The structural and functional changes of blood cells and molecular components in diabetes mellitus

2017 ◽  
Vol 398 (4) ◽  
pp. 411-423 ◽  
Author(s):  
Leszek Szablewski ◽  
Anna Sulima
Keyword(s):  
Diabetes Mellitus ◽  
Red Blood Cells ◽  
Blood Cells ◽  
White Blood Cells ◽  
Neutrophil Function ◽  
Cardiovascular Complications ◽  
Oxygen Binding ◽  
Functional Changes ◽  
Coronary Syndrome ◽  
Patients With Diabetes

Abstract It is known fact that diabetes mellitus (DM) affects blood cells. Changes in the erythrocyte membrane, disorder in hemoglobin oxygen-binding and modification in mechanical characteristics, are effects of hyperglycemia on red blood cells. Altered susceptibility infection of patients with diabetes has been ascribed to a depression in the function of polymorphonuclear leukocytes. Neutrophil function in patients with diabetes with good glucose control is slightly different than in healthy ones. DM causes significant changes in lymphocytes metabolism and their functions. Patients with diabetes, presenting with acute coronary syndrome, are at higher risk of cardiovascular complications and recurrent ischemic events in comparison to non-diabetic counterparts. Various mechanisms, including endothelial dysfunction, platelet hyperactivity, and abnormalities in coagulation and fibrynolysis have been implicated for this increased atherothrombotic risk. There are many other alterations of blood cells due to DM. In the present review we focused on modifications of blood cells due to DM. Then, as a second point, we explored how the changes affect functions of red blood cells, white blood cells and platelets.

scholarly journals Increased Atherothrombotic Burden in Patients with Diabetes Mellitus and Acute Coronary Syndrome: A Review of Antiplatelet Therapy

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Karthik Balasubramaniam ◽  
Girish N. Viswanathan ◽  
Sally M. Marshall ◽  
Azfar G. Zaman
Keyword(s):  
Diabetes Mellitus ◽  
Acute Coronary Syndrome ◽  
Platelet Inhibition ◽  
Cardiovascular Complications ◽  
Diabetic Patients ◽  
Coronary Syndrome ◽  
Patients With Diabetes ◽  
Thrombotic Complications ◽  
Underlying Pathophysiology ◽  
Ischemic Events

Patients with diabetes mellitus presenting with acute coronary syndrome have a higher risk of cardiovascular complications and recurrent ischemic events when compared to nondiabetic counterparts. Different mechanisms including endothelial dysfunction, platelet hyperactivity, and abnormalities in coagulation and fibrinolysis have been implicated for this increased atherothrombotic risk. Platelets play an important role in atherogenesis and its thrombotic complications in diabetic patients with acute coronary syndrome. Hence, potent platelet inhibition is of paramount importance in order to optimise outcomes of diabetic patients with acute coronary syndrome. The aim of this paper is to provide an overview of the increased thrombotic burden in diabetes and acute coronary syndrome, the underlying pathophysiology focussing on endothelial and platelet abnormalities, currently available antiplatelet therapies, their benefits and limitations in diabetic patients, and to describe potential future therapeutic strategies to overcome these limitations.

The Effect of Red Blood Cells on the ADP-induced Aggregation of Human Platelets in Flow Through Tubes

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Mean Transit Time ◽  
White Blood Cells ◽  
Aggregate Size ◽  
Human Platelets ◽  
Induced Aggregation

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

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