The role of policy in red blood cell storage and transfusion in children

2017 ◽  
Vol 82 (6) ◽  
pp. 894-896
Author(s):  
Jean L Raphael ◽  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Storage

In vitro evaluation of di(2-ethylhexyl)terephthalate-plasticized polyvinyl chloride blood bags for red blood cell storage in AS-1 and PAGGSM additive solutions

Transfusion ◽  
2018 ◽  
Vol 58 (5) ◽  
pp. 1100-1107 ◽  
Author(s):  
Sharon Graminske ◽  
Kathleen Puca ◽  
Anna Schmidt ◽  
Scott Brooks ◽  
Amanda Boerner ◽  
...  
Keyword(s):  
Blood Cell ◽  
Polyvinyl Chloride ◽  
Red Blood Cell ◽  
In Vitro Evaluation ◽  
Cell Storage

scholarly journals Recent insights into nitrite signaling processes in blood

2017 ◽  
Vol 398 (3) ◽  
pp. 319-329 ◽  
Author(s):  
Christine C. Helms ◽  
Xiaohua Liu ◽  
Daniel B. Kim-Shapiro
Keyword(s):  
Nitric Oxide ◽  
Human Physiology ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Nitrite Reduction ◽  
No Production ◽  
The Past ◽  
Acidic Conditions ◽  
Hypoxic Vasodilation

Abstract Nitrite was once thought to be inert in human physiology. However, research over the past few decades has established a link between nitrite and the production of nitric oxide (NO) that is potentiated under hypoxic and acidic conditions. Under this new role nitrite acts as a storage pool for bioavailable NO. The NO so produced is likely to play important roles in decreasing platelet activation, contributing to hypoxic vasodilation and minimizing blood-cell adhesion to endothelial cells. Researchers have proposed multiple mechanisms for nitrite reduction in the blood. However, NO production in blood must somehow overcome rapid scavenging by hemoglobin in order to be effective. Here we review the role of red blood cell hemoglobin in the reduction of nitrite and present recent research into mechanisms that may allow nitric oxide and other reactive nitrogen signaling species to escape the red blood cell.

Blood viscosity during the neonatal period: The role of plasma and red blood cell type

1982 ◽  
Vol 100 (3) ◽  
pp. 449-453 ◽  
Author(s):  
Lise Riopel ◽  
Jean-Claude Fouron ◽  
Harry Bard
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Blood Viscosity ◽  
Neonatal Period ◽  
Cell Type ◽  
Blood Cell Type

scholarly journals A Comparison of CO2 Excretion IA Spontaneously Ventilating Blood Perfused Trout Preparation and Salineperfused Gill Preparations: Contribution of the Branchial Epithelium and Red Blood Cell

1982 ◽  
Vol 101 (1) ◽  
pp. 47-60 ◽  
Author(s):  
STEVE F. PERRY ◽  
PETER S. DAVIE ◽  
DAVID J. RANDALL
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Coho Salmon ◽  
Disulfonic Acid ◽  
Gill Epithelium ◽  
Rate Limiting Step ◽  
Branchial Epithelium ◽  
Epithelium Cells ◽  
Co2 Excretion

A spontaneously ventilating blood-perfused trout preparation and saline perfused gill preparations were utilized to investigate the role of the erythrocyte and branchial epithelium in CO2 excretion and acid-base regulation. CO, excretion (MCOCO2) in blood-perfused preparations was positively correlated with haematocrit (Hct), and was abolished completely during plasma-perfusion. Elevating HCO3- concentration of input blood from 10 to 25 mM significantly increased MCOCO2. fourfold in blood-perfused preparations as a result of increased entry of HCO into the red blood cell and not into the gill epithelium. Increased HCO3- concentration was without effect in totally saline-perfused coho salmon (Onchorynchus kisutch). The addition of 4-acetamido-4′-wo-thiocyanatostilbene-2, 2 disulfonic acid (SITS; 10−4 M) to input blood significantly reduced MCO, and oxygen uptake (Mg,OO2) in blood-perfused fish due to inhibition of erythrocytic HCO3-exchange. Unlike blood-perfused preparations, no saline-perfused preparation (isolated holobranchs or totally perfused rainbow trout or coho salmon) displayed measureable CO, excretion at physiological Pco and pH. Increased input PCOt in both blood-perfused and saline-perfused preparations significantly increased MCOt due to enhanced branchial diffusion of molecular CO2. It is concluded that the entry of HCO3- into the erythrocyte is the rate-limiting step in CO, excretion and that movement of HCO3- from plasma to gill epithelium cells in no way contributes to overall CO3 elimination. Note: Department of Physiology and Anatomy, Massey University Palmerston North, New Zealand. Pacific Gamefish Foundation, P.O. Box 25115, Honolulu, Hawaii, U.S.A. 96825

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