scholarly journals Association between morphologic distortion of sickle cells and deoxygenation-induced cation permeability increase

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 450-454 ◽  
Author(s):  
N Mohandas ◽  
ME Rossi ◽  
MR Clark
Keyword(s):  
Mechanical Stress ◽  
Hemoglobin Concentration ◽  
Minimal Effect ◽  
Concomitant Increase ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Extensive Growth ◽  
Permeability Increase ◽  
K Permeability ◽  
Mean Cell Hemoglobin

Abstract We hypothesized that the deoxygenation-induced increase in cation permeability of sickle cells was related to mechanical distention of the membrane by growing HbS polymer within the cell. To test this hypothesis, we determined the effect of deoxygenation on cation fluxes in sickle cells under conditions that restricted or permitted extensive growth of polymer, producing different degrees of membrane distention. Manipulation of suspending medium osmolality for density-isolated high and low mean cell hemoglobin concentration (MCHC) cells was used to regulate the extensional growth of polymer bundles and hence membrane distortion. For initially low MCHC cells, the deoxygenation-induced increase in both Na and K fluxes was markedly suppressed when the MCHC was increased by increasing the osmolality. This suppression corresponded to the inhibition of extensive morphologic cellular distortion. For initially high MCHC, ISC-rich cells, deoxygenation had minimal effect on K permeability. However, reduction of MCHC by a decrease in osmolality produced a concomitant increase in cation permeability and cellular distortion. These observations support the idea that the sickling-associated increase in membrane permeability is related to mechanical stress imposed on the membrane by bundles of HbS polymer.

scholarly journals Association between morphologic distortion of sickle cells and deoxygenation-induced cation permeability increase

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 450-454 ◽  
Author(s):  
N Mohandas ◽  
ME Rossi ◽  
MR Clark
Keyword(s):  
Mechanical Stress ◽  
Hemoglobin Concentration ◽  
Minimal Effect ◽  
Concomitant Increase ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Extensive Growth ◽  
Permeability Increase ◽  
K Permeability ◽  
Mean Cell Hemoglobin

We hypothesized that the deoxygenation-induced increase in cation permeability of sickle cells was related to mechanical distention of the membrane by growing HbS polymer within the cell. To test this hypothesis, we determined the effect of deoxygenation on cation fluxes in sickle cells under conditions that restricted or permitted extensive growth of polymer, producing different degrees of membrane distention. Manipulation of suspending medium osmolality for density-isolated high and low mean cell hemoglobin concentration (MCHC) cells was used to regulate the extensional growth of polymer bundles and hence membrane distortion. For initially low MCHC cells, the deoxygenation-induced increase in both Na and K fluxes was markedly suppressed when the MCHC was increased by increasing the osmolality. This suppression corresponded to the inhibition of extensive morphologic cellular distortion. For initially high MCHC, ISC-rich cells, deoxygenation had minimal effect on K permeability. However, reduction of MCHC by a decrease in osmolality produced a concomitant increase in cation permeability and cellular distortion. These observations support the idea that the sickling-associated increase in membrane permeability is related to mechanical stress imposed on the membrane by bundles of HbS polymer.

scholarly journals Permeability characteristics of deoxygenated sickle cells

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 2139-2145 ◽  
Author(s):  
MR Clark ◽  
ME Rossi
Keyword(s):  
Membrane Permeability ◽  
Cytochalasin B ◽  
Monovalent Cation ◽  
Permeability Characteristics ◽  
First Order ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Permeability Increase ◽  
Induced Changes ◽  
Chloride Influx

Abstract This study investigated the effect of acute deoxygenation on membrane permeability characteristics of sickle cells. Measured fluxes of Na+ and K+ in ouabain-inhibited cells, of chloride and sulfate exchange in 4,4′-diisothiocyanostilbene-2,2′-disulfonate (DIDS)-inhibited and untreated cells, and of erythritol, mannitol, and arabinose in cytochalasin B-inhibited cells indicated that a deoxygenation-induced permeability change occurred in sickle cells only for cations and chloride. Monovalent cation permeabilities increased five-fold, and chloride influx into DIDS treated cells was enhanced nearly threefold on sickle cell deoxygenation. In contrast, no detectable increase in permeability to the other solutes was found. To gain perspective on these findings, similar measurements were performed in normal cells treated with diamide, an agent shown by others to induce a coupled increase in membrane permeability and phospholipid translocation, reminiscent of deoxygenation-induced changes in sickle cells. Although the increase in cation permeability was no greater than that in sickled cells, treatment with 2 mmol/L diamide also produced a twofold increase in the first order rate constants for sulfate exchange and mannitol efflux, indicating a relatively nonselective permeability increase that permitted flux of larger solutes than in the case of deoxygenated sickle cells. These results suggest that the deoxygenation of sickle cells induces a permeability increase that is relatively insensitive to charge, but is restrictive with respect to solute size.

scholarly journals Influence of red cell water content on the morphology of sickling

Blood ◽  
1980 ◽  
Vol 55 (5) ◽  
pp. 823-830 ◽  
Author(s):  
MR Clark ◽  
JC Guatelli ◽  
N Mohandas ◽  
SB Shohet
Keyword(s):  
Water Content ◽  
Hemoglobin Concentration ◽  
Major Influence ◽  
Red Cell ◽  
Hypotonic Medium ◽  
Cell Water ◽  
Sickle Cells ◽  
Membrane Rigidity ◽  
Internal Viscosity ◽  
Mean Cell Hemoglobin

Abstract The response of sickle cells with varying water content to alterations in oxygen tension has been studied. Cells that were severely dehydrated while sickled retained the characteristic sickled morphology even after prolonged reoxygenation. When the cell water content was increased by reduction of the suspending medium osmolality, the cells unsickled. Cells that were dehydrated before deoxygenation were unable to assume the spiculated morphology typical of sicked cells. This was true both for high mean cell hemoglobin concentration (MCHC) discoid sickle cells and for irreversibly sickled cells. When such cells were resuspended in hypotonic medium before deoxygenation, they sickled with the characteristic morphology of sickle cells with normal MCHC. The morphological behavior of Ca-loaded sickled cells as well as irreversibly sickled cells showed a major influence of increased hemoglobin concentration and extremely high internal viscosity. Constraint on cell morphology by putative membrane rigidity was not observed.

scholarly journals Influence of red cell water content on the morphology of sickling

Blood ◽  
1980 ◽  
Vol 55 (5) ◽  
pp. 823-830 ◽  
Author(s):  
MR Clark ◽  
JC Guatelli ◽  
N Mohandas ◽  
SB Shohet
Keyword(s):  
Water Content ◽  
Hemoglobin Concentration ◽  
Major Influence ◽  
Red Cell ◽  
Hypotonic Medium ◽  
Cell Water ◽  
Sickle Cells ◽  
Membrane Rigidity ◽  
Internal Viscosity ◽  
Mean Cell Hemoglobin

The response of sickle cells with varying water content to alterations in oxygen tension has been studied. Cells that were severely dehydrated while sickled retained the characteristic sickled morphology even after prolonged reoxygenation. When the cell water content was increased by reduction of the suspending medium osmolality, the cells unsickled. Cells that were dehydrated before deoxygenation were unable to assume the spiculated morphology typical of sicked cells. This was true both for high mean cell hemoglobin concentration (MCHC) discoid sickle cells and for irreversibly sickled cells. When such cells were resuspended in hypotonic medium before deoxygenation, they sickled with the characteristic morphology of sickle cells with normal MCHC. The morphological behavior of Ca-loaded sickled cells as well as irreversibly sickled cells showed a major influence of increased hemoglobin concentration and extremely high internal viscosity. Constraint on cell morphology by putative membrane rigidity was not observed.

scholarly journals Permeability characteristics of deoxygenated sickle cells

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 2139-2145 ◽  
Author(s):  
MR Clark ◽  
ME Rossi
Keyword(s):  
Membrane Permeability ◽  
Cytochalasin B ◽  
Monovalent Cation ◽  
Permeability Characteristics ◽  
First Order ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Permeability Increase ◽  
Induced Changes ◽  
Chloride Influx

This study investigated the effect of acute deoxygenation on membrane permeability characteristics of sickle cells. Measured fluxes of Na+ and K+ in ouabain-inhibited cells, of chloride and sulfate exchange in 4,4′-diisothiocyanostilbene-2,2′-disulfonate (DIDS)-inhibited and untreated cells, and of erythritol, mannitol, and arabinose in cytochalasin B-inhibited cells indicated that a deoxygenation-induced permeability change occurred in sickle cells only for cations and chloride. Monovalent cation permeabilities increased five-fold, and chloride influx into DIDS treated cells was enhanced nearly threefold on sickle cell deoxygenation. In contrast, no detectable increase in permeability to the other solutes was found. To gain perspective on these findings, similar measurements were performed in normal cells treated with diamide, an agent shown by others to induce a coupled increase in membrane permeability and phospholipid translocation, reminiscent of deoxygenation-induced changes in sickle cells. Although the increase in cation permeability was no greater than that in sickled cells, treatment with 2 mmol/L diamide also produced a twofold increase in the first order rate constants for sulfate exchange and mannitol efflux, indicating a relatively nonselective permeability increase that permitted flux of larger solutes than in the case of deoxygenated sickle cells. These results suggest that the deoxygenation of sickle cells induces a permeability increase that is relatively insensitive to charge, but is restrictive with respect to solute size.

Failure of prolonged exercise training to increase red cell mass in humans

1996 ◽  
Vol 270 (1) ◽  
pp. H121-H126 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. J. Green ◽  
J. Coates ◽  
M. Ali ◽  
S. Grant
Keyword(s):  
Exercise Training ◽  
Prolonged Exercise ◽  
Cell Mass ◽  
Hemoglobin Concentration ◽  
Red Cell ◽  
Total Blood ◽  
Mean Cell Volume ◽  
Red Cell Mass ◽  
Mean Cell Hemoglobin

The purpose of this study was to investigate the time-dependent effects of long-term prolonged exercise training on vascular volumes and hematological status. Training using seven untrained males [age 21.1 +/- 1.4 (SE) yr] initially consisted of cycling at 68% of peak aerobic power (VO2peak) for 2 h/day, 4-5 days/wk, for 11 wk. Absolute training intensity was increased every 3 wk. Red cell mass (RCM), obtained using 51Cr, was unchanged (P > 0.05) with training (2,142 +/- 95, 2,168 +/- 86, 2,003 +/- 112, and 2,080 +/- 116 ml at 0, 3, 6, and 11 wk, respectively) as were serum erythropoietin levels (17.1 +/- 4.3, 13.9 +/- 3.5, and 17.0 +/- 2.0 U/l at 0, 6, and 11 wk, respectively). Plasma volume measured with 125I-labeled albumin and total blood volume (TBV) were also not significantly altered. The increase in mean cell volume that occurred with training (89.7 +/- 0.95 vs. 91.0 +/- 1.0 fl, 0 vs. 6 wk, P < 0.05) was not accompanied by changes in either mean cell hemoglobin or mean cell hemoglobin concentration. Serum ferritin was reduced 73% with training (67.4 +/- 13 to 17.9 +/- 1 microgram/l, 0 vs. 11 wk, P < 0.05). Total hemoglobin (HbTot) calculated as the product of hemoglobin concentration and TBV was unaltered (P > 0.05) at both 6 and 11 wk of training. The 15% increase in VO2peak (3.39 +/- 0.16 to 3.87 +/- 0.14 l/min, 0 vs. 11 wk, P < 0.05) with training occurred despite a failure of training to change TBV, RCM, or HbTot.

scholarly journals Profil Darah Ikan Gelodok (Periophthalmodon schlosseri) dan (Boleophthalamus boddarti) di Desa Kuala Tambangan Pelaihari, Kalimantan Selatan

2020 ◽  
Vol 7 (2) ◽  
pp. 176
Author(s):  
Nita Azhari ◽  
Hidayaturrahmah Hidayaturrahmah
Keyword(s):  
Normal Limit ◽  
Hemoglobin Concentration ◽  
Mangrove Ecosystem ◽  
Normal Range ◽  
Blood Profile ◽  
Normal Limits ◽  
Range Type ◽  
Periophthalmodon Schlosseri ◽  
The Village ◽  
Mean Cell Hemoglobin

Profil darah memiliki peran yang sangat penting dalam fisiologi metabolisme dan aktifitas tubuh hewan. Kuala Tambangan memiliki banyak potensi sumber daya ikan salah satunya ikan gelodok. Ikan gelodok di kawasan ini mudah ditemukan, akan tetapi sampai sekarang belum dimanfaatkan dengan baik oleh masyarakat. Tujuan penelitian ini untuk mengetahui profil darah ikan gelodok jenis Periophthalmodon schlosseri dan Boleophthalamus boddarti pada ekosistem mangrove yang berada di desa Kuala Tambangan, Kabupaten Tanah Laut, Kalimantan Selatan. Metode yang digunakan pada penelitian ini yaitu metode penangkapan hewan langka yaitu line transek, metode hemositometer dan metode sahli parameter yang dihitung hemoglobin, eritrosit, leukosit, hematokrit, MCV (Mean Corpusculla Volume), MCH (Mean Cell Hemoglobin), MCHC (Mean Cell Hemoglobin Concentration) pada 2 jenis ikan gelodok 34 ekor P. schlosseri dan 34 ekor B. boddarti. Hasil yang didapatkan adalah eritrosit P. schlosseri 3,87±0,58 x 106 sel/μL; B. boddarti 3,78±0,73 x 106 sel/μL 2 jenis ikan gelodok ini memiliki nilai eritrosit diatas batas normal; leukosit P. schlosseri 11,91±5,61 x103 sel/μL dan B. boddartii 9,72±4,24 x103 sel/μL nilai leukosit pada 2 jenis ikan gelodok ini berada di atas batas normal; hemoglobin P. schlosseri 11,59±1,75 % dan B. boddartii 11,75±1,96 % dari hasil yang didapat kadar hemoglobin pada 2 jenis ikan gelodok ini berada di atas batas normal kadar hemoglobin ikan pada umumnya; hematokrit P. schlosseri 34,32±5,57 % dan B. boddartii 35,71±5,44 % hasil hematokrit yang didapat dari 2 jenis ikan gelodok ini yaitu di atas batas normal; jenis P. schlosseri memiliki nilai MCV 88,72±6,62 μm3 yang berada di bawah batas normal; MCH 29,92±0,69 pg/sel yang berada di bawah batas normal; MCHC 33,99±3,97 g/dL pada jenis ini nilai MCHC masih berada pada batas normal; jenis B. boddartii memiliki nilai MCV 96,16±17,96 μm3 yang berada di bawah batas normal; MCH 31,51±5,50 pg/sel yang masih berada di batas normal; MCHC 32,87±1,77 g/dL nilai MCHC pada jenis ini masih berada pada batas normal. Blood profile has a very important role in the physiology of metabolism and animal body activities. Kuala Tambangan has a lot of potential fish resources, one of which is the fish Mudskipper. Mudskipper fish in this area are easy to find, but until now it has not been utilized properly by the community. The purpose of this study was to determine the blood profile of the Periophthalmodon Schlosseri and Boleophthalamus boddarti fish species in the mangrove ecosystem in the village of Kuala Tambangan, Tanah Laut District, South Kalimantan . The method used in this study is the method of catching endangered animals namely trasnek line, hemocytometer method and parameter Sahli method which is calculated hemoglobin, erythrocytes, leukocytes, hematocrit, MCV (Mean Corpuscular Volume), MCH (Mean Cell Hemoglobin), MCHC (Mean Cell Hemoglobin Concentration) on 2 types of fish, 34 Periophthalmodon schlosseri and 34 Boleophthalmus boddarti. The results obtained were P. schlosseri erythrocytes 3.87 ± 0.58 x 106 cells / μL; B. boddarti 3.78 ± 0.73 x 106 cells / μL 2 types of fish Mudskipper has erythrocyte values above the normal limit; P. schlosseri leukocytes 11.91 ± 5.61 x103 cells / μL and B. boddartii 9.72 ± 4.24 x103 cells / μL leukocyte values in these 2 types of jagged fish are above normal limits; hemoglobin P. schlosseri 11.59 ± 1.75 % and B. boddartii 11.75 ± 1.96 % from the results obtained by the hemoglobin levels in these 2 types of fishes are above the normal limit of fish hemoglobin levels in general; hematocrit P.schlosseri 34.32 ± 5.57 % and B. boddartii 35.71 ± 5.44 % hematocrit results obtained from these 2 types of mudskipper fish are above normal limits; P.schlosseri species had MCV values of 88.72 ± 6.62 μm3 which were below normal limits; MCH 29.92 ± 0.69 pg / cell that is below the normal range; MCHC 33.99 ± 3.97 g / dL in this type the MCHC value is still in the normal range; type B. boddartii has a MCV value of 96.16 ± 17.96 μm3 which is below normal limits; MCH 31,51 ± 5.50 pg / cell which is still in the normal range; MCHC 32.87 ± 1.77 g / dL MCHC values in this type are still within normal limits.Keywords: gelodok, blood, kuala tambangan

scholarly journals Deoxygenation-induced cation fluxes in sickle cells: II. Inhibition by stilbene disulfonates

Blood ◽  
1990 ◽  
Vol 76 (1) ◽  
pp. 212-220 ◽  
Author(s):  
CH Joiner
Keyword(s):  
Binding Site ◽  
Anion Exchange ◽  
Anion Exchanger ◽  
Drug Exposure ◽  
External Surface ◽  
Anion Transport ◽  
Sickle Cells ◽  
Transport Inhibitor ◽  
Cation Permeability

Deoxygenation-induced cation movements in sickle cells were inhibited 80% to 85% by the anion transport inhibitor, 4,4′-diisothiocyano- 2,2′disulfostilbene (DIDS). Morphologic sickling was not altered by DIDS treatment, demonstrating that morphologic sickling was not sufficient to produce cation leaks in sickle cells. DIDS inhibition of deoxygenation-induced cation flux was not affected when l- replaced Cl- , indicating that conductive anion movements did not limit cation flux in deoxygenated cells treated with DIDS. Inhibition was irreversible after preincubation with DIDS at 37 degrees C for 20 minutes, and was not affected by the oxygenation state of cells at the time of drug exposure. Sulfate self-exchange was inhibited at lower DIDS concentrations than was deoxygenation-induced flux. Incubation of cells with DIDS at 4 degrees C produced progressive blockade of sulfate exchange, but did not alter deoxygenation-induced cation fluxes. Other stilbene disulfonates, including compounds incapable of covalent reactions, also inhibited deoxygenation-induced cation movements, although several other inhibitors of anion exchange did not. Dissociation of the inhibition of anion exchange and deoxygenation- induced cation flux indicates that the DIDS effect on deoxygenation- induced cation movements does not involve the well-characterized stilbene binding site of the anion exchanger. These data provide evidence for a membrane constituent on the external surface of oxygenated sickle cells capable of interacting with DIDS to prevent the increase in cation permeability associated with sickling.

scholarly journals The influence of oxygen tension, temperature, and hemoglobin concentration on the rheologic properties of sickle erythrocytes

Blood ◽  
1990 ◽  
Vol 76 (6) ◽  
pp. 1256-1261 ◽  
Author(s):  
LH Mackie ◽  
RM Hochmuth
Keyword(s):  
Recovery Time ◽  
Hemoglobin Concentration ◽  
Partial Pressure Of Oxygen ◽  
Normal Cells ◽  
Sickle Cells ◽  
Threefold Increase ◽  
Sickle Erythrocytes ◽  
Rheologic Properties ◽  
Oxygen Tensions ◽  
Cell Densities

Abstract With the use of micromanipulation techniques, the shear modulus or “rigidity” mu, the recovery time tc, and the unfolding time tf for individual sickle cells have been measured at different oxygen tensions, temperatures, and cell densities. In these experiments, the partial pressure of oxygen was varied from 156 to 40 mm Hg and the temperature was controlled at 25 degrees C or 37 degrees C. Three mean cellular hemoglobin concentrations were studied: 29 g/dL, 33 g/dL, and 46 g/dL. The lighter cells (29 and 33 g/dL) exhibited at most a threefold increase in rigidity as the pO2 was decreased from 156 to 40 mm Hg. At 25 degrees C, the densest cells (46 g/dL) also exhibited a threefold increase. However, at 37 degrees C, the rigidity of these cells increased eightfold between 156 to 40 mm Hg. Compared with normal cells, this gives a rigidity that is 18 times larger. In contrast to the values for mu, the values for tc and tf remained essentially unchanged (within the accuracy of the experiments) for the lighter cells and could not be measured for the densest cells.

Chronic sodium cyanate treatment induces "hypoxia-like" effects in rats

1986 ◽  
Vol 60 (4) ◽  
pp. 1145-1149 ◽  
Author(s):  
B. P. Teisseire ◽  
C. C. Vieilledent ◽  
L. J. Teisseire ◽  
M. O. Vallez ◽  
R. A. Herigault ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Hemoglobin Concentration ◽  
Normal Growth ◽  
Mean Cell Volume ◽  
Control Value ◽  
Normal Limits ◽  
Sodium Cyanate ◽  
Mean Cell Hemoglobin

Three weeks of sodium cyanate (NaCNO) intraperitoneal treatment in rats (n = 15) induced high hemoglobin O2 affinity, i.e., low PO2 at 50% hemoglobin saturation (P50), 20.5 +/- 1.4 Torr, in comparison with the mean control values, 34.5 +/- 1.6 Torr (n = 15). NaCNO rats showed a reduction in mean body weight, 376 +/- 27 g, in comparison with controls, 423 +/- 23 g (P less than 0.001). Despite arterial O2 partial pressure (PaO2) within normal limits NaCNO-treated rats had a higher systolic right ventricular pressure (SRVP), 33.7 +/- 3.1 Torr, in comparison with control value, 29.0 +/- 2.5 Torr (P less than 0.001). Right ventricle weights were significantly increased (P less than 0.001). After 60 min of an hypoxic challenge (fractional concentration of inspired O2 = 0.10) NaCNO-treated rats increased SRVP of only 7 +/- 4% compared with 46 +/- 9% in the control animals. Inducing high hemoglobin affinity in rats (n = 10; 6 wk NaCNO treatment) resulted in increases in hematocrit ratio and hemoglobin concentration (P less than 0.001). The characteristics of the red blood cell (RBC) itself changed; values of mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration being significantly increased (P less than 0.001) when compared with mean control values. The count of nucleated RBC′s appeared to be significantly higher from the 2nd wk of NaCNO treatment. Chronic NaCNO treatment was demonstrated to exert “hypoxia-like” effects since it induced prevention of normal growth, polycythemia, pulmonary hypertension, right ventricular hypertrophy, and blunted pulmonary pressor response to acute hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

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