tissue demand for oxygen at rest:

During strenuous exercise, the oxygen demand can increase as much as 16-fold to 4 L/min or more. Under such conditions, the cardiac output would have to be greater than 1000 L/min if physically dissolved oxygen were to supply all the oxygen required by the tissues. The maximum cardiac outputs attainable by normal adults during strenuous exercise are in the range of 25 L/min. Clearly, the physically dissolved oxygen in the blood cannot meet the metabolic demand for oxygen, even at rest.

Chemically Combined with Hemoglobin

The Structure of Hemoglobin

Hemoglobin is a complex molecule with a molecular weight of about 64,500. The protein portion (globin) has a tetrameric structure consisting of 4 linked polypeptide chains, each of which is attached to a protoporphyrin (heme) group. Each heme group consists of 4 symmetrically arranged pyrroles with a ferrous (Fe 2+ ) iron atom at its center. The iron atom is bound to each of the pyrrole groups and to 1 of the 4 polypeptide chains. A sixth binding site on the ferrous iron atom is freely available to bind with oxygen (or carbon monoxide). Therefore each of the 4 polypeptide chains can bind a molecule of oxygen (or carbon monoxide) to the iron atom in its own heme group, and so the tetrameric hemoglobin molecule can combine chemically with 4 oxygen molecules (or 8 oxygen atoms). Both the globin component and the heme component (with its iron atom in the ferrous state), in their proper spatial orientation to each other, are necessary for the chemical reaction with oxygen to take place—neither heme nor globin alone will combine with oxygen. Each of the tetrameric hemoglobin subunits can combine with oxygen by itself (see Figure 7–4C).

Variations in the amino acid sequences of the 4 globin subunits may have important physiologic consequences. Normal adult hemoglobin (HbA) consists of 2 alpha (α) chains, each of which has 141 amino acids, and 2 beta (β) chains, each of which has 146 amino acids. Fetal hemoglobin (HbF), which consists of 2 α chains and 2 gamma (γ) chains, has a higher affinity for oxygen than does HbA. Synthesis of β chains normally begins about 6 weeks before birth, and HbA usually replaces almost all the HbF by the time an infant is 4 months old. Other, abnormal hemoglobin molecules may be produced by genetic substitution of a single amino acid for the normal one in an α or β chain or (rarely) by alterations in the structure of heme groups. These alterations may produce changes in the affinity of the hemoglobin for oxygen, change the physical properties of hemoglobin, or alter the interaction of hemoglobin and other substances that affect its combination with oxygen, such as 2,3-bisphosphoglycerate (2,3-BPG) (discussed later in this chapter). More than 1000 abnormal variants of normal HbA have been demonstrated in patients. The best known of these, hemoglobin S, is present in sickle cell disease, an autosomal recessive genetic disorder caused by a single point mutation in the β chain. Hemoglobin S tends to polymerize and crystallize in the cytosol of the erythrocyte when it is not combined with oxygen. This polymerization and crystallization decreases the solubility of hemoglobin S within the erythrocyte and changes the shape of the cell from the normal biconcave disk to a crescent or “sickle” shape. A sickled cell is more fragile than a normal cell, causing hemolytic anemia. In addition, the cells have a tendency to stick to one another, which increases blood viscosity and also favors thrombosis or blockage of blood vessels.

Chemical Reaction of Oxygen and Hemoglobin

Hemoglobin rapidly combines reversibly with oxygen. It is the reversibility of the reaction that allows oxygen to be released to the tissues if the reaction did not proceed easily in both directions, hemoglobin would be of little use in delivering oxygen to satisfy metabolic needs. The reaction is very fast, with a half-time of 0.01 of a second or less. Each gram of hemoglobin is capable of combining with about 1.39 mL of oxygen under optimal conditions, but under normal circumstances some hemoglobin exists in forms such as methemoglobin (in which the iron atom is in the ferric state) or is combined with carbon monoxide, in which case the hemoglobin does not bind oxygen. For this reason, the oxygen-carrying capacity of hemoglobin is conventionally considered to be 1.34 mL O 2 /g Hb. That is, each gram of hemoglobin, when fully saturated with oxygen, binds 1.34 mL of oxygen. Therefore, a person with 15 g Hb/100 mL of blood has an oxygen-carrying capacity of 20.1 mL O 2 /100 mL of blood:

Pulmonary Toxicology


Efficient gas exchange depends on adequate respiratory drive, an intact and patent airway, strong muscles of respiration (diaphragm and chest wall), normal alveolar architecture, and adequate pulmonary capillary blood flow. Abnormalities among any of these components can cause respiratory compromise.

Respiratory drive is controlled by peripheral chemoreceptors located in the carotid body, as well as central chemoreceptors located in the brainstem. The peripheral receptors detect hypoxia, whereas the central receptors detect lowered CSF pH due to increases in CO2. Both respond to these signals by increasing the depth and rate of respiration. Toxicants that cause a decrease in these responses to respiratory drive can induce hypoxemia. Central nervous system depressants, such as barbiturates, can cause respiratory depression by blunting the normal physiologic response to stimulation of these chemorecpetors. Opioids interact at multiple receptor sites in the body. The μ-opioid receptors are responsible for most of the clinical effects seen with available opioids, and agents acting at the μ receptors show little or no selectivity between the two subtypes, designated μ1 and μ2. Stimulation of the μ1-opioid receptor causes analgesia and the pleasurable euphoria sought by abusers. Overstimulation at the μ2-opioid receptor is responsible for the respiratory depression seen in opioid overdoses.

Airway compromise can be caused by ingestion of local irritants, such as caustics or dieffenbachia, or airway swelling induced by allergic angioedema seen in anaphylaxis or the angioedema seen with angiotensin-converting enzyme inhibitors. Chest wall rigidity induced by fentanyl, as well as respiratory muscular weakness caused by organophosphates, carbamates, and botulinum toxin, can cause respiratory failure.

Acute lung injury, formerly known as noncardiogenic pulmonary edema, can be caused by a multitude of inhaled or ingested toxicants (see later). This condition causes pulmonary capillary fluid to leak into the alveolar space, disrupting efficient gas exchange and decreasing the normal pulmonary compliance. Late sequelae of acute lung injury can include bronchiolitis obliterans fibrosa, which permanently impairs gas exchange and causes a restrictive defect. Other pulmonary reactions, such as hypersensitivity pneumonitis and certain pneumoconiosis, can induce permanent pulmonary fibrosis with impairment of gas exchange and restrictive lung disease. Aspiration of gastric contents and subsequent pneumonia/pneumonitis can impair efficient gas exchange by inducing a ventilation-perfusion mismatch, in which blood flows to an area of the lung incapable of gas exchange.

Finally, impairment of pulmonary capillary blood flow can cause ventilation-perfusion mismatch, in which ventilated areas cannot perform gas exchange due to inadequate perfusion. This can occur with any drug causing pulmonary embolus (e.g., estrogen, oral contraceptives), as well as inert substances and debris injected intravenously by drug abusers (e.g., talc, vegetable matter, cotton). Septic emboli can occur in this setting from inadvertent injection of microorganisms.

Oxygen Transport via Metal Complexes

An adult at rest consumes the equivalent of 250 ml of pure oxygen per minute. This oxygen is used to provide energy for all the tissues and organs of the body, even when the body is at rest. The body's oxygen needs increase dramatically during exercise or other strenuous activities. The oxygen is carried in the blood from the lungs to the tissues where it is consumed. However, only about 1.5% of the oxygen transported in the blood is dissolved directly in the blood plasma. Transporting the large amount of oxygen required by the body, and allowing it to leave the blood when it reaches the tissues that demand the most oxygen, require a more sophisticated mechanism than simply dissolving the gas in the blood. To meet this challenge, the body is equipped with a finely-tuned transport system that centers on the metal complex heme.

Metal Complexes in the Body

The ability of metal ions to coordinate with (bind) and then release ligands in some processes, and to oxidize and reduce in other processes makes them ideal for use in biological systems. The most common metal used in the body is iron, and it plays a central role in almost all living cells. For example, iron complexes are used in the transport of oxygen in the blood and tissues.

Metal-ion complexes consist of a metal ion that is bonded via "coordinate-covalent bonds" (Figure 1) to a small number of anions or neutral molecules called ligands. For example the ammonia (NH3) ligand used in this experiment is a monodentate ligand i.e., each monodentate ligand in a metal-ion complex possesses a single electron-pair-donor atom and occupies only one site in the coordination sphere of a metal ion. Some ligands have two or more electron-pair-donor atoms that can simultaneously coordinate to a metal ion and occupy two or more coordination sites these ligands are called polydentate ligands. They are also known as chelating agents (from the Greek word meaning "claw"), because they appear to grasp the metal ion between two or more electron-pair-donor atoms. The coordination number for a metal refers to the total number of occupied coordination sites around the central metal ion (i.e., the total number of metal-ligand bonds in the complex).

Figure 1

You have already learned that a covalent bond forms when electrons are shared between atoms. A coordinate-covalent bond (represented by a green arrow in this diagram) forms when both of the shared electrons come from the same atom, called the donor atom (blue).

An anion or molecule containing the donor atom is known as a ligand. The top illustration shows a coordinate-covalent bond between a metal ion (e.g., Fe, shown in red) and a monodentate ligand (a ligand that contains only one electron-pair-donor atom, shown in light blue). The bottom illustration shows a metal ion with coordinate-covalent bonds to a bidentate ligand (a ligand that contains two donor atoms simultaneously coordinated to the metal ion, shown in yellow).

Art Connections

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The Respiratory System - Workings: how the respiratory system functions

The main function of the respiratory system is to provide oxygen for the body's cells and remove the carbon dioxide they produce. Oxygen is the most important energy source for the cells. They need it for cellular respiration: the process by which the simple sugar glucose is oxidized (combined with oxygen) to form the energy-rich compound adenosine triphosphate (ATP). Glucose is produced in cells by the breakdown of more complex carbohydrates, including starch, cellulose, and complex sugars such as sucrose (cane or beet sugar) and fructose (fruit sugar). ATP is the compound used by all cells to carry out their ordinary functions: growth, the production of new cell parts and chemicals, and the movement of compounds through cells and the body as a whole.


The mechanical process by which the body takes in oxygen and then releases carbon dioxide is called breathing or pulmonary ventilation. Inhalation (or inspiration) occurs when air flows into the lungs. Exhalation (or expiration) occurs when air flows out of the lungs. A single breath, called a respiratory cycle, consists of an inhalation followed by an exhalation. Breathing is brought about by the actions of the nervous system and the respiratory muscles.

When Earth was new, its atmosphere was probably composed of hydrogen, methane, and ammonia gases—much like the other planets in our solar system. Over billions of years, the composition of the atmosphere has changed considerably. Scientists theorize that a series of events that began when gases were released by early volcanic activity led to the formation of Earth's current atmosphere.

The air humans breathe in is Earth's atmosphere. The air humans breathe out, however, has a different composition. The following list breaks down the major components of those two types of air and their approximate percentages:

Nitrogen: 78% (inhaled air)/ 78% (exhaled air)

Oxygen: 21% (inhaled air)/ 16% (exhaled air)

Carbon dioxide: 0.04% (inhaled air)/ 4.5% (exhaled air)

Although most of Earth's atmosphere is composed of nitrogen, the human body cannot utilize this gas, so it is simply exhaled. Exhaled air has a decreased amount of oxygen and an increased amount of carbon dioxide. These amounts show how much oxygen is retained within the body for use by the cells and how much carbon dioxide is produced as a by-product of cellular metabolism.

The respiratory muscles are the diaphragm and the intercostal muscles. When the diaphragm (the dome-shaped sheet of muscle beneath the lungs that separates the thoracic chest cavity from the abdominal cavity) contracts, it flattens and moves downward. The intercostal muscles are found between the ribs. When the external intercostal muscles contract, they pull the ribs upward and outward. When the internal intercostal muscles contract, they pull the ribs downward and inward. The actions of all these muscles produce changes in the pressure within the alveoli and the bronchial tree.

All forms of matter—solid, liquid, and gas𠅎xert pressure. In the case of a gas (like air), that pressure is caused by the motion of the gas particles. Gas particles have a tendency to fly away rapidly from each other and fill any container in which they are placed. As they do so, they constantly collide against the walls of that container and each other. The collisions of the gas particles causes gas pressure. In a large container, the gas particles in a certain amount of gas will be far apart and less collisions will occur. As a result, the gas pressure will be low. In a smaller container, the gas particles in that same amount of gas will be closer together and more collisions will occur. This will result in high gas pressure.

Inhalation occurs when motor nerves from the medulla oblongata in the brain carry impulses to the diaphragm and intercostal muscles, stimulating them to contract. When the diaphragm is stimulated to contact, it moves downward. Its dome is flattened and the size of the chest cavity is increased. The external intercostal muscles are also stimulated to contract, and they move the ribs up and outward. This also increases the size of the chest cavity. Since the lungs are attached to the chest (thoracic) walls, as the chest expands, so do the lungs. This action reduces the pressure inside the lungs relative to the pressure of the outside atmospheric air. As a consequence, a partial vacuum is created in the lungs and air rushes in from the outside to fill them. The quantity of fresh air taken in during an inhalation is referred to as tidal air.

The reverse occurs in exhalation. In healthy people, exhalation is mostly a passive process that depends more on the elasticity of the lungs than on muscle contraction. During exhalation, motor nerve stimulation from the brain decreases. The diaphragm relaxes and its dome curves up into the chest cavity, while the external intercostal muscles relax and the ribs move back down and inward. As the chest cavity decreases in size, so do the lungs. The air in the lungs is forced more closely together and its pressure increases. When that pressure rises to a point higher than atmospheric pressure, the air is expelled or forced out of the lungs until the two pressures are equal again.

Under normal circumstances, energy is expended during inhalation, but not during exhalation. However, air can be forcefully expelled, such as during talking, singing, or playing a musical wind instrument. Forced exhalation is an active process that requires muscle contraction. In such a case, the internal intercostal muscles are stimulated to contract, pulling the ribs down and in. This forces more air out of the lungs. The abdominal muscles (rectus abdominis) may also be stimulated to contract, compressing the abdominal organs and pushing the diaphragm upward. This action forces even more air out of the lungs.

A healthy adult at rest breathes in and out—one respiratory cycle�out twelve to sixteen times per minute (children breathe more rapidly, about eighteen to twenty times per minute). Exercise and other factors can change this rate. Total lung capacity is about 12.5 pints (6 liters). Under normal circumstances, an individual inhales and exhales about 1 pint (475 milliliters) of air in each respiratory cycle. Only about three-quarters of this air reaches the alveoli. The rest of the air remains in the respiratory tract. Regardless of the volume of air breathed in and out (called the tidal volume), about 2.5 pints (1200 milliliters) remains in the respiratory passageways and alveoli. This amount of air, called the residual volume, keeps the alveoli inflated and allows gas exchange between the lungs and blood vessels to go on continuously.


Once air has filled the lungs, the oxygen in that air must be transported to all the cells in the body. In return, all cells in the body release carbon dioxide that must be transported back to the lungs to be exhaled. The exchanges of gases in the body is known as respiration. External respiration is the exchange of gases through the thin membranes of the alveoli and those of the blood capillaries surrounding them. Internal respiration is the exchange of gases between the blood capillaries and the tissue cells of the body. Within the body, all gases are exchanged through the process of diffusion.

Diffusion is the movement of molecules from an area of greater concentration (existing in greater numbers) to an area of lesser concentration (existing in lesser numbers). Diffusion takes place because molecules have free energy, meaning they are always in motion. This is the case especially with molecules in a gas, which move quicker than those in a solid or liquid. Oxygen and carbon dioxide, the gases that pass between the alveoli and their capillaries and between the blood and the interstitial fluid (fluid surrounding cells of the body), move by diffusion.

In 1943, French oceanographer Jacques-Yves Cousteau (1910�) and French engineer Emile Gagnan developed the aqualung or scuba gear. This scuba (an acronym for s elf- c ontained u nderwater b reathing a pparatus) system not only benefitted recreational divers, but scientists as well. It has become an indispensable tool in the study of marine biology.

The aqualung allows a diver to swim freely down to about 180 feet (55 meters). Recordsetting dives of over 300 feet (91 meters) have been made with scuba gear. It consists of a canister or canisters of highly compressed air that the diver wears on his or her back. The unit is connected to a demand regulator that automatically supplies air at the same pressure as that of the surrounding water. A mouthpiece attached to the regulator allows the diver to breathe.

EXTERNAL RESPIRATION. After inhalation, the air in the alveoli contains a high concentration of oxygen and a low concentration of carbon dioxide. Conversely, the blood in the pulmonary capillaries surrounding the alveoli (which has come from the body) has a low concentration of oxygen and a high concentration of carbon dioxide. Following the law of diffusion, oxygen molecules in the air in the alveoli flow into the pulmonary capillaries. Carbon dioxide molecules flow in the opposite direction, from the blood in pulmonary capillaries into the air in the alveoli.

After gas exchange occurs in the lungs, the pulmonary capillaries carry the oxygenated (carrying oxygen) blood toward the heart. They merge to form venules, which merge to form larger and larger veins. Finally, the oxygenated blood reaches the left atrium of the heart through the four pulmonary veins. After flowing into the left ventricle, the blood is pumped out to the rest of the body.

Almost all the oxygen that diffuses into the pulmonary capillaries attaches to red blood cells in the blood. The primary element of red blood cells is a protein pigment called hemoglobin. Hemoglobin molecules account for one-third the weight of each red blood cell. At the center of each hemoglobin molecule is a single atom of iron, which gives red blood cells their color. The oxygen molecules bond to the iron atoms to create compounds called oxyhemoglobins. The main function of red blood cells is to transport this form of oxygen to the cells throughout the body.

INTERNAL RESPIRATION. Internal respiration occurs between the cells in the body and the systemic capillaries (capillaries in the body outside of the lungs). The bond between the oxygen molecules and the iron atoms of hemoglobin is not a very strong or stable one. When red blood cells enter tissues in the body where the concentration of oxygen is low, the bond is readily broken and the oxygen molecules are released.

Fish and most other aquatic animals use gills for respiration. In fish, these external respiratory organs are located in gill chambers at the rear of the mouth. Gills are specialized tissues with many infoldings. Each gill is covered by a thin layer of cells and filled with blood capillaries.

Water taken in through a fish's mouth is forced through openings called gill slits. It then washes over the delicate gills. The exchange of gases—oxygen and carbon dioxide—occurs through diffusion, much like in human lungs. Oxygen that is dissolved in the water diffuses through the thin membranes of the gills and passes into the capillaries. Carbon dioxide, produced as a waste product by the fish's cells, diffuses from the capillaries through the gills into the passing water.

All higher vertebrates or animals that have a backbone or spinal column (including humans) have immature gill slits when they are in an embryo stage or initially developing. However, these gill slits never fully mature and become functional. They disappear as the vertebrate embryo develops.

This occurs when the systemic capillaries pass among the body cells. The blood in the systemic capillaries has a high concentration of oxygen molecules and a low concentration of carbon dioxide molecules. The body cells and the interstitial fluid surrounding them have just the opposite: a low concentration of oxygen molecules and a high concentration of carbon dioxide molecules (because cells use oxygen to create energy, giving off carbon dioxide as the waste product of human metabolism).

Thus, in internal respiration, oxygen diffuses from the capillaries into the interstitial fluid to be taken up by the cells. At the same time, carbon dioxide diffuses from the interstitial fluid into the capillaries. Red blood cells in the now deoxygenated (carrying very little oxygen) blood then transport the carbon dioxide molecules back to the heart through ever larger veins. Finally, the blood returns to the right atrium of the heart via the venae cavae. After flowing into the right ventricle, the deoxygenated blood is pumped through the pulmonary arteries to the lungs, where the cycle of respiration begins once again.

Plants do not ȫreathe" like animals. All animals have some mechanism for removing oxygen from the air and transmitting it into their bloodstreams, while expelling carbon dioxide from their bloodstreams in the process. Plants exchange oxygen and carbon dioxide with Earth's atmosphere, but in a different process.

Plants create energy for their cells through the process known as photosynthesis. Simply put, a plant absorbs sunlight into chlorophyll (green pigment located in plant cells called chloroplasts) and takes in carbon dioxide from the air through stomata (microscopic openings on the underside of its leaves). It also absorbs water from the soil through its roots. Using the energy from sunlight, the plant combines carbon dioxide and water to create the simple sugar glucose (which is later used to form more complex carbohydrates such as starch and cellulose). Oxygen is a by-product of this process.

In the second phase of photosynthesis, called respiration, the plant combines glucose and oxygen with enzymes to create adenosine triphosphate (ATP), a high-energy molecule used by cells of all organisms to store energy. Since plants use less oxygen during respiration than is created during photosynthesis, they expel that oxygen through their stomata. This action occurs mainly at night when photosynthesis cannot take place.


We demonstrate increased levels of intracellular NO in RBC from COVID-19 subjects. This is not due to the presence of hypoxia per se but may afford protection against the hypoxia seen in COVID-19 patients. During health, constitutive NO production in RBCs is largely NOS-dependent, whereas in hypoxic conditions NO production may involve nitrite reduction by deoxyhemoglobin carbonic anydrase and/or eNOS itself [14].

RBC-derived NO causes the vasodilation of small vessels allowing oxygen to be readily released to tissues. In our study, intracellular RBC NO of COVID-19 patients is significantly higher than in healthy controls and this may enable the release of oxygen to tissues resulting in the clinical manifestation of silent hypoxia in these patients. Pronounced arterial hypoxemia without proportional signs of respiratory distress is reported in COVID-19 patients [15,16,17,18]. For example, Tobin and colleagues recently reported three cases of silent hypoxemia with a PaO2 ranging between 36 and 45 mmHg in the absence of increased alveolar ventilation [16].

However, the mechanism(s) underlying this silent hypoxia have not been explored despite the need to understand why some COVID-19 patients are able to continue with their normal daily activities despite often pronounced hypoxia [19].

Many theories have been proposed to account for this silent hypoxia. For example, silent hypoxia may be due to the differential effect of O2 and CO2 on gas exchange which may produce a relative preservation of the lungs’ ability to excrete CO2 despite falling O2 levels. Since the body is better able to detect changes in CO2 than O2, the relatively normal CO2 levels may attenuate any drive to increase the patients breathing rate despite the presence of low oxygen levels and thereby prevent the sensation of shortness of breath.

The mechanism(s) underlying NO generation inside RBC is not well understood. However, acidosis, hypoxemia and tissue hypoxia lead to NO generation by RBC via SNO–protein transfer of NO activity [20, 21]. The efficiency of NO produced by RBC NOS to promote vasodilation is not well described however perfusion of blood vessel segments with pre-sheared RBC suspensions caused a significant dilation under hypoxic conditions, but not high oxygen, levels [22]. Vasodilation was abolished by pre-incubation of the RBC suspension with the NOS inhibitor L-NAME. These findings support the concept that RBC-derived NO has a functional role in the regulation of local blood flow [22]. Moreover, shear stress induces ATP release from hypoxic RBC as a consequence of their role as O2 sensors [21].

Since NO is a pulmonary vasodilator and also has antiviral activity against coronavirus strains it is likely that exogenous NO treatment may be effective in COVID-19 subjects. There is no evidence that direct oxygen therapy is beneficial in the management of breathlessness in severe COVID-19 patients but our data suggests that NO therapy may be beneficial in COVID-19 patients with hypoxia [23].

Autoimmune hemolytic anemia (AIHA) was recently described in COVID-19 patients [24, 25]. AIHA causes platelet cell death and RBCs can also modulate platelet activity directly through either chemical signalling or direct RBC-platelet interactions. In this way RBCs promote platelet aggregation and degranulation by releasing ATP and ADP under low pO2, low pH and in response to mechanical deformation [26, 27]. In addition, the release of extracellular hemoglobin can also cause platelet activation by lowering NO bioavailability [28]. Thus, our current finding and evidence for hemolysis in patients may account for the microvascular coagulation seen in COVID-19 patients. We were unable to explore the mechanism(s) causing the accumulation of intracellular NO in RBC of COVID-19 patients in this study but this will be the focus of future research.

In summary, COVID-19 patients show higher levels of NO inside RBC compared to non-COVID-19 hypoxemic patients. Whether higher levels of intracellular NO inside RBC of COVID-19 infected patients drive the unexpected silent hypoxia phenotype needs to be examined in future clinical studies using NO donors in hypoxemic COVID-19 patients.


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