Erythrocyte Survival and Blood Volume in the Rat as Determined by Labeling the Red Cells With Cr<sup>51</sup>

Hall, Charles A.; Nash, Joe B.; Hall, O.

doi:10.1152/ajplegacy.1957.190.2.327

Cited by 12 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The half-time survival of H.B.R.B.C.s (taking the numbers an hour after transfusion as 100%) in intact rats is seen to be approximately one day, whereas in splenectomized rats it is five and a half days. This value approaches that reported for normal red cells in normal rats (Hall, Nash, and Hall, 1957). These authors injected Cr5l-tagged red cells into normal rats, and taking the value found one hour later as 100%, obtained a half-time survival of about eight days.…”

Section: Discussionsupporting

confidence: 75%

The Response to Heinz Bodies in the Rat

Rofe¹

1959

Occupational and Environmental Medicine

View full text Add to dashboard Cite

Irregular refractile granules which occur within red blood cells were first described by Heinz in 1890. The precise nature of these bodies is unknown. The present work was undertaken in order to help to assess the significance of the presence of Heinz bodies in the blood over a considerable period.Heinz bodies have been produced in the red blood cells of intact and splenectomized rats over relatively long periods by continuous feeding of azo geranine. The proportion of Heinzbody red blood cells quickly rose to a peak and then fell to fluctuating lower values; there was a concurrent fall in the red blood cell count and reticulocytosis. There were more Heinz-body red blood cells and a greater fall in the red blood cell count in the splenectomized animals. Large deposits of haemosiderin were present in the livers of the splenectomized animals fed the dye. Little or no haemosiderin was found in the livers of intact animals fed the dye or in those of splenectomized animals not receiving dye. Splenic hyperplasia accompanied the initial increase in Heinz-body red blood cells and remained undiminished after the level had fallen. The halftime survival of Heinz-body red blood cells transfused into normal rats was approximately one day compared with over five days in splenectomized animals. The anaemia associated with the appearance of Heinz bodies was found to be hypochromic: the mean cell haemoglobin concentration fell from 35-7y% before feeding dye to 26-7y% at the time of peak Heinz-body red blood cell concentration after seven days of dye feeding. With the subsequent fall in Heinz-body red blood cell level, approximately half of the deficiency in the mean cell haemoglobin concentration was replaced, despite a substantial recovery in the packed cell volume without an increase in the red cell count. Twenty days after feeding the dye had been stopped, no Heinz-body red blood cells were found, and all values had returned to normal.

show abstract

Section: Discussionsupporting

confidence: 75%

The Response to Heinz Bodies in the Rat

Rofe¹

1959

Occupational and Environmental Medicine

View full text Add to dashboard Cite

show abstract

“…Estimation of Blood Volume. Total circulating blood volume was estimated at the completion of a 10-d experimental period by dilution of "Cr-labeled RBCs according to a modification of previously described methods (25). Heparinized syngeneic donor blood (18 ml) was incubated with 'Cr (2 mCi) for 45 min at 25°C.…”

Section: Methodsmentioning

confidence: 99%

Cachectin/tumor necrosis factor induces cachexia, anemia, and inflammation.

Tracey

Manogue

et al. 1988

The Journal of Experimental Medicine

696

272

View full text Add to dashboard Cite

Severe weight loss and debilitative wasting of lean body mass frequently complicate the treatment of patients suffering from malignancy or chronic infection. Termed cachexia, this syndrome of anorexia, anemia, and weakness further increases cancer mortality; some data indicate that as many as 30% of cancer patients die from cachexia, rather than tumor burden (1-3). The severity of cachexia may be unrelated to tumor size or parasite load, and profound wasting has been observed in patients with tumor burdens of only 0.01-5.0% body mass (4). If not reversed, cachexia-associated derangements of homeostasis lead to immunological deficiencies, organ failure, and multiple metabolic abnormalities . While it is clear that a variety of mechanisms participate in the pathogenesis of cachexia, and that cachexia adversely affects prognosis, the etiology of this syndrome is not known.For a number of years we have been searching for endogenous, humoral mediators of cachexia, beginning with the characterization of metabolic changes in trypanosome-infected rabbits that develop profound cachexia and lose up to 50% of lean body mass within weeks. In later stages of disease a paradoxical increase in circulating triglycerides occurs, attributable to systemic suppression of lipoprotein lipase (LPL)t (5). A bacterial LPS-inducible serum factor which suppresses LPL in mice, and several other key lipogenic enzymes in the adipocyte cell line 3T3-L1, was isolated and named cachectin (6, 7). Cachectin evokes a state of cellular cachexia by suppressing the expression of several mRNAs encoding essential lipogenic enzymes (8, 9). Myocytes also show changes in cellular metabolism after exposure to cachectin in vitro, including a prompt decrease in resting transmembrane potential difference and depletion of intracellular glycogen stores with increased lactate efflux, and a later increase in hexose transporters (10,11). It has been suggested that cachectin may play a

show abstract

“…The slight discrepancy can be explained by the fact that these workers have not corrected their data for changes in blood volume with growth during the course of their experiments. The lower values of 10 days quoted by Donohue et al (1955) and 8 days by Hall, Nash & Hall (1957) may be attributed to the use of low specific activity 5lCr (1-3 ,c/,g Cr) with the consequent incorporation into the labelled blood of amounts of metallic chromium sufficient to cause irreversible damage to the red cells. Giblett et al (1956) observed abnormally shortened survival at chromium concentrations of 20-25 Kg/ml.…”

mentioning

confidence: 92%

“…Intravenously injected 59Fe by contrast is more rapidly incorporated into red cell precursors in the erythropoietic tissues. However, since under normal conditions iron returned to the metabolic pool from destroyed red cells is largely re-utilized for new taemoglobin synthesis (Gibson, Aub, Evans, Peacock, Irvine & Sack, 1947) it is Escober & Baldwin (1934) Creskoff & Fitzhugh (1937) Harne, Lutz & Davis (1938) Ponticorvo, Rittenberg & Bloch (1949) Berlin, Huff & Hennessy (1951Berlin, Meyer & Lazarus (1951 Berlin & Lotz (1951) Fryers & Berlin (1952) Berlin, Van Dyke & Lotz (1953) Burwell, Brickley & Finch (1953) Davis, Alpen & Davis (1955) Van Dyke, Asling, Berlin & Harrison (1955) Donohue, Motulsky, Giblett, Pirzio-Biroli, Viranuvatti & Finch (1955) Giblett, Motulsky, Casserd, Houghton & Finch (1956) Hall, Nash & Hall (1957) The use of 51Cr in red cell survival studies is complicated by the fact that the 51Cr concentration in the blood falls more rapidly than would be expected from red cell destruction alone, a finding usually explained in terms of a slow elution of the isotopic label from the red cells in the circulation. Measurements of the 5lCr content of the blood must therefore be corrected for elution loss if true survival is to be estimated.…”

mentioning

confidence: 99%