|
|
 Previous Article | Table of Contents | Next Article 
Blood, 1970, Vol. 36, No. 5, pp. 566-575.
© 1970 American Society of Hematology, Inc.
Acquisition of Autophagic Vacuoles by Human Erythrocytes
Physiological Role of the Spleen
CHRISTOPHER P. HOLROYDE 1 and
FRANK H. GARDNER 1
1 Hematology Research Laboratory, Presbyterian-University of Pennsylvania
Medical Center and the Department of Medicine, University of Pennsylvania School of
Medicine, Philadelphia. Pa.
Using interference-contrast microscopy,
erythrocyte vacuoles can be rapidly and
easily distinguished. Because of the shadowing effect inherent in this optical
system they appear as surface indentations. Twenty splenectomized patients
with both normal and abnormal erythropoiesis had 54.3 per cent vacuolated cells
as compared to 2.1 per cent in a control
group of normal adults. A splenectomized
patient with pure red cell aplasia, whose
erythrocyte mass was maintained with
fresh normal blood, had 44 per cent
vacuolated cells. Electron microscopy
thin sections showed numerous erythrocyte inclusions and vacuoles which were
morphologically suggestive of hemoglobin degeneration. Similar inclusions were
noted in all splenectomized subjects
studied, and were found in greater numbers in patients with young cell populations. They were rare in normals with
intact spleens. Transfusion studies show
that these inclusions can be acquired by
normal mature erythrocytes when circulating in an asplenic patient. Further,
they are cleared from the circulation in
the presence of an intact spleen without
measurable loss of red cell viability. The
evidence suggests that, in the absence of
a spleen, autophagic vacuoles may occur
in situ in all circulating red cells. It is
presumed that these inclusions would
normally be removed as a physiological
process by a functioning spleen.
Submitted on January 29, 1970
Revised on June 4, 1970
Accepted on June 9, 1970
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
V. L. Lew and R. M. Bookchin
Ion Transport Pathology in the Mechanism of Sickle Cell Dehydration
Physiol Rev,
January 1, 2005;
85(1):
179 - 200.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. N. COLEMAN, I. R. MCDOUGALL, M. O. DAILEY, P. AGER, S. BUSH, and H. S. KAPLAN
Functional Hyposplenia After Splenic Irradiation for Hodgkin's Disease
Ann Intern Med,
January 1, 1982;
96(1):
44 - 47.
[Abstract]
[PDF]
|
|
|
|
|
|
|
B. A. Neilan and J. F. Perry Jr
Persistence of Vacuolated RBCs After Splenectomy in Adults
JAMA,
May 2, 1980;
243(17):
1741 - 1742.
[Abstract]
[PDF]
|
|
|
|
|
|
|
R. H. Sills and F. A. Oski
RBC Surface Pits in the Sickle Hemoglobinopathies
Arch Pediatr Adolesc Med,
May 1, 1979;
133(5):
526 - 527.
[Abstract]
[PDF]
|
|
|
|
|
|
|
R. W. Hilberg, R. D. Ringle, and S. P. Balcerzak
Howell-Jolly Bodies: Intracellular or Extracellular?
Arch Intern Med,
February 1, 1973;
131(2):
236 - 237.
[Abstract]
[PDF]
|
|
|
|
|
