scholarly journals Thrombin Preconditioning Attenuates Brain Edema Induced by Erythrocytes and Iron

2003 ◽  
Vol 23 (12) ◽  
pp. 1448-1454 ◽  
Author(s):  
Ya Hua ◽  
Richard F. Keep ◽  
Julian T. Hoff ◽  
Guohua Xi
Keyword(s):  
Red Blood Cells ◽  
Brain Edema ◽  
Blood Cells ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Dry Weight ◽  
Edema Formation ◽  
Mitogen Activated Protein ◽  
Weight Method ◽  
The Brain

Pretreatment with a low intracerebral dose of thrombin reduces brain edema after hemorrhagic and thromboembolic stroke. We have termed this phenomena thrombin preconditioning (TPC) or thrombin-induced brain tolerance. Red blood cell lysis and iron overload contribute to delayed edema formation after intracerebral hemorrhage. The present study examined whether TPC can attenuate the brain edema induced by lysed red blood cells or iron. It also examined whether TPC is associated with increasing hypoxia inducible factor-1α (HIF-1α) levels and alterations in two HIF-1α target genes, transferrin (Tf) and transferrin receptor (TfR), within the brain. Brain edema was measured by wet/dry weight method. HIF-1α, Tf, and TfR were measured by Western blot analysis and immunohistochemistry. We found that TPC reduces the edema induced by infusion of lysed red blood cells and iron. Thrombin increases HIF-1α levels through p44/42 mitogen activated protein kinases pathway. Thrombin also increases Tf and TfR levels in the brain. These results indicate that HIF-1α and its target genes may be involved in thrombin-induced brain tolerance.

Complement activation in the brain after experimental intracerebral hemorrhage

2000 ◽  
Vol 92 (6) ◽  
pp. 1016-1022 ◽  
Author(s):  
Ya Hua ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
Julian T. Hoff
Keyword(s):  
Brain Edema ◽  
Complement Activation ◽  
Autologous Blood ◽  
Complement Cascade ◽  
Edema Formation ◽  
Content Type ◽  
Erythrocyte Lysis ◽  
The Brain ◽  
Brain Edema Formation ◽  
Fine Print

Object. Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the complement cascade is activated after ICH and whether inhibition of complement attenuates brain edema around the hematoma.Methods. This study was divided into three parts. In the first part, 100 µl of autologous blood was infused into the rats' right basal ganglia, and the animals were killed at 24 and 72 hours after intracerebral infusion. Their brains were tested for complement factors C9, C3d, and clusterin (a naturally occurring complement inhibitor) by using immunohistochemical analysis. In the second part of the study, the rats were killed at 24 or 72 hours after injection of 100 µl of blood. The C9 and clusterin proteins were quantitated using Western blot analysis. In the third part, the rats received either 100 µl of blood or 100 µl of blood plus 10 µg of N-acetylheparin (a complement activation inhibitor). Then they were killed 24 or 72 hours later for measurement of brain water and ion contents. It was demonstrated on Western blot analysis that there had been a sixfold increase in C9 around the hematoma 24 hours after the infusion of 100 µl of autologous blood. Marked perihematomal C9 immunoreactivity was detected at 72 hours. Clusterin also increased after ICH and was expressed in neurons 72 hours later. The addition of N-acetylheparin significantly reduced brain edema formation in the ipsilateral basal ganglia at 24 hours (78.5 ± 0.5% compared with 81.6 ± 0.8% in control animals, p < 0.001) and at 72 hours (80.9 ± 2.2% compared with 83.6 ± 0.9% in control animals, p < 0.05) after ICH.Conclusions. It was found that ICH causes complement activation in the brain. Activation of complement and the formation of membrane attack complex contributes to brain edema formation after ICH. Blocking the complement cascade could be an important step in the therapy for ICH.

scholarly journals Red blood cells release microparticles containing human argonaute 2 and miRNAs to target genes of Plasmodium falciparum

2017 ◽  
Vol 6 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Zhensheng Wang ◽  
Juemin Xi ◽  
Xiao Hao ◽  
Weiwei Deng ◽  
Juan Liu ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Target Genes ◽  
Argonaute 2

Electrolyte changes in blood, urine, and tissues after lipid and other test meals

1963 ◽  
Vol 204 (6) ◽  
pp. 1071-1076 ◽  
Author(s):  
Roy L. Swank ◽  
Lavelle Jackson
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Potassium Excretion ◽  
Cod Liver Oil ◽  
The Brain

Hamsters were fed large (8 g/kg) test meals of cream, cod liver oil, carbohydrate, and protein and the Ca, Na, and K levels in red blood cells, serum, urine, and tissues were determined. 1) Urinary changes consisted of a decrease in Ca and Na 4–7 hr after both cream and cod liver oil meals. These changes were most marked after cream. Potassium excretion also decreased after cod liver oil meals, but increased after cream meals. 2) Seven hours after lipid meals both Ca and K were decreased in red blood cells. At the same time Ca and Na decreased in serum after cod liver oil meals, and the K initially increased after both lipid meals. 3) Cation changes in the heart 7 hr after feeding consisted of a reduction in Ca and Na, and a possible increase in K after cream. These changes did not occur after test meals of water, protein, carbohydrate, or cod liver oil. 4) In the brain, Ca, Na, and K were all decreased 7 hr after cream meals, and increased by all other meals. 5) Significant dehydration of all tissues was present 7 hr after cream meals. This was not observed after any other test meals.

scholarly journals Tissue Albumin and Water Content in the Early Stages of Vasogenic Brain Edema Formation

1979 ◽  
Vol 6 (4) ◽  
pp. 423-426 ◽  
Author(s):  
Michael P. Pash ◽  
W. Arnold Tweed
Keyword(s):  
Brain Edema ◽  
Plasma Volume ◽  
Animal Experiments ◽  
Dry Weight ◽  
Blue Staining ◽  
Tissue Water ◽  
Edema Formation ◽  
Early Stages ◽  
Wet Weight ◽  
Brain Edema Formation

SUMMARY:Brain edema (BE) research lacks quantitative regional methods. We modified the method of Pappius and McCann (1969), who used radioactive iodinated I125 serum albumin (RISA) as a label for vasogenic BE fluid. To correct for intravascular plasma volume we used Cr51 labelled red blood cells and calculated equivalent extravascular plasma volume (EVPV). The modified RISA method was compared with a standard method for measuring increased tissue water, i.e. the change in wef.dry weights. Anesthetized rabbits were subjected to unilateral cortical freeze injury and sacrificed three hours later. The lesion corresponding to the area of blood brain barrier (BBB) breakdown was delineated by Evan's blue staining. That area and the two adjacent poles were sectioned. The contralateral hemisphere was used as the control. Good agreement was found between the two methods. By the modified RISA method, 4.08% of the wet weight of the injured hemisphere was EVPV while the decrease in dry weight corresponded to 5.56% edema. In the freeze lesion, however, where BBB breakdown occurred extravascular (EV)protein exceeded EV water, while adjacent to the lesion in the area with intact BBB, EV water exceeded EV protein. This suggests that the diffusion rate for water through brain tissue exceeds that of albumin in the early stages of vasogenic BE formation. We conclude that the modified RISA method is a satisfactory measure of regional vasogenic BE in acute animal experiments.

scholarly journals Iron is prioritized to red blood cells over the brain in phlebotomized anemic newborn lambs

2016 ◽  
Vol 79 (6) ◽  
pp. 922-928 ◽  
Author(s):  
Tara G Zamora ◽  
Sixto F Guiang ◽  
John A Widness ◽  
Michael K Georgieff
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
The Brain

scholarly journals MAMMALIAN RED CELLS AS A SOURCE OF "SMALL PARTICLES"

1943 ◽  
Vol 77 (4) ◽  
pp. 315-322 ◽  
Author(s):  
Björn Sigurdsson
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Dry Weight ◽  
Red Cells ◽  
Small Particles ◽  
Horse Blood ◽  
Foreign Species

1. Small particles essentially similar to those previously isolated from other tissues have been isolated from mammalian red blood cells (horse blood). 2. About one-third of the dry weight of the particles is lipids. 3. The particles produce hemolysins against the homologous erythrocytes when inoculated into a foreign species. 4. The fact that the particles can be isolated from mammalian red cells which do not contain visible granules is taken to indicate that some at least of the particles isolated from whole organs represent disintegrated "stroma."

scholarly journals Effects on Brain Edema of Crystalloid and Albumin Fluid Resuscitation after Brain Trauma and Hemorrhage in the Rat

2010 ◽  
Vol 112 (5) ◽  
pp. 1194-1203 ◽  
Author(s):  
Mårten Jungner ◽  
Per-Olof Grände ◽  
Gustav Mattiasson ◽  
Peter Bentzer
Keyword(s):  
Water Content ◽  
Brain Edema ◽  
Blood Volume ◽  
Dry Weight ◽  
Brain Trauma ◽  
Intravascular Volume ◽  
Oncotic Pressure ◽  
Fluid Percussion Injury ◽  
Weight Method ◽  
The Subject

Background It has been hypothesized that resuscitation with crystalloids after brain trauma increases brain edema compared with colloids, but previous studies on the subject have been inconclusive. To test this hypothesis, the authors compared groups resuscitated with either colloid or crystalloid. Methods After fluid percussion injury, rats were subjected to a controlled hemorrhage of 20 ml/kg and were randomized to 5% albumin at 20 ml/kg (A20), isotonic Ringer's acetate at 50 ml/kg (C50), or 90 ml/kg (C90). After 3 or 24 h, water content in the injured cortex was determined using a wet/dry weight method. Blood volume was calculated from plasma volume, measured by 125I-albumin dilution, and hematocrit. Oncotic pressure and osmolality were measured with osmometers. Results At 3 h, blood volume was equal in the A20 and C90 groups and lower in the C50 group. Oncotic pressure was reduced by 35-40% in the crystalloid groups and unchanged in the albumin group. Cortical water content in the A20 group was lower than in the C90 group (81.3 +/- 0.5% vs. 82.1 +/- 1.1%, P &lt; 0.05), but it was not different from the C50 group (81.8 +/- 1.1%). At 24 h, oncotic pressure and blood volume were normalized in all groups, and cortical water content was significantly lower in the albumin group than in the crystalloid groups. Osmolality and arterial pressure were equal in all groups throughout the experiment. Conclusions When given to the same intravascular volume expansion, isotonic crystalloids caused greater posttraumatic brain edema than 5% albumin at 3 and 24 h after trauma.

scholarly journals High Levels of β-Amyloid, Tau, and Phospho-Tau in Red Blood Cells as Biomarkers of Neuropathology in Senescence-Accelerated Mouse

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Rebecca Piccarducci ◽  
Deborah Pietrobono ◽  
Carolina Pellegrini ◽  
Simona Daniele ◽  
Matteo Fornai ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Inflammatory Marker ◽  
Interleukin 1 ◽  
Biochemical Alterations ◽  
Amyloid A ◽  
Accumulation Kinetics ◽  
Samp8 Mice ◽  
The Brain ◽  
Senescence Accelerated Mouse

Alzheimer’s Disease (AD) is the most common Neurodegenerative Disease (ND), primarily characterised by neuroinflammation, neuronal plaques of β-amyloid (Aβ), and neurofibrillary tangles of hyperphosphorylated tau. α-Synuclein (α-syn) and its heteroaggregates with Aβ and tau have been recently included among the neuropathological elements of NDs. These pathological traits are not restricted to the brain, but they reach peripheral fluids as well. In this sense, Red Blood Cells (RBCs) are emerging as a good model to investigate the biochemical alterations of aging and NDs. Herein, the levels of homo- and heteroaggregates of ND-related proteins were analysed at different stages of disease progression. In particular, a validated animal model of AD, the SAMP8 (Senescence-Accelerated Mouse-Prone) and its control strain SAMR1 (Senescence-Accelerated Mouse-Resistant) were used in parallel experiments. The levels of the aforementioned proteins and of the inflammatory marker interleukin-1β (IL-1β) were examined in both brain and RBCs of SAMP8 and SAMR1 at 6 and 8 months. Brain Aβ, tau, and phospho-tau (p-tau) were higher in SAMP8 mice than in control mice and increased with AD progression. Similar accumulation kinetics were found in RBCs, even if slower. By contrast, α-syn and its heterocomplexes (α-syn-Aβ and α-syn-tau) displayed different accumulation kinetics between brain tissue and RBCs. Both brain and peripheral IL-1β levels were higher in SAMP8 mice, but increased sooner in RBCs, suggesting that inflammation might initiate at a peripheral level before affecting the brain. In conclusion, these results confirm RBCs as a valuable model for monitoring neurodegeneration, suggesting peripheral Aβ, tau, and p-tau as potential early biomarkers of AD.

Non invasive method to measure red blood cells transit time through the microcirculation of the brain

2016 ◽  
Vol 8 (3-4) ◽  
pp. 461-466
Author(s):  
T. Herrmann ◽  
E. Gremillet ◽  
J. Juge ◽  
A. Champailler ◽  
P. Rusch ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Transit Time ◽  
Blood Cells ◽  
Non Invasive ◽  
Invasive Method ◽  
The Brain
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