Abstract
There is considerable evidence that blood viscosity is greater than normal in diabetes, and decreased red blood cell deformability has been suggested as the cause. However, viscosity can be influenced by changes in the properties of blood proteins in addition to red cells. Direct interpretation of red cell filtrometry data in terms of deformability has been complicated by the interfering effect of white cells and platelets and clogging of micropores. We have thus used the cell transit time analyzer, a new filtrometric procedure that eliminates these complications and produces an individual red cell micropore transit time profile, to reassess diabetic red cell deformability. Samples from 26 patients with diabetes and an equal number of subjects without diabetes who served as controls were assayed by the cell transit time analyzer at 2 and at 4 cm hydrostatic pressure. Samples from patients with diabetes and controls were sex and age matched for daily runs. At 2 cm H 2O, red blood cell transit time for the patients with diabetes was 2.73 ± 0.05 milliseconds as compared with 2.67 ± 0.05 milliseconds for controls (p not significant). The ratio of transit time for patients with diabetes to that of controls (T(d)/T(nd)) was 1.03 ± 0.01 (p <0.05, Wilcoxon) at 2 cm H 2O and 1.02 ± 0.01 (p not significant) at 4 cm H 2O. This small difference at 2 cm appeared to be caused by an increase in transit times for patients with diabetes with poor glycemic control: T(d)/T(nd) was 1.05 ± 0.02 for patients with glycohemoglobin >9.5% (p <0.05 compared with unity, Wilcoxon) and 1.07 ± 0.02 for glucose concentration >300 mg/dl (p <0.05, Wilcoxon). Patients with glucose and glycohemoglobin in the well-controlled range or intermediate range of control showed no increase in T(d)/T(nd). Erythrocytes from controls without diabetes incubated at several different glucose concentrations for 1 hour at 37° C showed no changes in transit times. There thus appears to be a very small decrease in red cell deformability demonstrable by cell transit time analysis in diabetes. This decrease is related to hyperglycemia but is not the result of an immediate effect of elevated serum glucose level.
| Original language | English |
|---|---|
| Pages (from-to) | 500-504 |
| Number of pages | 5 |
| Journal | The Journal of Laboratory and Clinical Medicine |
| Volume | 117 |
| Issue number | 6 |
| State | Published - 1991 |
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All Science Journal Classification (ASJC) codes
- Medicine(all)
- Pathology and Forensic Medicine
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Effects of glycemic control on red cell deformability determined by using the cell transit time analyzer. / Rendell, M.; Fox, M.; Knox, S.; Lastovica, J.; Kirchain, W.; Meiselman, H. J.
In: The Journal of Laboratory and Clinical Medicine, Vol. 117, No. 6, 1991, p. 500-504.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of glycemic control on red cell deformability determined by using the cell transit time analyzer
AU - Rendell, M.
AU - Fox, M.
AU - Knox, S.
AU - Lastovica, J.
AU - Kirchain, W.
AU - Meiselman, H. J.
PY - 1991
Y1 - 1991
N2 - There is considerable evidence that blood viscosity is greater than normal in diabetes, and decreased red blood cell deformability has been suggested as the cause. However, viscosity can be influenced by changes in the properties of blood proteins in addition to red cells. Direct interpretation of red cell filtrometry data in terms of deformability has been complicated by the interfering effect of white cells and platelets and clogging of micropores. We have thus used the cell transit time analyzer, a new filtrometric procedure that eliminates these complications and produces an individual red cell micropore transit time profile, to reassess diabetic red cell deformability. Samples from 26 patients with diabetes and an equal number of subjects without diabetes who served as controls were assayed by the cell transit time analyzer at 2 and at 4 cm hydrostatic pressure. Samples from patients with diabetes and controls were sex and age matched for daily runs. At 2 cm H 2O, red blood cell transit time for the patients with diabetes was 2.73 ± 0.05 milliseconds as compared with 2.67 ± 0.05 milliseconds for controls (p not significant). The ratio of transit time for patients with diabetes to that of controls (T(d)/T(nd)) was 1.03 ± 0.01 (p <0.05, Wilcoxon) at 2 cm H 2O and 1.02 ± 0.01 (p not significant) at 4 cm H 2O. This small difference at 2 cm appeared to be caused by an increase in transit times for patients with diabetes with poor glycemic control: T(d)/T(nd) was 1.05 ± 0.02 for patients with glycohemoglobin >9.5% (p <0.05 compared with unity, Wilcoxon) and 1.07 ± 0.02 for glucose concentration >300 mg/dl (p <0.05, Wilcoxon). Patients with glucose and glycohemoglobin in the well-controlled range or intermediate range of control showed no increase in T(d)/T(nd). Erythrocytes from controls without diabetes incubated at several different glucose concentrations for 1 hour at 37° C showed no changes in transit times. There thus appears to be a very small decrease in red cell deformability demonstrable by cell transit time analysis in diabetes. This decrease is related to hyperglycemia but is not the result of an immediate effect of elevated serum glucose level.
AB - There is considerable evidence that blood viscosity is greater than normal in diabetes, and decreased red blood cell deformability has been suggested as the cause. However, viscosity can be influenced by changes in the properties of blood proteins in addition to red cells. Direct interpretation of red cell filtrometry data in terms of deformability has been complicated by the interfering effect of white cells and platelets and clogging of micropores. We have thus used the cell transit time analyzer, a new filtrometric procedure that eliminates these complications and produces an individual red cell micropore transit time profile, to reassess diabetic red cell deformability. Samples from 26 patients with diabetes and an equal number of subjects without diabetes who served as controls were assayed by the cell transit time analyzer at 2 and at 4 cm hydrostatic pressure. Samples from patients with diabetes and controls were sex and age matched for daily runs. At 2 cm H 2O, red blood cell transit time for the patients with diabetes was 2.73 ± 0.05 milliseconds as compared with 2.67 ± 0.05 milliseconds for controls (p not significant). The ratio of transit time for patients with diabetes to that of controls (T(d)/T(nd)) was 1.03 ± 0.01 (p <0.05, Wilcoxon) at 2 cm H 2O and 1.02 ± 0.01 (p not significant) at 4 cm H 2O. This small difference at 2 cm appeared to be caused by an increase in transit times for patients with diabetes with poor glycemic control: T(d)/T(nd) was 1.05 ± 0.02 for patients with glycohemoglobin >9.5% (p <0.05 compared with unity, Wilcoxon) and 1.07 ± 0.02 for glucose concentration >300 mg/dl (p <0.05, Wilcoxon). Patients with glucose and glycohemoglobin in the well-controlled range or intermediate range of control showed no increase in T(d)/T(nd). Erythrocytes from controls without diabetes incubated at several different glucose concentrations for 1 hour at 37° C showed no changes in transit times. There thus appears to be a very small decrease in red cell deformability demonstrable by cell transit time analysis in diabetes. This decrease is related to hyperglycemia but is not the result of an immediate effect of elevated serum glucose level.
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M3 - Article
VL - 117
SP - 500
EP - 504
JO - Translational Research
JF - Translational Research
SN - 1931-5244
IS - 6
ER -