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Hematocrit

About: Hematocrit is a research topic. Over the lifetime, 17038 publications have been published within this topic receiving 425666 citations. The topic is also known as: HCT & Ht.


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Journal ArticleDOI
TL;DR: Changes in PV calculated from the increase in plasma protein concentration averaged 7.5(z compared with 12.2 y0 calculated from changes in Hb and Hct, the difference could be accounted for by a loss of 6v10 plasma protein from the circulation.
Abstract: DILL, D. B., AND I>. L. &STILL. Calculation of pcrccntage changes in volumes of blood, plasma, and red cells in dehydration. J. Appl. Physiol. 37(2): 247-248. 1974.-Observations on hematocrit (Hct) and hemoglobin (Hb) were Inade in six men before and after running long enough to cause a 4y0 decrease in body weight. Subscripts B and A were used to denote before dehydration and after dehydration, respectively. Relations were derived between BVn, BVA, Hbn, HbA, Hctg, and HctA with which one can calculate the percentage decreases in BV, CV, and PV, as well as the concentration of hemoglobin in red cells, g. 100 ml-l (MCHC). When subjects reach the same level of dehydration the water loss from the various body compartments may vary reflecting difference in salt losses in sweat. Changes in PV calculated from the increase in plasma protein concentration averaged 7.5(z compared with 12.2 y0 calculated from changes in Hb and Hct. The difference could be accounted for by a loss of 6v10 plasma protein from the circulation.

3,405 citations

Journal ArticleDOI
TL;DR: It is demonstrated that recombinant human erythropoietin is effective, can eliminate the need for transfusions with their risks of immunologic sensitization, infection, and iron overload, and can restore the hematocrit to normal in many patients with the anemia of end-stage renal disease.
Abstract: We administered recombinant human erythropoietin to 25 anemic patients with end-stage renal disease who were undergoing hemodialysis. The recombinant human erythropoietin was given intravenously three times weekly after dialysis, and transfusion requirements, hematocrit, ferrokinetics, and reticulocyte responses were monitored. Over a range of doses between 15 and 500 units per kilogram of body weight, dose-dependent increases in effective erythropoiesis were noted. At 500 units per kilogram, changes in the hematocrit of as much as 10 percentage points were seen within three weeks, and increases in ferrokinetics of three to four times basal values, as measured by erythron transferrin uptake, were observed. Of 18 patients receiving effective doses of recombinant human erythropoietin, 12 who had required transfusions no longer needed them, and in 11 the hematocrit increased to 35 percent or more. Along with the rise in hematocrit, four patients had an increase in blood pressure, and a majority had ...

1,958 citations

Journal ArticleDOI
TL;DR: In patients with clinically evident congestive heart failure or ischemic heart disease who are receiving hemodialysis, administration of epoetin to raise their hematocrit to 42 percent is not recommended.
Abstract: Background In patients with end-stage renal disease, anemia develops as a result of erythropoietin deficiency, and recombinant human erythropoietin (epoetin) is prescribed to correct the anemia partially. We examined the risks and benefits of normalizing the hematocrit in patients with cardiac disease who were undergoing hemodialysis. Methods We studied 1233 patients with clinical evidence of congestive heart failure or ischemic heart disease who were undergoing hemodialysis: 618 patients were assigned to receive increasing doses of epoetin to achieve and maintain a hematocrit of 42 percent, and 615 were assigned to receive doses of epoetin sufficient to maintain a hematocrit of 30 percent throughout the study. The median duration of treatment was 14 months. The primary end point was the length of time to death or a first nonfatal myocardial infarction. Results After 29 months, there were 183 deaths and 19 first nonfatal myocardial infarctions among the patients in the normal-hematocrit group and 150 deat...

1,944 citations

Journal Article
TL;DR: The current knowledge of these three parameters for normal and neoplastic tissues, the methods of their measurements, and the implications of the results in the growth and metastasis formation as well as in the detection and treatment of tumors are reviewed.
Abstract: Blood flow rate in a vascular network is proportional to the pressure difference between the arterial and venous sides and inversely proportional to the viscous and geometric resistances. Despite rapid progress in recent years, there is a paucity of quantitative data on these three determinants of blood flow in tumors and several questions remain unanswered. This paper reviews our current knowledge of these three parameters for normal and neoplastic tissues, the methods of their measurements, and the implications of the results in the growth and metastasis formation as well as in the detection and treatment of tumors. Microvascular pressures in the arterial side are nearly equal in tumor and nontumorous vessels. Pressures in venular vessels, which are numerically dominant in tumors, are significantly lower in a tumor than those in a nontumorous tissue. Decreased intravascular pressure and increased interstitial pressure in tumors are partly responsible for the vessel collapse as well as the flow stasis and reversal in tumors. The apparent viscosity (viscous resistance) of blood is governed by the viscosity of plasma and the number, size, and rigidity of blood cells. Plasma viscosity can be increased by adding certain solutes. The concentration of cells can be increased by adding cells to blood or by reducing plasma volume. The rigidity of RBC, which are numerically dominant in blood, can be increased by lowering pH, elevating temperature, increasing extracellular glucose concentration, or making the suspending medium hypo- or hypertonic. Effective size of blood cells can be increased by forming RBC aggregates (also referred to as rouleaux). RBC aggregation can be facilitated by lowering the shear rate (i.e., decreasing velocity gradients) or by adding macromolecules (e.g., fibrinogen, globulins, dextrans). Since cancer cells and WBC are significantly more rigid than RBC, their presence in a vessel may also increase blood viscosity and may even cause transient stasis. Finally, due to the relatively large diameters of tumor microvessels the Fahraeus effect (i.e., reduction in hematocrit in small vessels) and the Fahraeus-Lindqvist effect (i.e., reduction in blood viscosity in small vessels) may be less pronounced in tumors than in normal tissues. Geometric resistance for a network of vessels is a complex function of the vascular morphology, i.e., the number of vessels of various types, their branching pattern, and their length and diameter. Geometric resistance to flow in a single vessel is proportional to the vessel length and inversely proportional to vessel diameter to the fourth power.(ABSTRACT TRUNCATED AT 400 WORDS)

1,452 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023531
20221,190
2021446
2020489
2019444
2018457