Why tissue damage hinders active transport

This can cause problems in transporting enough of the material for the cell to function properly. When all of the proteins are bound to their ligands, they are saturated and the rate of transport is at its maximum. Increasing the concentration gradient at this point will not result in an increased rate of transport.

Figure 5. Some substances are able to move down their concentration gradient across the plasma membrane with the aid of carrier proteins. Carrier proteins change shape as they move molecules across the membrane. An example of this process occurs in the kidney.

Glucose, water, salts, ions, and amino acids needed by the body are filtered in one part of the kidney.

This filtrate, which includes glucose, is then reabsorbed in another part of the kidney. Because there are only a finite number of carrier proteins for glucose, if more glucose is present than the proteins can handle, the excess is not transported and it is excreted from the body in the urine. Channel and carrier proteins transport material at different rates.

Channel proteins transport much more quickly than do carrier proteins. Channel proteins facilitate diffusion at a rate of tens of millions of molecules per second, whereas carrier proteins work at a rate of a thousand to a million molecules per second. Osmosis is the movement of water through a semipermeable membrane according to the concentration gradient of water across the membrane, which is inversely proportional to the concentration of solutes.

While diffusion transports material across membranes and within cells, osmosis transports only water across a membrane and the membrane limits the diffusion of solutes in the water. Not surprisingly, the aquaporins that facilitate water movement play a large role in osmosis, most prominently in red blood cells and the membranes of kidney tubules.

Figure 6. In osmosis, water always moves from an area of higher water concentration to one of lower concentration. In the diagram shown, the solute cannot pass through the selectively permeable membrane, but the water can. Osmosis is a special case of diffusion. Water, like other substances, moves from an area of high concentration to one of low concentration. An obvious question is what makes water move at all?

Imagine a beaker with a semipermeable membrane separating the two sides or halves Figure 6. On both sides of the membrane the water level is the same, but there are different concentrations of a dissolved substance, or solute , that cannot cross the membrane otherwise the concentrations on each side would be balanced by the solute crossing the membrane. If the volume of the solution on both sides of the membrane is the same, but the concentrations of solute are different, then there are different amounts of water, the solvent, on either side of the membrane.

To illustrate this, imagine two full glasses of water. One has a single teaspoon of sugar in it, whereas the second one contains one-quarter cup of sugar. If the total volume of the solutions in both cups is the same, which cup contains more water?

Because the large amount of sugar in the second cup takes up much more space than the teaspoon of sugar in the first cup, the first cup has more water in it. Returning to the beaker example, recall that it has a mixture of solutes on either side of the membrane. A principle of diffusion is that the molecules move around and will spread evenly throughout the medium if they can.

However, only the material capable of getting through the membrane will diffuse through it. In this example, the solute cannot diffuse through the membrane, but the water can. Water has a concentration gradient in this system. Thus, water will diffuse down its concentration gradient, crossing the membrane to the side where it is less concentrated.

This diffusion of water through the membrane—osmosis—will continue until the concentration gradient of water goes to zero or until the hydrostatic pressure of the water balances the osmotic pressure. Osmosis proceeds constantly in living systems. Tonicity describes how an extracellular solution can change the volume of a cell by affecting osmosis.

Osmolarity describes the total solute concentration of the solution. A solution with low osmolarity has a greater number of water molecules relative to the number of solute particles; a solution with high osmolarity has fewer water molecules with respect to solute particles.

In a situation in which solutions of two different osmolarities are separated by a membrane permeable to water, though not to the solute, water will move from the side of the membrane with lower osmolarity and more water to the side with higher osmolarity and less water.

This effect makes sense if you remember that the solute cannot move across the membrane, and thus the only component in the system that can move—the water—moves along its own concentration gradient. An important distinction that concerns living systems is that osmolarity measures the number of particles which may be molecules in a solution.

Therefore, a solution that is cloudy with cells may have a lower osmolarity than a solution that is clear, if the second solution contains more dissolved molecules than there are cells.

Three terms—hypotonic, isotonic, and hypertonic—are used to relate the osmolarity of a cell to the osmolarity of the extracellular fluid that contains the cells. In a hypotonic situation, the extracellular fluid has lower osmolarity than the fluid inside the cell, and water enters the cell. In living systems, the point of reference is always the cytoplasm, so the prefix hypo — means that the extracellular fluid has a lower concentration of solutes, or a lower osmolarity, than the cell cytoplasm.

It also means that the extracellular fluid has a higher concentration of water in the solution than does the cell. In this situation, water will follow its concentration gradient and enter the cell. Because the cell has a relatively higher concentration of water, water will leave the cell. In an isotonic solution, the extracellular fluid has the same osmolarity as the cell.

If the osmolarity of the cell matches that of the extracellular fluid, there will be no net movement of water into or out of the cell, although water will still move in and out. Blood cells and plant cells Figure 7 in hypertonic, isotonic, and hypotonic solutions take on characteristic appearances. Figure 7. Osmotic pressure changes the shape of red blood cells in hypertonic, isotonic, and hypotonic solutions.

The turgor pressure within a plant cell depends on the tonicity of the solution that it is bathed in. A doctor injects a patient with what the doctor thinks is an isotonic saline solution. The patient dies, and an autopsy reveals that many red blood cells have been destroyed.

Do you think the solution the doctor injected was really isotonic? In a hypotonic environment, water enters a cell, and the cell swells. In an isotonic condition, the relative concentrations of solute and solvent are equal on both sides of the membrane. There is no net water movement; therefore, there is no change in the size of the cell.

In a hypertonic solution, water leaves a cell and the cell shrinks. Remember, the membrane resembles a mosaic, with discrete spaces between the molecules composing it. If the cell swells, and the spaces between the lipids and proteins become too large, the cell will break apart.

In contrast, when excessive amounts of water leave a red blood cell, the cell shrinks, or crenates. This has the effect of concentrating the solutes left in the cell, making the cytosol denser and interfering with diffusion within the cell. Various living things have ways of controlling the effects of osmosis—a mechanism called osmoregulation. Some organisms, such as plants, fungi, bacteria, and some protists, have cell walls that surround the plasma membrane and prevent cell lysis in a hypotonic solution.

The plasma membrane can only expand to the limit of the cell wall, so the cell will not lyse. In fact, the cytoplasm in plants is always slightly hypertonic to the cellular environment, and water will always enter a cell if water is available. This inflow of water produces turgor pressure, which stiffens the cell walls of the plant Figure 7. In nonwoody plants, turgor pressure supports the plant.

Conversly, if the plant is not watered, the extracellular fluid will become hypertonic, causing water to leave the cell. In this condition, the cell does not shrink because the cell wall is not flexible.

However, the cell membrane detaches from the wall and constricts the cytoplasm. This is called plasmolysis. Plants lose turgor pressure in this condition and wilt Figure 8. Figure 8. Without adequate water, the plant on the left has lost turgor pressure, visible in its wilting; the turgor pressure is restored by watering it right. Vicente Selvas. Figure 9. Tonicity is a concern for all living things. For example, paramecia and amoebas, which are protists that lack cell walls, have contractile vacuoles.

This vesicle collects excess water from the cell and pumps it out, keeping the cell from lysing as it takes on water from its environment Figure 9. Intracellular calcium is an important signalling system responsible for activation of phospholipases and proteases, and its derangement results in membrane disruption and remodelling Zuccarelli, As a result, calcium accumulates in the mitochondria, causing structural derangement of the organelles, and may be the hallmark of irreversible cellular injury and, eventually, death Buckman et al, An imbalance between oxygen supply and tissue demands is fundamental to the nature of the insult.

Oxygen supply and demand is maintained in balance as long as supplies of oxygen are available and carbon dioxide is eliminated through ventilation, perfusion, diffusion and cell metabolism. Any alteration of any part of these processes cause impaired gas exchange.

Oxygen supply and demand deficits may relate to pulmonary trauma, causing damage to the chest wall and pulmonary contusions. However, deficits in oxygen supply may exist when the lungs are not directly injured, as any insult may give rise to an increase in demand over supply, due to the neuroendocrine response, leading to cellular hypoxia, production of lactic acid and the lowering of blood pH.

In an acid environment chemoreceptors are stimulated, and consequently this increases respiratory rate in an attempt to eliminate the excess acid.

This can exhaust the patient, leading to increased demands for oxygen. When these processes become overwhelmed, the victim is at risk of pulmonary complications, leading to a supply-demand deficit that gives rise to an oxygen debt. The nurse is responsible for administrating humidified oxygen, the continuous frequent monitoring of respiratory rate, depth and pattern of breathing and any signs of change. There are detailed arterial blood gas tests that can be done to determine acid base balance, but these are not always available in all clinical situations.

The release of mediators effects the microvasculature, organs, and the regional circulation causing vasodilatation, permeability changes, and coagulation. The vasodilatation in certain areas increases blood flow, the movement of fluid from the circulation due to permeability changes, which causes tissue oedema in the area, and contributes to the disruption of the normal circulation Edwards, The coagulation may cause blockage of the vasculature as a result of microvascular thrombi, which causes further tissue damage.

The consequence of selective vasoconstriction and dilatation is a maldistribution of circulating volume and may lead to organ dysfunction Huddleston, The movement of fluid and vasodilatation impede cell movement, function and result in a relative rather than true hypovolaemia Edwards, With the stimulation of the neuroendocrine system there is a substantial increase in metabolic rate, oxygen consumption, and the production of carbon dioxide and heat.

This amplification of energy production is accomplished at the expense of lean body mass. A patient with profound injuries will have hypermetabolism due to stress, and use mixed fuel sources.

Energy requirements are amplified to supply nutrients and oxygen to active tissues and organs involved in the defence against the results of injury. Inflammation, immune function and tissue repair all require an increase in nutritional substrates to support their function Lehmann, All potential sources of glucose are mobilised as sources of fuel.

Amino acids and glycerol are converted into glucose via gluconeogenesis, and glycogen stores are converted via glycogenolysis. The result is a hyperglycaemia. The release of catecholamines causes decreased deposition of fat stores lipogenesis , and increased breakdown of fat lipolysis.

The liver degrades fatty acids for use as fuel, and fat deposits may accumulate in the liver, leading to signs and symptoms of liver failure, including hyperbilirubinaemia, elevated levels of liver enzymes, and hepatic encephalopathy Cheevers, Zinc distributed via the liver becomes deficient, which is associated with impaired wound healing Tan, As protein continues to be broken down and used for energy serum, levels of proteins reduce Chee-vers, Circulating proteins are responsible for maintaining stability of the colloidal oncotic pressure of the vascular bed.

A decreased level of these proteins, such as albumin, result in decreased colloidal oncotic pressure, and hypoalbuminaemia, causing pooling of fluid in the interstitial space, characterised by oedema. Protein loss is accompanied by potassium, magnesium and phosphate loss Tan, The use of all energy sources following an insult causes an exhaustion of energy stores and sources, and deprives cells of nutrients, reducing their function.

There is an increase in cellular metabolism, oxygen consumption, cardiac work and carbon dioxide production. The myocardium becomes depressed, leading to dysfunction.

Clearly protein depletion and starvation contribute to morbidity and mortality following an insult. Therefore it is imperative to initiate feeding regimens early Edwards, The timing and the route of nutritional support can favourably influence the metabolic response to injury. Treatments for conditions such as heart failure, trauma and so on, generally focus on haemodynamic abnormalities, and interventions that maintain circulating volume, administration of oxygen to meet supply and demand, and the prevention of shock.

This type of nursing is demanding and intense. There has recently been a steady increase in research looking at the release of mediators following cell injury, the effects of which can continue for months or years after the initial event Edward, It is now being proposed that it is the cellular, chemical involvement and the complex activation of neurohormones released within minutes of the initial injury that are the true culprits in death and disability associated with certain conditions.

Immediate pharmacological intervention aimed at deterring the onset or progress of cell death could define the future of emergency care Zimmerman et al, There are continued efforts to discover new drugs that could prove essential as our understanding of the epidemiology of disease develops. The interconnections between cellular elements, their secretions, the immune system, and the nervous system are highly regulated and serve to benefit human body functions.

When there is traumatic or hypoxic injury to cells, the interconnections between these systems becomes evident. They act together to choke the tissue, depriving it of control over its micro-circulation and necessary oxygen, rendering membrane potentials useless to maintain organ function.

It is now thought that the progressive worsening of some conditions results from neurohormonal changes, which occur as the body tries to compensate for haemodynamic abnormalities. Therefore, when treating victims with any physiological insult there is a possibility of further injury and even death from events totally unrelated to the initial injury.

There is hope for effective pharmacological intervention at the initial stages, before further injury begins. In contrast to these methods of moving material into a cell is the process of exocytosis. Exocytosis is the opposite of the processes discussed above in that its purpose is to expel material from the cell into the extracellular fluid. A particle enveloped in membrane fuses with the interior of the plasma membrane.

This fusion opens the membranous envelope to the exterior of the cell, and the particle is expelled into the extracellular space Figure 4. The combined gradient that affects an ion includes its concentration gradient and its electrical gradient. Living cells need certain substances in concentrations greater than they exist in the extracellular space. Moving substances up their electrochemical gradients requires energy from the cell.

Active transport uses energy stored in ATP to fuel the transport. Active transport of small molecular-size material uses integral proteins in the cell membrane to move the material—these proteins are analogous to pumps.

Some pumps, which carry out primary active transport, couple directly with ATP to drive their action. In secondary transport, energy from primary transport can be used to move another substance into the cell and up its concentration gradient. Endocytosis methods require the direct use of ATP to fuel the transport of large particles such as macromolecules; parts of cells or whole cells can be engulfed by other cells in a process called phagocytosis.

In phagocytosis, a portion of the membrane invaginates and flows around the particle, eventually pinching off and leaving the particle wholly enclosed by an envelope of plasma membrane. Vacuoles are broken down by the cell, with the particles used as food or dispatched in some other way.

Pinocytosis is a similar process on a smaller scale. The cell expels waste and other particles through the reverse process, exocytosis.

Wastes are moved outside the cell, pushing a membranous vesicle to the plasma membrane, allowing the vesicle to fuse with the membrane and incorporating itself into the membrane structure, releasing its contents to the exterior of the cell.

Skip to main content. Structure and Function of Plasma Membrane. Search for:. Active Transport Learning Objectives By the end of this section, you will be able to: Understand how electrochemical gradients affect ions Describe endocytosis, including phagocytosis, pinocytosis, and receptor-mediated endocytosis Understand the process of exocytosis.

Electrochemical Gradient Figure 1. Additional Self Check Question 1. Where does the cell get energy for active transport processes? Answer 1.