Search Results (99)

Background/Objectives: Chronic ethanol consumption damages erythrocyte membranes, reducing their deformability and disrupting erythropoiesis. Dopaminergic signalling plays an important role in regulating haematopoietic stem cells. However, the impact of genetic alterations in the dopamine system on the functional properties of erythrocytes and their resistance to the toxic effects of alcohol remains understudied. In this study, we evaluated haematological parameters and the sensitivity of erythrocytes to chronic ethanol exposure in DAT-HET rats (heterozygous for the dopamine transporter gene) compared to Wistar rats. Methods: Both lines of rats were subjected to chronic alcoholisation (10% ethanol for six months). Flow cytometry was used to assess reticulocyte production, intracellular esterase activity (cell viability), and membrane lipid asymmetry disruptions. Laser diffraction was used to evaluate osmotic resistance (deformability). Results: The partial knockout of the DAT gene significantly altered the baseline haematological profile, resulting in pronounced leukopenia, moderate thrombocytopenia, moderate erythrocyte macrocytosis, and reduced intracellular esterase activity. The consequences of chronic ethanol consumption in Wistar rats (anaemia, decreased reticulocyte count, increased osmotic rigidity of erythrocytes, and an increased proportion of annexin-positive cells) were similar to those observed in humans, thus confirming the validity of the experimental model. In contrast, chronic alcohol exposure did not significantly influence haematopoiesis parameters or erythrocyte biophysical properties in DAT-HET rats, indicating that even a 50% loss of the dopamine transporter strongly prevented ethanol’s damaging effects on blood cells. Conclusions: The marked contrast between Wistar rats (which develop alcohol-induced anaemia and erythrocyte dysfunction similar to humans) and DAT-HET rats (which remain largely unaffected) demonstrates that dopaminergic signalling plays a previously unrecognised role in determining erythrocyte sensitivity to alcohol toxicity. Full article

Two spectrin-sensitive relaxations have been reported in the RBC plasma membrane: β_s (1.4 MHz, related to the interface β-relaxation) and γ1_s (9 MHz, rotation alignment of spectrin-bound dipoles by penetrating electric field). Here, a third (α_s) relaxation type is reported within the frequency region of surface (α) relaxation. With low-ion-strength outside media, the adsorption of blood plasma immunoglobulins on RBCs was found to inhibit β_s and γ1_s relaxations, while α_s relaxation was enforced with strong inflammation. The three relaxations are represented by three consecutive segments on the Cole′s plots: Δε_rd″.ω against Δε_r′ and Δε_rd″/ω against Δε_r′. Here, ω is the frequency of the field and Δε_r* = Δε_r′ + j.Δε_rd″ is the change in the relative complex dielectric permittivity of RBC suspension at the denaturation temperature of spectrin. The β_s segment in Δε_rd″.ω against the Δε_r′ plot could be regarded as a vector (complex number) whose projection on the vertical axis (the irreversible loss in energy) could express the ability of the plasma membrane to deform (under the impact of shear stress). Full article

Hereditary spherocytosis (HS) is the most common inherited red blood cell (RBC) membrane disorder and has traditionally been attributed to defects in cytoskeletal proteins such as spectrin, ankyrin, band 3, and protein 4.2. Growing evidence, however, shows that disturbances in ion transport also contribute to HS pathophysiology. This review summarizes current understanding of HS by integrating membrane structural defects with abnormalities in ion homeostasis and highlights the diagnostic value of osmotic gradient ektacytometry (OGE). Beyond membrane instability, HS erythrocytes exhibit increased cation permeability with abnormal Na⁺ influx and K⁺ loss, leading to cellular dehydration, elevated mean corpuscular hemoglobin concentration (MCHC), and reduced deformability. Dysregulation of mechanosensitive and Ca²⁺-activated K⁺ channels (PIEZO1, KCNN4) may modulate disease expression. OGE—now the reference functional test for RBC deformability—identifies reproducible phenotypes reflecting hydration status, including dehydrated (HS1) and partially hydrated (HS2) HS profiles. When combined with next-generation sequencing (NGS), OGE improves differentiation between HS and overlapping membranopathies such as hereditary xerocytosis or stomatocytosis. In conclusion, HS is a multifactorial disorder resulting from the interplay between cytoskeletal fragility, oxidative stress, and dysregulated ion transport. Integrated diagnostic strategies that combine hematologic indices, OGE, and targeted NGS enhance diagnostic accuracy, support genotype–phenotype interpretation, and guide individualized clinical management. Future efforts should focus on ion-channel modulation and wider adoption of functional assays in precision hematology. Full article

The study aimed to determine the effect of acute, one-time physical effort performed under different environmental temperature conditions on erythrocyte deformability in healthy young men. This exploratory randomized parallel-group study involved 30 men randomly assigned to an experimental group exercising at −10 °C in a climatic chamber and a control group exercising under thermoneutral outdoor conditions. Erythrocyte deformability was assessed using the elongation index (EI), reflecting erythrocyte elasticity and the ability to pass through microcirculation vessels. Participants performed an incremental 20 m shuttle run test. Venous blood samples were collected before and immediately after exercise, and erythrocyte deformability was analyzed using a Lorrca analyzer across a shear stress range of 0.30–60.00 Pa. A two-factor repeated-measures analysis of variance was applied. An increase in EI after exercise was observed in both groups, predominantly at higher shear stress values, indicating enhanced erythrocyte deformability under conditions of increased shear forces. However, the magnitude of post-exertion changes differed between groups. At lower shear stress levels (0.30 Pa and 0.58 Pa), EI tended to decrease after exercise. These findings indicate that a single bout of physical effort influences erythrocyte deformability, while the potential effects of cold exposure on this response remain uncertain and warrant further investigation. Full article

Zinc oxide nanoparticles (ZnO NPs) are increasingly applied in medicine, cosmetics, and environmental technologies, yet their interactions with blood cells remain poorly understood, raising cross-species safety concerns. Using frog (nucleated) and human (anucleate) erythrocytes as comparative models, we show that cellular architecture fundamentally shapes responses to ZnO NPs exposure. Human erythrocytes exhibited a dose-dependent progression from membrane deformation to eryptosis and hemolysis, reflecting the pronounced vulnerability of anucleate cells. In contrast, frog erythrocytes sustained nuclear DNA damage while largely preserving membrane integrity, highlighting the protective or reparative role of the nucleus. Molecular docking revealed energetically favorable interactions of ZnO NPs with ERα-LBD and DNA (ΔG = −4.28 and −5.68 kcal/mol, respectively), while quantum chemical analyses indicated electron-accepting properties and a narrow HOMO–LUMO gap, suggesting efficient macromolecular interactions and intracellular ROS generation. Together, these findings demonstrate that the presence of a nucleus shifts the primary target of nanoparticle toxicity from membrane to genome, providing novel mechanistic insights. This comparative study offers a robust framework for understanding nanomaterial reactivity across taxa and informs One Health-oriented risk assessments. Full article

Calcium (Ca²⁺) is a signal messenger for ion flow in and out of microbial, parasitic, and host defense cells. Manipulation of calcium ion signaling with ion blockers and calcineurin inhibitors may improve host defense while decreasing microbial/parasitic resistance to therapy. Ca²⁺ release from intracellular storage sites controls many host defense functions (cell integrity, movement, and growth). The transformation of phospholipids in the erythrocyte membrane is associated with changes in deformability. This type of lipid bilayer defense mechanism helps to prevent attack by Plasmodium. Patients with sickle cell disease (SS hemoglobin) do not have this protection and are extremely vulnerable to massive hemolysis from parasitic infestation. Patients with thalassemia major also lack parasite protection. Alteration of Ca²⁺ ion channels responsive to environmental stimuli (transient receptor potential) results in erythrocyte protection from Plasmodium. Similarly, calcineurin inhibitors (cyclosporine) reduce heart and brain inflammation injury with Trypanosoma and Taenia. Ca²⁺ channel blockers interfere with malarial life cycles. Several species of parasites are known to invade hepatocytes: Plasmodium, Echinococcus, Schistosoma, Taenia, and Toxoplasma. Ligand-specific membrane channel constituents (inositol triphosphate and sphingosine phospholipid) constitute membrane surface signal messengers. Plasmodium requires Ca²⁺ for energy to grow and to occupy red blood cells. A cascade of signals proceeds from Ca²⁺ to two proteins: calmodulin and calcineurin. Inhibitors of calmodulin were found to blunt the population growth of Plasmodium. An inhibitor of calcineurin (cyclosporine) was found to retard population growth of both Plasmodium and Schistosoma. Calcineurin also controls sensitivity and resistance to antibiotics. After exposure to cyclosporine, the liver directs Ca²⁺ ions into storage sites in the endoplasmic reticulum and mitochondria. Storage of large amounts of Ca²⁺ would be useful if pathogens began to occupy both red blood cells and liver cells. We present scientific evidence supporting the benefits of calcium channel blockers and calcineurin inhibitors to potentiate current antiparasitic therapies. Full article

Background: The intravascular laser irradiation of blood (ILIB) is a low-power laser technique that has been studied since the 1970s, and it is associated with the substantial capability to modulate various physiological processes. Indeed, ILIB involves the irradiation of blood with low-intensity light, typically within the red or near-infrared spectrum, to trigger a cascade of photochemical and photobiological events. Objective: This study aimed to analyze previous findings regarding ILIB effects on physical performance. Methods: This study is a narrative review of the literature, addressing the effects of ILIB on multiple organ systems and its impact on physical performance. Results: The most found effects include antioxidant activation, inhibition of inflammatory processes, increased blood fluidity, and improved hemorheological properties. The ILIB affects blood rheological properties based on vasodilatation and decreasing aggregation of thrombocytes. Other effects include improved deformability of erythrocytes, which results in a better supply of oxygen and a decrease in the partial pressure of carbon dioxide. Since ILIB is a photobiomodulation procedure, other applications can be considered, such as ergogenic intervention. In this context, ILIB may favor performance in aerobic exercises and contribute to practices involving anaerobic metabolism by facilitating phosphocreatine resynthesis and ATP restoration. Conclusions: Multiple findings seek to support the potential benefits of ILIB on metabolic and cardiovascular responses associated with exercise training, providing potential improvements in athletic performance. Full article

Background: Chronic venous insufficiency (CVI) is one of the main causes of venous leg ulcers. Rheological disorders of the blood, such as changes in viscosity, hematocrit, and erythrocyte aggregation and deformability, can impair microcirculation and impede healing. Carbonic acid (CO₂) dry baths are a non-invasive physical method that can affect microcirculation and blood parameters, and this study aimed to assess their effectiveness in ulcer healing and in modifying selected blood rheological parameters in patients with CVI. Methods: This prospective, controlled study enrolled 23 participants (11 patients with active venous leg ulcers and 12 healthy controls). The intervention group underwent ten sessions of dry CO₂ baths, performed twice weekly for 5 weeks. No randomization was applied. Ulcer healing was assessed planimetrically, and blood rheological parameters (hematocrit, blood and plasma viscosity, erythrocyte deformability index [EI], aggregation index [AI], aggregation amplitude [AMP], and half-time of aggregation [T_1/2]) were measured before and after therapy. Results: Following the intervention, the ulcer area decreased significantly (median 3.35 cm² to 1.74 cm²; p < 0.01), as did ulcer circumference (7.33 cm to 5.87 cm; p < 0.01). Hematocrit increased (median 40.25% to 41.50%; p < 0.05), and blood viscosity values at low shear rates approached those of the control group. In contrast, erythrocyte deformability (EI) and aggregation indices (AI, AMP, T_1/2) showed no statistically significant intragroup changes, although intergroup differences persisted. Pain intensity decreased significantly (VAS 6.0 to 3.5 cm; p < 0.05). Conclusions: CO₂ dry baths support the treatment of venous ulcers by improving microcirculation and reducing pain. Their impact on blood rheology may have clinical significance, especially as an adjunct to therapy in chronic venous insufficiency. However, the relatively small sample size (n = 23) should be considered a limitation when interpreting these findings. Full article

In reconstructive surgery, usage of different flaps is essential to cover tissue defects. Twisting, stretching or damaging the vascular pedicle may jeopardize the flaps’ viability. The aim of our experiment was to monitor tissue perfusion parameters of local versus rotated musculocutaneous flaps. In rats, musculus cutaneus maximus-based muscle–skin flaps were prepared bilaterally: one was sutured back to its original position, while the other flap was rotated to the ventral chest region (Flap group). In the Control group, flaps were not prepared. Tissue microcirculation was monitored intraoperatively, and on the 7th and 14th postoperative days. Blood samples were taken for testing hematological and hemorheological parameters. At the end of the observation period, biopsies were taken for biomechanical (tensile strengths) and histological investigations. We found that leukocyte and platelet counts significantly increased in the Flap group, while erythrocyte deformability decreased and aggregation increased. Although both local and rotated flaps survived and wound healing progressed well, in microcirculatory recordings, hypoperfusion and visible red blood cell aggregates were seen mostly in the rotated flaps. The rotated flaps were biomechanically weaker compared to local flaps or intact skin regions. This new model seems to be suitable for studying further flap pathophysiology focusing on tissue perfusion. Full article

Background/Objectives: To prevent flap failure, adequate tissue perfusion and effective regenerative processes, undisturbed wound healing are essential, among others. To improve wound healing, various locally and systematically administered pharmacons can be used. This study investigated the effect of PACAP 1-38 (pituitary adenylate cyclase activating polypeptide) and BGP-15 (a nicotinic amidoxime derivative) on the healing of epigastric fasciocutaneous flaps exposed to ischemia–reperfusion (I/R). Methods: Wistar rats were randomly divided into control (no substance), PACAP 1-38, and BGP-15 groups. Groin flaps were prepared bilaterally. The left flap was exposed to 120 min of ischemia prior to suturing it back. We applied wound gels containing substances. Laboratory tests (hematology, erythrocyte deformability, and aggregation) were performed before surgery on the 1st, 3rd, and 7th postoperative days. Lastly, flap skin samples were taken for histological and tensile strength measurements. Results: Impaired erythrocyte deformability and enhanced aggregation were found because of flap I/R. The pharmacons were able to reduce the systemic micro-rheological impairment to varying degrees. The tensile strength increased in the areas of better perfusion. Conclusions: The anti-inflammatory effects of PACAP 1-38 and BPG-15, as well as the impact of PACAP 1-38 on collagen and elastic fiber composition, have been demonstrated. Full article

Red blood cell (RBC), accounting for approximately 45% of total blood volume, are essential for oxygen delivery and carbon dioxide removal. Their unique biconcave morphology, high surface area-to-volume ratio, and remarkable deformability enable them to navigate microvessels narrower than their resting diameter, ensuring efficient microcirculation. RBC deformability is primarily determined by membrane viscoelasticity, cytoplasmic viscosity, and cell geometry, all of which can be altered under various physiological and pathological conditions. Reduced deformability is a hallmark of numerous diseases, including sickle cell disease, malaria, diabetes mellitus, sepsis, ischemia–reperfusion injury, and storage lesions in transfused blood. As these mechanical changes often precede overt clinical symptoms, RBC deformability is increasingly recognized as a sensitive biomarker for disease diagnosis, prognosis, and treatment monitoring. Over the past decades, diverse techniques have been developed to measure RBC deformability. These include single-cell methods such as micropipette aspiration, optical tweezers, atomic force microscopy, magnetic twisting cytometry, and quantitative phase imaging; bulk approaches like blood viscometry, ektacytometry, filtration assays, and erythrocyte sedimentation rate; and emerging microfluidic platforms capable of high-throughput, physiologically relevant measurements. Each method captures distinct aspects of RBC mechanics, offering unique advantages and limitations. This review synthesizes current knowledge on the pathophysiological significance of RBC deformability and the methods for its measurement. We discuss disease contexts in which deformability is altered, outline mechanical models describing RBC viscoelasticity, and provide a comparative analysis of measurement techniques. Our aim is to guide the selection of appropriate approaches for research and clinical applications, and to highlight opportunities for developing robust, clinically translatable diagnostic tools. Full article

Microfluidic methods are an important tool for studying the microrheology of blood and the mechanical properties of blood cells—erythrocytes, leukocytes, and platelets. In patients with diabetes, hypertension, obesity, sickle cell anemia, or cerebrovascular or peripheral vascular diseases, hemorheological alterations are commonly observed. These include increased blood viscosity and red blood cell (RBC) aggregation, along with reduced RBC deformability. Such disturbances significantly contribute to impaired microcirculation and microvascular perfusion. In blood vessels, abnormal hemorheological parameters can elevate resistance to blood flow, exert greater mechanical stress on the endothelial wall, and lead to microvascular complications. Among these parameters, erythrocyte deformability is a potential biomarker for diseases including diabetes, malaria, and cancer. This review highlights recent advances in microfluidic technologies for in vitro assays of RBC deformability and aggregation, as well as leukocyte aggregation and adhesion. It summarizes the core principles of microfluidic platforms and the experimental findings related to hemodynamic parameters. The advantages and limitations of each technique are discussed, and future directions for improving these devices are explored. Additionally, some aspects of the modeling of the microrheological properties of blood cells are considered. Overall, the described microfluidic systems represent promising tools for investigating erythrocyte mechanics and leukocyte behavior. Full article

The mechanical stability and deformability of erythrocytes are vital for their function as they traverse capillaries, where shear stress can reach up to 10 Pa under physiological conditions. Human serum albumin (HSA) is known to help maintain erythrocyte stability by influencing cell shape, membrane integrity, and resistance to hemolysis. However, the precise mechanisms by which albumin exerts these effects remain debated, with some studies indicating a stabilizing role and others suggesting the opposite. This review highlights that under high shear rates, albumin molecules may undergo unfolding due to normal stress differences. Such structural changes can significantly alter albumin’s interactions with the erythrocyte membrane, thereby affecting cell mechanical stability. We discuss two potential scenarios explaining how albumin influences erythrocyte mechanics under shear stress, considering both the viscoelastic properties of blood and those of the erythrocyte membrane. Based on theoretical analyses and experimental evidence from the literature, we propose that albumin’s effect on erythrocyte mechanical stability depends on (i) the transition between unfolded and folded states of the protein and (ii) the impact of shear stress on the erythrocyte membrane’s ζ-potential. Understanding these factors is essential for elucidating the complex relationship between albumin and erythrocyte mechanics in physiological and pathological conditions. Full article

Hemorheology is a branch of science that studies and explains the causes of blood flow disorders. In many vascular disorders whole blood viscosity, plasma viscosity, aggregability, and deformability of erythrocytes can be a diagnostic factor. In this paper we analyze whether statin therapy affects hemorheological values in a group of patients with clinically diagnosed silent ischemic foci of the brain (CSVCL). The study includes an analysis of the hemorheological parameter values such as whole blood viscosity, plasma viscosity, and selected biochemical parameters. Aggregability and deformability of erythrocytes were determined using the mathematical Quemada model. Our results indicate a modifying effect of statins on hemorheological parameters. Full article

Background: Venous thromboembolism is more prevalent among patients with inflammatory bowel disease (IBD). This study aimed to identify prothrombotic hemorheological alterations in IBD. Methods: We conducted a case–control study with patients with ulcerative colitis, Crohn’s disease, and non-IBD control subjects. We measured hemorheological indicators including plasma viscosity (PV), whole blood viscosity (WBV), erythrocyte aggregation (EA), and erythrocyte deformability (ED). Uni- and multivariate tests were employed for analysis. Results: A total of 53 IBD patients and 77 control subjects were recruited. IBD patients showed significantly higher aggregation index (68.8% (35.3–83.5%) vs. 66.9% (35.2–83.5%), p = 0.003) and threshold shear rate (120 1/s (55–325 1/s) vs. 110 1/s (55–325 1/s), p < 0.001), with lower aggregation half-time (1.6 s (0.6–7.1 s) vs. 1.8 s (0.6–7.1 s), p = 0.004), indicating enhanced EA. However, after adjusting for covariates, including inflammatory markers, IBD no longer predicted EA. There were no significant differences in EA. PV, WBV, and ED between the groups. Fibrinogen, rather than the Crohn’s Disease Activity Index, was the strongest predictor of the outcomes. Conclusions: Our study demonstrates that IBD patients exhibit enhanced EA, predicted mainly by fibrinogen. These results confirm that inflammation plays the cardinal role in the increased tendency for venous thromboembolism in IBD. Full article