Erythrocyte Mechanical Fragility Research Articles

Red Blood Cells Fragility among Sudanese Patients with Type 2 Diabetic Mellitus

Background: Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia and has become a major public health problem globally. Diabetes is the risk factor for osmotic fragility. Objective: The aim of the present study is to describe erythrocyte osmotic fragility changes in type II diabetes. The osmotic fragility test is a measure of the resistance of erythrocytes to hemolysis by osmotic stress. Material and method: In this study 50 diabetic type 2 patients were informed about the study and parameters selected for the study are : median corpuscular fragility (MCF), hemoglobin(HB) , hemoglobin A1c(HA1c) , Fasting blood glucose (FBG) . Result: The analyzed results showed: Patients with type 2 diabetes have a significantly higher erythrocyte mechanical fragility. And that fasting blood glucose and anemia are also strongest correlate of increased mechanical fragility of erythrocytes. Conclusion: The result of FBG, HBA1c and OFT were significantly increased in diabetic’s type 2 patient (p value < 0.05), furthermore hemoglobin (HB) estimation was significantly decreased in diabetic’s type 2 patient (p value <0.05). The correlation between OFT and duration of type 2 DM were positive significant correlation (p value < 0.05).

Rapid in vitro screening model for drugs affecting calcium ion mediated erythrocyte mechanical fragility

Rapid in vitro screening model for drugs affecting calcium ion mediated erythrocyte mechanical fragility

Erythrocyte mechanical fragility is increased in patients with type 2 diabetes

BackgroundAnemia is common among patients with type 2 diabetes. We determined whether type 2 diabetic patients significantly differed in erythrocyte mechanical fragility as compared with nondiabetic subjects. MethodsWe recruited 25 Caucasian patients with type 2 diabetes (14 men and 11 women; mean age 58±8years) and 25 age-, race- and sex-matched nondiabetic individuals. The fragility of erythrocytes was tested by inducing mechanical hemolysis by double aspiration of K2EDTA blood through a 0.5mL insulin syringe equipped with a very thin needle. The plasma was then separated from the blood cells by centrifugation at 2000xg for 15min at room temperature. A Beckman Coulter DxC 800 was used to measure the hemolysis index by direct spectrophotometry. ResultsCompared with matched nondiabetic controls, type 2 diabetic patients had a significantly increased mechanical fragility of erythrocytes (hemolysis index ratio 21±13 vs. 14±10, p=0.02). Univariable linear regression analysis revealed that there was a strong positive association between percent hemolysis and fasting plasma glucose (r=0.669, p<0.001) and hemoglobin A1c (r=0.549, p<0.005) in type 2 diabetic subjects, but not in matched nondiabetic controls. ConclusionsOur data suggest that patients with type 2 diabetes have a significantly higher erythrocyte mechanical fragility than matched nondiabetic subjects, and that fasting plasma glucose is the strongest correlate of increased mechanical fragility of erythrocytes in this patients group.

Species Differences in Erythrocyte Mechanical Fragility

The erythrocyte destruction rate under constant shear stress was measured to clarify species differences in red blood cell (RBC) mechanical fragility between human, bovine, and ovine cells. Blood was collected from healthy donors by venipuncture. RBC age fractionation was performed by high speed centrifugation (20 min at 12,000 g). Relatively young, middle, and old age RBCs was suspended in Dulbecco's phosphate buffered saline to adjust the hematocrit to 35%. Uniform shear stress was applied to each sample contained in a concavo-convex Couette flow testing machine. Young and old aged samples were exposed to 300 dyne-sec-cm2 for 0 and 15 min. Middle aged samples were exposed to 300 dyne-sec-cm2 for 0, 5, 10 and 15 min. Liberated hemoglobin was estimated by tetramethylbenzidine colorimetric measurement and the erythrocyte destruction rate was calculated. Older samples had a higher hemolysis rate than younger samples in every species. The destruction under constant shear stress is approximately linear in time. Mechanical fragility of ovine and bovine RBCs was 1.8 and 0.5 times as large as human RBCs, respectively. These values could serve as universal standards when extrapolating animal hemolysis data for any blood pump to predict its safety and biocompatibility in human clinical trials.

Studies on hemolysis in canine dirofilarial hemoglobinuria. Lipid alterations in blood serum and red cell membrane.

Changes of free cholesterol (F Ch) and phospholipid (Pl) collcentrations in the serum and the contents in the red cell membranes were investigated in the case of dirofilarial hemoglobinuria (Hb-uria) and compared with those in normal dogs and dogs suffering from chronic serious filariasis without Hb-emia and Hb-uria. There was a significant increase in serum F Ch concentration and in the Ch and Pl contents in the red cell membranes of the serious filariasis group, as compared with the normal one. Marked increases in the F Ch and Pl concentrations and F Ch/Pl ratio were found in the serum, the Ch content and Ch/Pl ratio in the red cell membranes in the Hb-uria group, as compared with the normal one. Also, as opposed to the serious filariasis group, serum F Ch concentration showed an appreciable rise, but the Ch/Pl ratio was insignificant in the red cell membranes. There were no significant findings as to the serum lipoprotein fractions in the Hb-uria or the normal group. In the Hb-uria group, however, the α-lipoprotein concentration and α/total β-ratio were significantly higher and the total β-lipoprotein concentration was significantly lower in the serum than in the serious filariasis group. There were significant correlations between the serum and red cell membranes as to F Ch concentration and Ch content, or Ch/Pl ratio, in the normal and whole groups, but not in the Hb-uria group. Both filariasis groups showed an appreciable increase in erythrocyte mechanical fragility, as compared with the normal group, and they displayed a lower minimum and higher maximum resistance to osmotic fragility than the normal group.

Temporary left ventricular bypass: factors affecting patient survival.

Circulatory support (range, 2 hours-8 days) was undertaken in eight cardiac surgical patients (with two survivors) exhibiting intractable cardiogenic shock. A paracorporeal, pneumatic, xenograft-valve pump was interposed between the left ventricular apex and ascending aorta. Pumping lowered left atrial and ventricular pressure while maintaining cardiac output (1.8--2.6 l/min/m2). Following implantation, plasma hemoglobin and erythrocyte mechanical fragility values were elevated but decreased to normal when renal function was not impaired. Mild thrombocytopenia was noted in three patients and was severe in five others with persistent hemorrhage. Anticoagulation agents were used during tapering of pump flow (three patients) after 100, 105 and 120 hours of bypass. Otherwise, for the major portion of the interval of mechanical circulatory support, anticoagulants were not administered. Despite this fact, no systemic embolization was detected in any of the patients. It appears that assist pump support can be life-saving in acute left ventricular failure in patients following cardiac surgery.

An Appraisal of Blood Trauma and the Blood-Prosthetic Interface during Left Ventricular Bypass in the Calf and Humans

Mechanical circulatory support was accomplished in 20 calves (mean, 140 days) and in 5 patients following operation for acquired heart disease (range, 1 hour to 8 days) employing a pneumatically actuated xenograft-valved assist pump interposed between the left ventricular apex and aorta. Following pump implantation in calves, hematocrit and platelets decreased transiently and returned to normal within 14 days. Plasma hemoglobin and erythrocyte mechanical fragility values were elevated for 48 hours. Platelet survival was slightly reduced, but erythrocyte survival values were similar to controls. In patients who received assist pumps, plasma hemoglobin and erythrocyte mechanical fragility were transiently elevated, but rapidly decreased to normal. Thrombocytopenia occurred only in the presence of bleeding and renal failure requiring hemodialysis. Pump flow of the left ventricular assist device was maintained above 2.0 L/min/m 2 despite serious arrhythmias. Postmortem examination revealed no evidence of thromboemboli in the clinical patients although anticoagulant agents were not administered.

Comparative Effects of Selenium and Vitamin E in Lead-poisoned Rats

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.

Lead Poisoning in Vitamin E-deficient Rats

Weanling male rats were fed either a vitamin E-deficient Torula yeast diet or the same diet supplemented with 100 ppm vitamin E for a period of 3 months. One group of animals fed each diet received 250 ppm lead in the drinking water, whereas another group of animals fed each diet received no lead in the water. Vitamin E deficiency per se had little or no effect on hematocrit value, reticulocyte count, spleen weight, or erythrocyte mechanical fragility in rats not poisoned with lead. On the other hand, the decreased hematocrit, increased reticulocyte count, and splenic enlargement due to lead poisoning were much more pronounced in vitamin E-deficient rats than in rats supplemented with vitamin E. The resistance to mechanical trauma of red blood cells from vitamin E-deficient lead-poisoned rats was much less than that of red cells from vitamin E-adequate lead-poisoned rats. Dietary vitamin E status had no significant influence on the increased mechanical fragility of erythrocytes from nonpoisoned rats caused by exposure to lead in vitro. These results suggest that vitamin E deficiency enhances the susceptibility of animals to the in vivo hemolytic effect of lead poisoning.

THE EFFECTS OF DRUGS ON ERYTHROCYTES in vitro: HEINZ BODY FORMATION, GLUTATHIONE PEROXIDASE INHIBITION AND CHANGES IN MECHANICAL FRAGILITY

1 The relationship between mechanical fragility, glutathione peroxidase inhibition and Heinz body formation, in erythrocytes exposed to oxidant drugs in vitro, has been investigated. All drugs tested caused Heinz body formation, and with the exception of acetyl salicylic acid and salicylic acid, also caused increased erythrocyte mechanical fragility. 2 There was a direct relationship between mechanical fragility and drug concentration. Mechanical fragility increased in parallel with Heinz body formation, with primaquine, gentisic acid, ascorbic acid and potassium chlorate. In contrast Heinz body formation occurred at drug concentrations which did not cause a marked increase in mechanical fragility in the case of menadione, acetyl phenylhydrazine and phenylhydrazine. 3 The degree of inhibition of glutathione peroxidase was directly related to increased mechanical fragility with menadione, gentisic acid and potassium chlorate. However other substances causing increased mechanical fragility resulted in little or no loss of glutathione peroxidase activity. 4 The results show that there is no constant relationship between mechanical fragility caused by drugs, the formation of Heinz bodies and the inhibition of glutathione peroxidase. The factors contributing to oxidant drug-induced haemolysis appear to be variable and depend upon the drug concerned.

Erythrocyte mechanical fragility test.

Erythrocyte mechanical fragility test.

The biophysics of the variants of sickle-cell disease.

Previous studies have demonstrated that the unique behavior of hemoglobin S with respect to polymerization, molecular orientation,1and decreased solubility consequent upon deoxygenation* is responsible for the sickling phenomenon and that blood from patients with sickle-cell disease shows increased number of sickled cells, increased erythrocyte mechanical fragility, and increased whole blood viscosity at reduced oxygen tensions.4The erythrocytes of sickle-cell anemia contain hemoglobin S in sufficient concentration to allow these changes to occur within the physiologic range of oxygen tensions; the erythrocytes of sickle-cell trait contain a concentration of hemoglobin S insufficient to show these changes except upon extreme reduction of the oxygen tension, to levels usually considered nonphysiologic. The relationship of these effects of dexoygenation to the mechanism of production of the hematologic abnormalities and circulatory alterations clinically seen in patients with sickle-cell disease has been discussed by Harris and his associates.4 The identification and description of patients in