Impaired deformability of erythrocytes in diabetic rat and human: Investigation by the nickel-mesh-filtration technique

Comprehensive research to quantify the deformability of erythrocytes in diabetic animals and humans has been lacking. The objective of this study was to compare the impairment of erythrocyte deformability in diabetic rats and patients by use of the same rheologic method. Deformability was investigated in streptozotocin-induced diabetic rats and diabetic patients, by using the highly sensitive and quantitative nickel-mesh-filtration technique. Erythrocyte filterability (whole-cell deformability) was defined as flow rate of hematocrit-adjusted erythrocyte suspension relative to that of saline (%). Hematological and biochemical data for diabetic rats did not differ from those for age-matched control rats except for hyperglycemia and malnutrition. Erythrocyte filterability for diabetic rats was significantly lower than that for control rats (69. 4 ± 10. 1%, n = 8, compared with 83. 1 ± 4. 2%, n = 8; p < 0. 001). Likewise, erythrocyte filterability for diabetic patients was significantly impaired compared with that for controls (87. 6 ± 3. 4%, n = 174, compared with 88. 6 ± 2. 1%, n = 51; p = 0. 046). Stepwise multiple regression analysis revealed that this impairment was mostly attributable to associated obesity (BMI, p = 0. 029) and glycemic stress (HbA1c(JDS), p = 0. 046). We therefore conclude that erythrocyte filterability is commonly impaired in diabetic rats and in humans. Moreover, metabolic risk accumulation further impairs erythrocyte filterability, resulting in derangement of the microcirculation.