Information

What is the oxygen carrying capacity of reticulocytes?

What is the oxygen carrying capacity of reticulocytes?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

What is the oxygen carrying capacity of immature red blood cells, or reticulocytes? Is there any difference between oxygen carrying capacity of mature and immature red blood cells?


This was studied by Steve Fishbone et al and concluded that the Hb content of a Reticulocyte is slightly higher than that of a mature RBC. The CHr, which is the Hb content of a reticulocyte in CRF patients receiving Erythropoetin is around 27.5 +/- 2.5 pg

Ref: Fishbone S, et al. Reticulocyte Hemoglobin Content in the Evaluation of Iron Status of Hemodialysis Patients. Kid. Int., 1997; 52: 217-222


Novel red cell indices indicating reduced availability of iron are associated with high erythropoietin concentration and low ph level in the venous cord blood of newborns

There is evidence that an elevated erythropoietin (EPO) concentration is associated with signs of iron deficient erythropoiesis. The aim of this study was to evaluate the iron status by means of novel cellular indices and serum iron markers and to determine whether these are associated with EPO and pH in the venous cord blood of 193 full-term newborns. There were positive correlations between EPO and the percentage of hypochromic red blood cells (%HYPOm) and reticulocytes (%HYPOr) [r = 0.45 (p < 0.001) and r = 0.56 (p < 0.001), respectively]. %HYPOm and %HYPOr also had negative correlations with pH [r = -0.53 (p = 0.001) and r = -0.46 (p = 0.001), respectively]. Newborns who had low pH (pH < or =7.15, n = 16) had significantly higher %HYPOm, %HYPOr, and serum transferrin receptor and transferrin concentrations in their cord blood than newborns with normal pH. Thus, in newborn cord blood, the higher number of red cells and reticulocytes with lower Hb content may have impaired the oxygen carrying capacity that has been a trigger for EPO production. Furthermore, signs of lower hemoglobinization of red cells are associated with low umbilical vein pH in the newborns, indicating an increased risk of birth asphyxia.


A carrying capacity is defined as a constant that explains how a population grows within a certain area.

How to calculate a carrying capacity?

    First, determine the rate of population increase.

Calculate the rate of population increase.

Calculate the total population size.

Calculate the total change in size.

Calculate the carrying capacity using the formula above.

A carrying capacity is a constant used in ecology when using the logistic population growth equation.


Ecology and Evolution of Blood Oxygen-Carrying Capacity in Birds

Blood oxygen-carrying capacity is one of the important determinants of the amount of oxygen supplied to the tissue per unit time and plays a key role in oxidative metabolism. In wild vertebrates, blood oxygen-carrying capacity is most commonly measured with the total blood hemoglobin concentration (Hb) and hematocrit (Hct), which is the volume percentage of red blood cells in blood. Here, I used published estimates of avian Hb and Hct (nearly 1,000 estimates from 300 species) to examine macroevolutionary patterns in the oxygen-carrying capacity of blood in birds. Phylogenetically informed comparative analysis indicated that blood oxygen-carrying capacity was primarily determined by species distribution (latitude and elevation) and morphological constraints (body mass). I found little support for the effect of life-history components on blood oxygen-carrying capacity except for a positive association of Hct with clutch size. Hb was also positively associated with diving behavior, but I found no effect of migratoriness on either Hb or Hct. Fluctuating selection was identified as the major force shaping the evolution of blood oxygen-carrying capacity. The results offer novel insights into the evolution of Hb and Hct in birds, and they provide a general, phylogenetically robust support for some long-standing hypotheses in avian ecophysiology.


Ecological Footprint, Concept of

Glossary

Usually defined as the average maximum number of individuals of a given species that can occupy a particular habitat without permanently impairing the productive capacity of that habitat.

The displacement of one species from its habitat or ecological niche by another. When humans appropriate other species’ ecological space, it often leads to the local or even the global extinction of the nonhuman organism.

An ecological deficit exists when the load imposed by a given human population on its own territory or habitat (e.g., region, country) exceeds the productive capacity of that habitat. Under these circumstances, if it wishes to avoid permanent damage to its local ecosystems, the population must use some biophysical goods and services imported from elsewhere (or, alternatively, lower its material standards).

The total human load imposed on the environment by a specified population is the product of population size times average per capita resource consumption and waste production. The concept of load recognizes that human carrying capacity is a function not only of population size but also of aggregate material and energy throughput. Thus, the human carrying capacity of a defined habitat is its maximum sustainability supportable load.

A population is in overshoot when it exceeds available carrying capacity. A population in overshoot may permanently impair the long-term productive potential of its habitat, reducing future carrying capacity. It may survive temporarily but will eventually crash as it depletes vital natural capital (resource) stocks.

The measurable habitat and ecosystem modification caused by large animals, including humans, as they forage for food or other resources. Patch disturbance is most pronounced near the den site, temporary camp, or other central place within the overall home range of the individual or group.

The global ecological deficit – that is, the difference between any excessive human load on the ecosphere and the long-term carrying (or load-bearing) capacity of the planet.


Oxygen Carrying Capacity Of Blood At Its Peak

If you have ever felt out of breath or fatigued, it’s most likely because not enough oxygen is being supplied to your cells. Our bodies work tirelessly to keep a sufficient supply of oxygen to our tissues crucial components of this oxygen transport system are red blood cells. Equipped with hemoglobin, a specialized iron/protein hybrid, red blood cells can pick up oxygen in the lungs and release it in the body tissues. This system is pushed to its limit in high altitude oxygen poor environments. To learn how humans adapt to these challenging conditions, Lauren Earthman and 20 other volunteers set out for the Bolivian Andes as part of the AltitudeOmics study.

The group was taken the ski resort atop Mount Chacaltaya, 5260 meters above sea level. Lauren – being a comparative 1500m runner – felt prepared for the challenging conditions the mountain posed but was in for a terrible surprise. Once leaving the comfort of the oxygen equipped bus even the simplest tasks like climbing a flight of stairs proved harrowing.

From her experiences of the first day on the mountain, Lauren would have never guessed she would be able to complete a 3.2 kilometer up hill run at this altitude a few weeks later.

So what allows humans to adapt to these oxygen poor environments?

At 5290 meters above sea level the amount of oxygen in the atmosphere is only 53% of that at sea level making breathing difficult – let alone exercise!

The body can produce more red blood cells in response to low oxygen levels increasing oxygen transport to muscles and vital organs. It has long been thought this has allowed humans can adapt to, and live in such extreme conditions.

But something in this traditional explanation doesn’t add up.

It can take weeks to make new red blood cells yet the group involved in the AltitudeOmics study saw improvements to their fitness within days. The study published this month in the Journal of Proteome Research found red blood cells begin a radical transformation after just a day at high altitude. Chemical changes within red blood cells mean that, while they are able to pick up slightly less oxygen in the lungs, they can dump much more oxygen in the tissues. This allows red blood cells to supply the body with a similar amount of oxygen as it would normally at sea level.

This transformation is both rapid and long lasting, persisting for the life of the red blood cell. As the average life expectancy for a red blood cell is 120 days, people can remain acclimatized to low oxygen levels for months, even after returning to low altitudes.

Understanding the mechanisms that allow the human body to cope in oxygen-poor environments has wide reaching applications from medicine to space travel.

In instances where the oxygen transport system is compromised by trauma causing blood loss, or when crippled by the effects of diseases, including cancer, heart disease, stroke and anaemia, there can be dire, even fatal consequences. This study gives insights into improving oxygen transport efficiency and so may save lives.

For astronauts understanding how people can survive long periods of time with little oxygen may lay the ground work for trips beyond our mountain peaks, to distant planets.


What is the oxygen carrying capacity of reticulocytes? - Biology

Reticulocytes are newly produced, relatively immature red blood cells (RBCs). A reticulocyte count helps to determine the number and/or percentage of reticulocytes in the blood and is a reflection of recent bone marrow function or activity.

Red blood cells are produced in the bone marrow, where blood-forming (hematopoietic) stem cells differentiate and develop, eventually forming reticulocytes and finally becoming mature RBCs. Reticulocytes are visually, slightly larger than mature RBCs. Unlike most other cells in the body, mature RBCs have no nucleus, but reticulocytes still have some remnant genetic material (RNA). As reticulocytes mature, they lose the last residual RNA and most are fully developed within one day of being released from the bone marrow into the blood. The reticulocyte count or percentage is a good indicator of the ability of a person's bone marrow to adequately produce red blood cells (erythropoiesis).

RBCs typically survive for about 120 days in circulation, and the bone marrow is continually producing new RBCs to replace those that age and degrade or are lost through bleeding. Normally, a stable number of RBCs is maintained in the blood through continual replacement of degraded or lost RBCs.

A variety of diseases and conditions can affect the production of new RBCs and/or their survival, in addition to those conditions that may result in significant bleeding. These conditions may lead to a rise or drop in the number of RBCs and may affect the reticulocyte count.

Higher than normal percentage of reticulocytes: Acute or chronic bleeding (hemorrhage) or increased RBC destruction (hemolysis) can lead to fewer RBCs in the blood, resulting in anemia. The body compensates for this loss or to treatment of deficiency anemias (such as iron deficiency anemia or pernicious anemia) by increasing the rate of RBC production and by releasing RBCs sooner into the blood, before they become more mature. When this happens, the number and percentage of reticulocytes in the blood increases until a sufficient number of RBCs replaces those that were lost or until the production capacity of the bone marrow is reached.

Lower than normal percentage of reticulocytes: Decreased RBC production may occur when the bone marrow is not functioning normally. This can result from a bone marrow disorder such as aplastic anemia. Diminished production can also be due to other factors, for example, cirrhosis of the liver, kidney disease, radiation or chemotherapy treatments for cancer, a low level of the hormone erythropoietin, or deficiencies in certain nutrients such as iron, vitamin B12 or folate. Decreased production leads to fewer RBCs in circulation, decreased hemoglobin and oxygen-carrying capacity, a lower hematocrit, and a reduced number of reticulocytes as old RBCs are removed from the blood but not fully replaced.

Occasionally, both the reticulocyte count and the RBC count will be increased because of excess RBC production by the bone marrow. This may be due to an increased production of erythropoietin, disorders that cause chronic overproduction of RBCs (polycythemia vera), and cigarette smoking.


What is the oxygen carrying capacity of reticulocytes? - Biology

People with sickle cell anemia, since many die before they reach reprodctive age or are physically debilitated as adults. People with sickle cell anemia are not sterile and some do have offspring, but the percentage is much lower than people with sickle cell disease.

Dd Localization of the Genetic Defect

If sickle cell anemia is indeed a genetically-determined disease, then in which component of the red blood cell does the defect lie? There are three major components of the red blood cell that could be site of the defect: the cell membrane, the cell's internal scaffolding or cytoskeleton (composed mostly of the protein actin and tubulin), and the hemoglobin molecules that are packed inside (red blood cells do not have most of the other complex internal organelles, including a nucleus, characteristics of other cells, hence among other things, red blood cells do not reproduce).

In-Text Question 4: In general, what sort of experimental design would you have to devise in order to determine which component of the cell -- membrane, cyto-skeletal protein, or hemoglobin -- might be the defective element in sickle cell anemia?

Two simple experiments are able to rule out the membrane and the cytoskeleton as the locus of sickling.

Red blood cell "ghosts" (cells that have been broken open by physical means -- usually by placing the cells in a hyposmotic medium such as distilled water) can be prepared in such a way that they retain their basic bi-concave shape, even though their hemoglobin contents have been spilled out into the surrounding medium. In 1927 E. Vernon Hahn and Elizabeth Gillespie, a surgeon and intern, respectively, at the University of Indiana Medical School in Indianapolis, used "ghosts" to make an important prediction. They reasoned that: IF . . . sickling is due to defects in the red blood cell membrane, and IF . . . "ghosts" from sickle cell anemic patients were subjected to lowered oxygen tension (pressure) THEN . . . "ghost cells" ought to show the same sickling phenomenon found in whole cells.

Performing this simple experiment Hahn and Gillespie found that "ghosts" did not sickle, even when the oxygen tension was reduced to zero. They were thus able to reject the membrane hypothesis. This left either the cytoskeleton or the hemoglobin molecule as the likely cause of the sickling phenomenon.

Another experiment, carried out much later, eliminated the cytoskeleton as the source of the sickling process. The proteins actin and tubulin, the most common proteins that make up the cytoskeleton, are composed of many subunits, joined together much as is a builder's scaffolding, where many similar pieces are joined together to produce a lattice-like support. Now, it is possible to produce red blood cells that lack cytoskeleton, and then to subject them to low oxygen concentrations. When this is done on cells from people with sickle cell anemia, it is found that sickling occurs just as it does in normal red blood cells. The cytoskeleton can also be ruled out as the source of the sickling defect. This leaves hemoglobin as the most likely culprit. What, then, is the nature of that defect? The answer to this question is the subject of Web Page II.

Further evidence corroborating the idea that sickle cell disease might be caused by defective hemoglobin molecules was supplied by the discovery, as early as 1925, of Thalassemia, or Cooley's Anemia, that was also thought to be due to defective hemoglobin. Not quite as debilitating as sickle cell, Thalassemia was known to be more prevalent in the Middle East and Africa then elsewhere, and like all anemias, produced unusual fatigue and other side effects in its victims.

A QUESTION OF CERTAINTY

British philosopher of science Karl Popper emphasized some forty years ago that from a logical point of view it is more certain to reject an hypothesis than to confirm one. By this he meant that while adding one more piece of evidence in favor of an hypothesis provides support for the hypothesis, it does not establish the hypothesis with logical certainty. For example, consider the hypothesis that "All green apples are sour." Tasting 10, 100 or 1,000 green apples and finding them all to be sour confirms the hypothesis, but since it is impossible to taste every green apple in existence now or in the future, we can never be sure that all green apples are sour. However, if one green apple turns out to be sweet, then that negative result allows us to reject the hypothesis with certainty . That is, it is logically impossible for all green apples to be sour if just one turns out to be sweet. Thus, only a negative result leads only to certainty in rejecting an hypothesis, while a positive result leads to an uncertain (but not logically wrong) confirmation. In the case of Hahn and Gillespie's work, for example, by obtaining a negative conclusion from their prediction, they could reject with certainty the hypothesis that sickling was due to a membrane-based defect.

In real life, of course, there are ways around Popper's certainty argument. Scientists do not always give up a cherished hypothesis even in the face of negative evidence. For example, proponents of the membrane-based defect in sickle cell anemia could argue that the process of disrupting the cell by experimental means altered the membrane structure so that it no longer responded to low oxygen tension. Such a response would not be illogical or unjustified, but it would take further experimental work to establish that rupturing the cell did not significantly alter membrane structure and thus change the conditions under which sickling would take place. This is biology's version of the uncertainty principle (from physics) in which the act of maniupulating the system alters the very conditions that are being investigated.

E. A Little Philosophy

The slowly evolving picture of sickle cell anemia and its cause represents a process called consilience by nineteenth-century philosopher of science William Whewell (1794-1866) in his monumental work, The Philosophy of the Inductive Sciences (1840). By consilience Whewell meant the coming together of two or more lines of evidence leading to the same conclusions, or theoretical interpretation. For example, Newtonian physics was a classic example of consilience, since it brought together under one explanation (the inverse-square law of gravitation) observations on the motion of the planets, the moon, falling bodies on the earth's surface, and the tides. In the later nineteenth century Darwin's theory of evolution by natural selection would also turn out to be a good example of consilience. Darwin's explanatory principle (descent by modification through the mechanism of natural selection) brought together observations from comparative anatomy, paleontology, biogeography, embryology and animal and plant breeding). The power of consilience lies in the fact that since each line of evidence is independently derived, the fact that they can be brought together under a single explanatory scheme gives weight and probability to the whole scheme.

  1. Pedigree analysis shows that sickle cell anemia runs in families and can be interpreted as inherited in a simple Mendelian fashion
  2. Microscopic observation of the blood of people with sickle cell trait shows that their cells sickle, too, but only when oxygen or general air pressure reaches a very low level
  3. Biochemical studies showed that the hemoglobin molecules of people with sickle cell disease differed from normal hemoglobin molecules

By themselves, none of these lines of evidence would have been as convincing as they were when considered together.

Recently, it has been discovered that several individuals who have been diagnosed as homozygous recessive for sickle cell hemoglobin (Hb s /Hb s ) do not show any noticeable effects of sickle cell anemia. In examining these patients it was found that they continue to produce fetal hemoglobin, a form of the protein that is normally synthesized during fetal development, but which is turned off within a few months after birth. Fetal hemoglobin is similar to adult hemoglobin, though it has a greater affinity for oxygen than adult hemoglobin, and is coded by a different gene. The hemoglobin F gene (Hb F) does not carry the mutation found in the sickle cell gene. Although the individuals examined still had sickle cell hemoglobin circulating in their blood, the presence of fetal hemoglobin meant that the oxygen tension of the blood remains high, so the red blood cells do not sickle. What this finding illustrates, in addition to a possible therapeutic potential (see Web Page IV of this website, Part B), is that genetic effects are influenced by the individual organism's own genetic background (the other genes it possesses) as well as by environmental input. It is extremely important to recognize that simply having a gene does not necessarily indicate what the pehnotype will be. Today with a great deal of hype in the press about genes determining all sorts of physical as well as mental and emotional illnesses, it is wise to keep in mind that there is no one-to-one correlation between genotype and phenotype.


What is the oxygen carrying capacity of reticulocytes? - Biology

To help evaluate the bone marrow's ability to produce red blood cells (RBCs) and to help distinguish between anaemia related to blood loss or destruction and anaemia related to decreased RBC production to help monitor bone marrow response and the return of normal marrow function following chemotherapy, bone marrow transplant, or post-treatment follow-up for iron deficiency anaemia

When you have a decreased (or increased) RBC count, haemoglobin, haematocrit or platelet count and your doctor wants to evaluate bone marrow activity

A blood sample obtained by inserting a needle into a vein in the arm or sometimes from pricking a finger or the heel in the case of infants.

Test samples are collected into sample tubes containing EDTA preservatives.

No test preparation is needed. Blood sample can be collected at any time of the day, before or after a meal.

On average it takes 7 working days for the blood test results to come back from the hospital, depending on the exact tests requested. Some specialist test results may take longer, if samples have to be sent to a reference (specialist) laboratory. The X-ray & scan results may take longer. If you are registered to use the online services of your local practice, you may be able to access your results online. Your GP practice will be able to provide specific details.

If the doctor wants to see you about the result(s), you will be offered an appointment. If you are concerned about your test results, you will need to arrange an appointment with your doctor so that all relevant information including age, ethnicity, health history, signs and symptoms, laboratory and other procedures (radiology, endoscopy, etc.), can be considered.

Lab Tests Online-UK is an educational website designed to provide patients and carers with information on laboratory tests used in medical care. We are not a laboratory and are unable to comment on an individual's health and treatment.

Reference ranges are dependent on many factors, including patient age, sex, sample population, and test method, and numeric test results can have different meanings in different laboratories.

For these reasons, you will not find reference ranges for the majority of tests described on this web site. The lab report containing your test results should include the relevant reference range for your test(s). Please consult your doctor or the laboratory that performed the test(s) to obtain the reference range if you do not have the lab report.

For more information on reference ranges, please read Reference Ranges and What They Mean.

Reticulocytes are immature red blood cells (RBCs). They are produced in the bone marrow when stem cells differentiate and progress toward RBC development, eventually forming reticulocytes and finally mature RBCs. Most RBCs are fully mature before they are released from the bone marrow into the blood, but about 0.5 – 2% of the RBCs in circulation will be reticulocytes. This test measures the number and percentage of reticulocytes in the blood and serves as an indicator of the adequacy of bone marrow red blood cell (RBC) production.

Normal RBCs have a lifespan of about 120 days. The body attempts to maintain a stable number of RBCs in circulation by continually removing old RBCs and producing new ones in the bone marrow. If this steady state is disrupted by an increased loss of RBCs or by decreased production, then anaemia will develop. Increased loss of red blood cells may be due to severe and short term (acute) or chronic bleeding haemorrhage) or haemolysis. The body compensates for this loss by increasing the rate of RBC production. When this happens, the number and percentage of reticulocytes in the blood increases until a sufficient number of RBCs is present and the balance is restored or until the production capacity of the marrow is reached.

Decreased RBC production may occur when the bone marrow is not functioning normally, due to a bone marrow disorder such as aplastic anaemia or due to marrow suppression from a variety of causes including radiation and chemotherapy treatments for cancer, because of insufficient erythropoietin, or because of deficiencies in certain nutrients such as iron, vitamin B12, or folate. This decreased production leads to fewer RBCs in circulation, decreased haemoglobin and oxygen-carrying capacity, a lower haematocrit, and to a reduction in the number of reticulocytes as old RBCs are removed from the bloodstream, but not fully replaced.

Occasionally, both the reticulocyte count and the RBC count will be increased because of excess RBC production. This may be due to a variety of causes including inappropriately increased production of erythropoietin, disorders that chronically produce increased numbers of RBCs (polycythemia vera), and cigarette smoking.

How is the sample collected for testing?

A blood sample is obtained by inserting a needle into a vein in the arm or sometimes from pricking a finger or the heel of an infant.

Is any test preparation needed to ensure the quality of the sample?

No test preparation is needed. Blood sample can be collected at any time of the day, before or after a meal.

The reticulocyte count is used to help determine if the bone marrow is responding adequately to the body’s need for red blood cells (RBCs) and to help determine the cause of and classify different types of anaemia. The number of reticulocytes must be compared to the number of RBCs to calculate a percentage of reticulocytes and haemoglobin and/or haematocrit are also usually requested to help evaluate the severity of anaemia.

The RBC, haemoglobin, and haematocrit are frequently measured as part of a full blood count (FBC). The FBC usually includes an evaluation of red blood cells (RBCs), White blood cells (WBCs) and Platelets (PLT) characteristics, such as cell size, volume, and shape. Based on these results, a reticulocyte count may be requested to further examine the RBCs. Reticulocytes can be distinguished from mature RBCs because they still contain remnant genetic material (RNA), a characteristic not found in mature RBCs which do not contain genetic material. Circulating reticulocytes generally lose their RNA within one to two days, thus becoming mature RBCs.

A reticulocyte count may be requested when you have a decreased RBC count and/or a decreased haemoglobin and haematocrit and your doctor wants to evaluate bone marrow function. If you have no apparent symptoms, these findings may be found during routine blood testing. Reticulocyte count may also be used when you have symptoms such as paleness, tiredness, weakness, shortness of breath, and/or blood in the stool.

A Reticulocyte count is useful after a recent episode of blood loss or in cases where the lifespan of red cell is shortened as seen in some haemolytic anaemia.

Reticulocyte count may also be used when you have a known iron or vitamin vitamin B12 or folate deficiency, known kidney disease, known bone marrow suppression as may occur during chemotherapy or bone marrow transplant. Reticulocyte count may be requested with a RBC count, haematocrit, and haemoglobin at intervals recommended by your doctor to monitor marrow function and response to treatment.

When you have an increased number of RBCs and elevated haemoglobin and haematocrit, the reticulocyte count may be used to help work out the degree and rate of overproduction of RBCs.

What your doctor is looking for is an appropriate response from the bone marrow, to confirm that your bone marrow is working properly to an increased demand for red blood cells. In a healthy patient, the reticulocyte percentage is stable. When the number of RBCs and haematocrit decreases, the percentage of reticulocytes may appear increased compared to the overall number of RBCs. In order to get a more accurate assessment of bone marrow function, the calculated reticulocyte percentage (%) is often corrected with a calculation called a corrected reticulocyte count or a reticulocyte index (RI). This calculation compares the patient’s haematocrit with a normal haematocrit value. An additional calculation called the reticulocyte production index (RPI) is sometimes calculated to correct for the degree of reticulocyte immaturity – reflecting how quickly the reticulocytes were released from the bone marrow and how long it will take them to mature in the bloodstream. The RPI and maturation time vary with the haematocrit.

Reticulocyte (%) = [Number of Reticulocytes / Number of Red Blood Cells] X 100

Reticulocyte Index = Reticulocyte count (%) X [Measured haematocrit / Normal haematocrit]

Reticulocyte Production Index = (Reticulocyte Index) X (1/maturation time)

Some automated reticulocyte counts may have an immature reticulocyte fraction (IRF) and a mean reticulocyte volume (MRV) reported. They are primarily research parameters at this time. The reticulocyte count is a reflection of recent bone marrow activity. If your bone marrow is responding appropriately to the demand for increased numbers of RBCs, then the bone marrow will allow for the early release of more immature RBCs, increasing the number of reticulocytes in the blood.

An increased reticulocyte percentage may indicate conditions such as:

  • Bleeding: If you bleed ((haemorrhage), then the number of reticulocytes will rise a few days later in an attempt to compensate for the red cell loss. If you have long-term (chronic) blood loss, then the number of reticulocytes will stay at an increased level as the marrow tries to keep up with the demand for new RBCs.

If your marrow is unable to keep up or is not functioning normally, then the number of reticulocytes may be normal or only slightly elevated despite demand but will eventually decrease due to lack of adequate production. If the number of reticulocytes is not elevated when you are anaemic, then it is likely that there is some degree of bone marrow disease or failure and/or a deficiency of erythropoietin. Decreased reticulocyte percentages may be seen, for example, with:

The reticulocyte count gives an indication of what may be happening but cannot diagnose of any one particular disease. Reticulocyte count can show whether further investigations may be necessary and can help monitor the effectiveness of therapy.

If reticulocyte numbers rise following chemotherapy, a bone marrow transplant, or treatment of an iron or vitamin B12 or folate deficiency, then bone marrow RBC production is beginning to recover. In conditions causing RBC overproduction, the number of reticulocytes and RBCs, the concentration of haemoglobin, and percentage of haematocrit will all be increased.

Patients who move to higher altitudes may have increased reticulocyte counts as their body adapts to the lower oxygen content of their new location. Smokers also may demonstrate an increased number of RBCs and reticulocytes.

Reticulocyte counts may be increased during pregnancy. Newborns have a higher percentage of reticulocytes, but the number drops to near adult levels within a few weeks.

Traditionally, reticulocyte counts have been done manually by looking at a specially stained slide under the microscope and counting the number of reticulocytes in a number of fields of view. This method is still in use, but it is in the process of being replaced by automated methods that allow for a greater number of cells to be counted, thus enhancing the accuracy of reticulocyte counts.

Yes. If anaemia is detected during a routine blood test, the doctor may request additional testing (including a reticulocyte count) on the same tube of blood, but it must be done on the same day, before the reticulocytes mature.

Yes. Your doctor will decide how long you should wait after a transfusion before having a reticulocyte count performed.

In some cases, a procedure called a bone marrow aspiration may be performed to obtain a sample of marrow to evaluate under the microscope. Sometimes this is the best way for a doctor to determine how well the bone marrow is functioning.

Most laboratories provide a reticulocyte count result t within 24 hours of sample collection.


MALES

No pre-menstrual syndrome: no mood swings, no irritability, no fatigue, no food craving, and no depression.

FEMALES

Pre-menstrual syndrome: monthly and irregular mood swings, irritability, fatigue, food craving, and depression.

Wanna read more about biological differences in gender?

A meta-analysis of sex differences in human brain structure (Combining 126 studies)
U.S. National Library of Medicine - National Institutes of Health.

Skeletal muscle mass and distribution in 468 men and women aged 18–88 yr - School of Physical and Health Education, Queen’s University, Kingston, Ontario, Canada K7L 3N6 and 2 Obesity Research Center, St. Luke’s/Roosevelt Hospital, Columbia University, College of Physicians and Surgeons, New York, New York 10025


Watch the video: Retic count test in hindi. corrected reticulocyte count formula. Retic count manual formula (May 2022).