scholarly journals Photostimulation of lymphatic clearance of red blood cells from the mouse brain after intraventricular hemorrhage

2020 ◽  
Author(s):  
Dong-Yu Li ◽  
Shao-Jun Liu ◽  
Ting-Ting Yu ◽  
Zhang Liu ◽  
Si-Lin Sun ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Intraventricular Hemorrhage ◽  
Therapeutic Effects ◽  
Invasive Therapy ◽  
Non Invasive ◽  
Clearing Functions ◽  
Promising Therapeutic Target ◽  
Fatal Form ◽  
Stimulation Of

AbstractIntraventricular hemorrhage (IVH) is the most fatal form of brain injury, yet a therapy directed at ameliorating intraventricular clot is very limited. There is accumulating evidence that an augmentation of the meningeal lymphatic (MLVs) functions might be a promising therapeutic target for IVH. In particular, the photostimulation (PS) of MLVs could be promising for non-invasive therapy of IVH via PS of clearance of red blood cells (RBCs) from the brain via MLVs. Indeed, we uncover that PS has therapeutic effects on IVH in mice reducing the mortality, improving the emotional status, accelerating the RBCs evacuation from the ventricles and increasing the ICP recovery. Our findings strongly suggest that the PS-mediated stimulation of drainage and clearing functions of MLVs can be a novel bedside, readily applicable and commercially viable technologies for treatment of IVH. These pilot results open new horizons in a non-invasive therapy of IVH via PS stimulation of regenerative lymphatic mechanisms.

Noninvasive technology of photostimulation of lymphatic clearance of red blood cells from the mouse brain after intraventricular hemorrhage.

2021 ◽  
Author(s):  
Dongyu Li ◽  
Shaojun Liu ◽  
Tingting Yu ◽  
Zhang Liu ◽  
Silin Sun ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Intraventricular Hemorrhage ◽  
Lymphatic Vessels ◽  
Hematoma Expansion ◽  
Non Invasive ◽  
Clearing Functions ◽  
Fatal Form ◽  
First Time ◽  
New Strategies

Abstract Intraventricular hemorrhage (IVH) is the most fatal form of brain injury in adults and infants. However, therapy of IVH is very limited, and new strategies are needed to reduce hematoma expansion. For the first time, in our experiments on mice with IVH, we clearly demonstrate that transcranial low-level infra-red photostimulation (PS) accelerates the red blood cells (RBCs) evacuation from the ventricles that is associated with reducing the mortality in 1.57 times, improving emotional status and recovery of intracranial pressure. We revealed the mechanisms of PS-modulation of lymphatic contractility and tone of the lymphatic vessels underlying the lymphatic clearing functions. Our findings strongly suggest that PS-mediated stimulation of lymphatic clearance of RBCs can be a novel non-invasive, bedside, readily applicable, and commercially viable technology for the treatment of IVH.

Adenosine causes cAMP-dependent activation of chick embryo red cell carbonic anhydrase and 2,3-DPG synthesis

1996 ◽  
Vol 271 (4) ◽  
pp. R973-R981 ◽  
Author(s):  
S. Glombitza ◽  
S. Dragon ◽  
M. Berghammer ◽  
M. Pannermayr ◽  
R. Baumann
Keyword(s):  
Carbonic Anhydrase ◽  
Red Blood Cells ◽  
Adenylyl Cyclase ◽  
Adenosine Receptor ◽  
Blood Cells ◽  
Cell Protein ◽  
Red Cell ◽  
Receptor Stimulation ◽  
2,3 Dpg ◽  
Stimulation Of

In late chick embryos, coordinate activation of red cell carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis is initiated by hypoxia. The effects are mediated by unidentified hormonal effectors resident in chick plasma. In the present investigation, we have analyzed the effect of adenosine receptor stimulation on embryonic red cell CAII and 2,3-DPG synthesis. We find that primitive and definitive embryonic red blood cells from chick have an A2a adenosine receptor. Stimulation of the receptor with metabolically stable adenosine analogues causes a large increase of red cell adenosine 3',5'-cyclic monophosphate (cAMP) and subsequent activation of red cell CAII and 2,3-DPG production in definitive red blood cells and of CAII synthesis in primitive red blood cells. Direct stimulation of adenylyl cyclase with forskolin has the same effect. Analysis of red cell protein pattern after labeling with [35S]methionine shows that stimulation of red cell cAMP levels activates synthesis of several other proteins aside from CAII. Presence of actinomycin D inhibits cAMP-dependent changes of protein synthesis, indicating that cAMP-dependent transcriptional activation is required. In contrast to the stable adenosine receptor analogues, adenosine itself was a very weak agonist, unless its metabolism was significantly inhibited. Thus, besides adenosine, other effectors of the adenylyl cyclase system are likely to be involved in the O2 pressure-dependent regulation of red cell metabolism in late development of avian embryos.

scholarly journals Activation of electroneutral K flux in Amphiuma red blood cells by N-ethylmaleimide. Distinction between K/H exchange and KCl cotransport.

1987 ◽  
Vol 90 (2) ◽  
pp. 209-227 ◽  
Author(s):  
J S Adorante ◽  
P M Cala
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Driving Force ◽  
Flow Analysis ◽  
Cell Swelling ◽  
Direct Effects ◽  
Kcl Cotransport ◽  
Thermodynamic Forces ◽  
Exchange Flux ◽  
Stimulation Of

Exposure of Amphiuma red blood cells to millimolar concentrations of N-ethylmaleimide (NEM) resulted in net K loss. In order to determine whether net K loss was conductive or was by electroneutral K/H exchange or KCl cotransport, studies were performed evaluating K flux in terms of the thermodynamic forces to which K flux by the above pathways should couple. The direction and magnitude of the NEM-induced net K flux did not correspond with the direction and magnitude of the forces relevant to K conductance or electroneutral KCl cotransport. Both the magnitude and direction of the NEM-activated K flux responded to the driving force for K/H exchange. We therefore conclude that NEM-induced K loss, like that by osmotically swollen Amphiuma red blood cells, is by an electroneutral K/H exchanger. In addition to the above studies, we evaluated the kinetic behavior of the volume- and NEM-induced K/H exchange flux pathways in media where Cl was replaced by SCN, NO3, para-aminohippurate (PAH), or gluconate. The anion replacement studies did not permit a distinction between K/H exchange and KCl cotransport, since, depending upon the anion used as a Cl replacement, partial inhibition or stimulation of volume-activated K/H exchange fluxes was observed. In contrast, all anions used were stimulatory to the NEM-induced K loss. Since, on the basis of force-flow analysis, both volume-and NEM-induced K loss are K/H exchange, it was necessary to reevaluate assumptions (i.e., anions serve as substrates and therefore probe the translocation step) associated with the use of anion replacement as a means of flux route identification. When viewed together with the force-flow studies, the Cl replacement studies suggest that anion effects upon K/H exchange are indirect. The different anions appear to alter mechanisms that couple NEM exposure and cell swelling to the activation of K/H exchange, as opposed to exerting direct effects upon K and H translocation.

Stimulation of K-C1 cotransport in rat red cells by a hemolytic anemia-producing metabolite of dapsone

1989 ◽  
Vol 256 (2) ◽  
pp. C265-C272 ◽  
Author(s):  
M. Haas ◽  
J. H. Harrison
Keyword(s):  
Red Blood Cells ◽  
Hemolytic Anemia ◽  
Blood Cells ◽  
Pneumocystis Carinii ◽  
Fold Increase ◽  
Sh Groups ◽  
Splenic Uptake ◽  
Stimulation Of ◽  
In Cells

Dapsone, a sulfone compound used in the treatment of leprosy and, more recently, Pneumocystis carinii pneumonia, produces as a major side effect a hemolytic anemia. This anemia is characterized by oxidation of hemoglobin to methemoglobin and increased splenic uptake of red blood cells. Using a rat model, Grossman and Jollow (J. Pharmacol. Exp. Ther. 244: 118-125, 1988) found that dapsone hydroxylamine (DDS-NOH), a dapsone metabolite, is responsible for its hemolytic effect in vivo. DDS-NOH also promotes hemoglobin binding to SH groups on rat red cell membrane proteins (Budinsky et al., FASEB J. 2: A801, 1988). Since the binding of hemoglobin and other reagents (e.g., N-ethylmaleimide) to membrane SH groups has been associated with increased K transport in red blood cells, we examined the effect of DDS-NOH on K efflux from rat red blood cells in vitro. Cells shrink when exposed to DDS-NOH (100 microM) in media with plasma-like ionic composition. This shrinkage is prevented if extracellular K is raised to 110 mM or if intra- and extracellular Cl are replaced by methylsulfate (MeSO4), suggesting involvement of a K-Cl cotransport pathway. Indeed, 100 microM DDS-NOH produces a 4- to 5-fold increase in K efflux in cells containing Cl but less than a 2-fold increase in cells containing MeSO4. This stimulatory effect is specific for K; Na efflux is slightly inhibited by 100 microM DDS-NOH. The concentrations of DDS-NOH required for half-maximal stimulation of Cl-dependent K efflux (53 microM) is similar to its half-maximal hemolytic concentration in rats (approximately 100 microM). Furthermore, the stimulation of Cl-dependent K efflux by DDS-NOH is greater than 80% reversed by subsequent treatment of the cells with dithiothreitol, suggesting involvement of SH groups. Our results indicate that DDS-NOH exposure stimulates an apparent K-Cl cotransport in rat red blood cells, resulting in cell shrinkage under physiological ionic conditions. Since shrinkage of red blood cells renders them less deformable (Mohandas et al., J. Clin. Invest. 66: 563-573, 1980), this suggests a pathophysiological mechanism whereby DDS-NOH exposure in vivo could promote increased splenic uptake of red blood cells and hemolytic anemia.

Passive calcium movements in dog red blood cells: anion effects

1983 ◽  
Vol 244 (5) ◽  
pp. C318-C323 ◽  
Author(s):  
J. C. Parker
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Transport ◽  
Calcium Influx ◽  
Low Ph ◽  
Irreversible Change ◽  
Cell Shrinkage ◽  
Sodium Efflux ◽  
Sodium Dependent ◽  
Stimulation Of

Calcium influx in dog red blood cells was stimulated by replacing chloride in the medium with nitrate or thiocyanate. These anion effects were due to stimulation of a sodium-dependent calcium pathway, because calcium influx in the presence of nitrate or thiocyanate was 1) inhibited by external sodium, 2) dependent on internal sodium, 3) inhibited by cell shrinkage and low pH, and 4) inhibited by quinidine. All these characteristics had previously been shown to hold for calcium movements in the presence of chloride. Neither nitrate nor thiocyanate caused an irreversible change in calcium transport in the concentrations studied. Calcium-stimulated sodium efflux is stimulated when chloride is replaced by thiocyanate but not by nitrate. Several limiting features of the system are discussed, which preclude a conclusive interpretation of the data. The possibility is considered that the rates of sodium-dependent calcium transport in the presence of chloride, nitrate, and thiocyanate are a function of the conductance of these anions.

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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