Isolation of autologous RBCs in transfused β-thalassemia patients using hypotonic saline

2016 ◽  
Vol 26 (5) ◽  
pp. 385-386 ◽  
Author(s):  
A. Sheladiya ◽  
K. Mendapara ◽  
S. R. Joshi
Keyword(s):  
Hypotonic Saline

scholarly journals STUDY OF THALASSEMIA MINOR IN THREE GENERATIONS OF AN ITALIAN FAMILY

Blood ◽  
1948 ◽  
Vol 3 (4) ◽  
pp. 449-456
Author(s):  
ROBERT W. HEINLE ◽  
MARGARET RUTH READ
Keyword(s):  
Life Expectancy ◽  
General Health ◽  
Hypochromic Anemia ◽  
Thalassemia Major ◽  
Genetic Studies ◽  
Italian Family ◽  
Three Generations ◽  
Thalassemia Minor ◽  
Hypotonic Saline

Abstract 1. Three generations of a family of Italian descent were studied. Nine of 13 members were found to have thalassemia minor. 2. Genetic studies indicate that this mild, microcytic hypochromic anemia characterized by the presence of target and elliptical cells and other bizarre forms and by increased resistance to hypotonic saline, results from heterozygosity of an inherited factor, which, when homozygous, produces thalassemia major or Cooley’s Mediterranean anemia. 3. If individuals heterozygous for this factor (thalassemia minor) marry other heterozygous individuals, one quarter of the offspring can be expected to be homozygous (thalassemia major), one half heterozygous (thalassemia minor) and one quarter free of the trait. 4. The presence of thalassemia minor apparently did not interfere with the general health of affected members of this family and did not appear to shorten life expectancy. The importance of the condition lies in its relation to thalassemia major.

scholarly journals Observations on the Anemia of Cryptogenetic Splenomegaly. I. Hemolysis

Blood ◽  
1958 ◽  
Vol 13 (6) ◽  
pp. 513-523 ◽  
Author(s):  
A. J. S. MCFADZEAN ◽  
DAVID TODD ◽  
K. C. TSANG
Keyword(s):  
Life Span ◽  
Survival Time ◽  
Liver Damage ◽  
Marked Reduction ◽  
Osmotic Fragility ◽  
Mixed Population ◽  
Red Cells ◽  
Hypotonic Saline

Abstract Excessive hemolysis has been shown to occur in patients with cryptogenetic splenomegaly. This is corrected by splenectomy. The survival of normal red cells transfused to such patients is greatly reduced. Following splenectomy normal red cells so transfused survive normally. The survival of red cells from such patients upon transfusion to healthy recipients, including a splenectomized recipient, is greatly reduced. Following splenectomy the survival of red cells from such patients upon transfusion to healthy recipients is significantly increased, although still significantly less than normal. However, upon transfusion into splenectomized but otherwise healthy recipients the survival time is normal. Study of osmotic fragility before splenectomy demonstrates the existence of a mixed population showing both increased and decreased fragility to hypotonic saline. Following splenectomy there emerges a population with increased resistance to hypotonic saline. It is concluded that prior to splenectomy the pathologic spleen exerts an effect upon circulating erythrocytes including transfused normal red cells which results in marked reduction in their survival. Following splenectomy a second defect in the erythrocytes becomes apparent and this also results in reduction in life-span, although the presence of the spleen would appear necessary for this reduction to occur. It is suggested that this second defect develops as the result of liver damage.

Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion

1979 ◽  
Vol 236 (2) ◽  
pp. H314-H322 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton ◽  
T. G. Coleman ◽  
R. E. McCaa
Keyword(s):  
Arterial Pressure ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Experimental Hypertension ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Hypotonic Saline

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.

EFFECTS OF DEOXYCORTICOSTERONE ACETATE AND CORTISONE ON THE EXCRETION OF HYPOTONIC SALINE BY ADRENALECTOMIZED RATS

1954 ◽  
Vol 11 (3) ◽  
pp. 261-268 ◽  
Author(s):  
D. F. COLE
Keyword(s):  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
The Body ◽  
Renal Tubules ◽  
Water Diuresis ◽  
Deoxycorticosterone Acetate ◽  
Water Excretion ◽  
Normal Water ◽  
Hypotonic Saline ◽  
Adrenalectomized Rats

SUMMARY The response to loads of hypotonic saline has been investigated in intact and in adrenalectomized rats treated with deoxycorticosterone acetate, with cortisone acetate and with both steroids. The response of untreated adrenalectomized animals was also studied. Intact rats excreted more water than sodium during the 5 hr after loading with hypotonic saline. There was a reduction of the proportion of water reabsorbed in the renal tubules, but the proportion of sodium reabsorbed was unaltered. Adrenalectomized rats, either with or without deoxycorticosterone treatment, did not show this diuretic response, and there was evidence that sodium was lost from the body cells. Rats in these two groups reabsorbed a smaller proportion of sodium in their renal tubules than intactrats. Adrenalectomized rats treated with cortisone showed partial restoration of the ability to excrete water, but the renal loss of sodium was greater than in intact animals. Treatment of adrenalectomized rats with both cortisone and deoxycorticosterone restored water excretion to normal values, but excessive amounts of sodium were lost. In neither group which received cortisone was there any indication of loss of cell sodium. The response of rats in the group receiving both steroids was not a normal water diuresis because the animals were unable to excrete water without loss of sodium. It appeared unlikely that there was excessive antidiuretic hormone activity in the rats receiving cortisone and that some factor other than reduction of pituitary antidiuretic hormone secretion was essential for normal water diuresis.

The osmotic fragility of some fish erythrocytes in hypotonic saline

1969 ◽  
Vol 28 (1) ◽  
pp. 409-415 ◽  
Author(s):  
George H. Ezell ◽  
L.L. Sulya ◽  
C.L. Dodgen
Keyword(s):  
Osmotic Fragility ◽  
Hypotonic Saline

scholarly journals RENAL RESPONSE TO HYPOTONIC SALINE LOAD IN FETAL AND NEW-BORN PIGS

1982 ◽  
Vol 67 (1) ◽  
pp. 133-141 ◽  
Author(s):  
J. M. Alt ◽  
B. Colenbrander ◽  
A. A. MacDonald ◽  
M. L. Forsling
Keyword(s):  
Renal Response ◽  
New Born ◽  
Hypotonic Saline

Failure of Oral Water Loading and Intravenous Hypotonic Saline to Suppress Plasma Prolactin in Man

1975 ◽  
Vol 41 (2) ◽  
pp. 383-389 ◽  
Author(s):  
ROBERT A. ADLER ◽  
GORDON L. NOEL ◽  
LEONARD WARTOFSKY ◽  
ANDREW G. FRANTZ
Keyword(s):  
Plasma Prolactin ◽  
Water Loading ◽  
Hypotonic Saline
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