The behaviour of red cells in narrow tubes in vitro as a model of the microcirculation

Abstract

To investigate the behaviour of red cells in the microcirculation, we established a new capillary method using narrow fluorinated ethylenepropylene copolymer tubes with internal diameters of 12.5 and 25.0 microns. Red cell flow in the tubes under a given range of pressure was analysed through a video system connected to a microscope. The experimental condition was adjusted so that the velocity of the control normocytes would be compatible with that in corresponding vessels in vivo, 0.5-1.5 mm/s. In the 12.5 microns tube, normocytes obtained from 12 young normal volunteers ran in an axisymmetric edge-on orientation with a folded shape at higher pressures, but rolled along freely without deformation at lower pressures. Deformation during the passage of the microcytes obtained from four patients with polycythaemia vera complicated with iron-deficient microcytosis and 10 patients with iron deficiency anaemia was relatively mild, whereas that of the macrocytes obtained from eight patients with refractory anaemia was marked. Even after the screening effect at the tube entrance was taken into consideration, the velocities of both microcytes and macrocytes were found to be significantly lower than the control normocytes. Therefore this method may be a new way to investigate the flow properties of red cells in the microcirculation.

Direct Tracking of Particles and Quantification of Margination in Blood Flow

“…A pressure-driven pump system with a flow controller (Fluigent, Villejuif, France) was used to pump each solution through the microfluidic device at a physiologically relevant average velocity of 1 mm/s (44)(45)(46)(47). This velocity corresponds to a volumetric flow rate of 0.24 mL/min and an apparent wall shear rate of 61 s À1 for our channel dimensions.…”

Comparisons Between Hemodynamics, During and After Bathing, and Prognosis in Patients With Myocardial Infarction

“…11 As for plaque disruption, the cardiac events that occurred during bathing in group A seemed to show that the drastic hemodynamic change triggered this. Some reports, referring to thrombosis, have indicated that decreased fibrinolytic activity and platelet hyperaggregability, caused by the hyperthermal stress of bathing, activates blood hyperviscosity, 12,13 and as for vasoconstriction, Tanabe et al suggested that for patients with MI the physical stress caused by bathing seems to bring about coronary artery spasm, a speculation derived from the number of transient ischemic ST-T changes observed with ECG monitoring during bathing. 14 According to these reports, bathing in patients with MI may trigger coronary thrombosis because it causes vasospasm, leading to endothelial impairment of the coronary artery, which results in plaque disruption, while simultaneously, the hyperthermal from bathing activates platelet function and inactivates the fibrinolytic system.…”

Could an analysis of mean corpuscular volume help to improve risk stratification in non-anemic patients with acute myocardial infarction?

“…Possible pathomechanisms can be more or less direct. A direct mechanism would be associated with a hindered flow of larger, less flexible erythrocytes through microcirculation, which is a phenomenon that might contribute to myocardial ischemia [23,24]. Patients with high MCV commonly develop hyperhomocysteinemia [25], which is known to augment cardiovascular risk [26][27][28].…”