Masao Soutani

FLOW DYNAMICS OF ERYTHROCYTES IN MICROVESSELS OF ISOLATED RABBIT MESENTERY: CELL-FREE LAYER AND FLOW RESISTANCE

A part of microvascular bed isolated from rabbit mesentery (composed of a few branches of superior mesenteric artery) was used for the study of the flow dynamics of erythrocytes in microvessels. The flow resistance in the microvascular bed was analyzed with respect to the thickness of a cell-free layer formed along the inner wall of vessels and the suspension viscosity of erythrocytes (in terms of hematocrit and erythrocyte deformability). The thickness of the cell-free layer increased with the increase in the inner diameter of microvessels. By lowering the hematocrit, the thickness increased and the flow resistance decreased. Meanwhile, by decreasing the erythrocyte deformability with diamide, the thickness decreased and the flow resistance increased. However, the thickness was not altered in microvessels less than 10 microns by the diamide treatment. The maximum inner diameter of microvessel required to induce parachute- and/or slipper-like deformation (at flow velocity of erythrocytes less than 2 mm s-1) was 13 microns for control cells and 6 microns for diamide-treated cells. The thickness of the cell-free layer could not be closely related to the flow resistance, while a good relationship applicable to both control and diamide-treated cells was obtained between the flow resistance and the suspension viscosity. The present results conclude that the flow resistance in the isolated microvascular bed is mainly provided by both hematocrit and erythrocyte deformability.

Deformation of Erythrocytes in Microvessels and Glass Capillaries: Effects of Erythrocyte Deformability

Objective: The deformation of erythrocytes in microvessels less than 15 μm in inner diameter was analyzed using a microvascular bed isolated from rabbit mesentery. The deformation was compared with that found in glass capillaries.

Flow Behavior of Erythrocytes in Microvessels and Glass Capillaries: Effects of Erythrocyte Deformation and Erythrocyte Aggregation

Flow behavior of erythrocytes in microvessels and glass capillaries with an inner diameter of 10-50 microns was compared in relation to erythrocyte deformation and erythrocyte aggregation. This study was focused on the formation of a marginal cell-free layer, and the thickness was determined using an image processor. Human erythrocytes were perfused through a part of microvascular networks isolated from rabbit mesentery and through glass capillaries. Erythrocyte deformability was modified by treating erythrocytes with diamide, diazene-dicarboxylic acid bis[N,N-dimethylamide], and erythrocyte aggregation was accelerated by adding dextran (with a molecular weight of 70,400) to the perfusion medium. The thickness of the cell-free layer increased with an increase of the inner diameter of flow channel, with lowering the hematocrit, and with increasing the flow velocity of erythrocytes, in both microvessels and glass capillaries. Furthermore, the thickness of cell-free layer decreased with decreasing erythrocyte deformability, while it increased with accelerating erythrocyte aggregation. However, the alteration of the cell-free layer in response to the changes of these hemorheological conditions was more sensitive in microvessels than in glass capillaries. The present study concludes that flow behavior of erythrocytes in microvessels is qualitatively similar to, but quantitatively different from those in glass capillaries, as far as evaluated by the change of the thickness of the marginal cell-free layer.

Different roles of neuronal and endothelial nitric oxide synthases on ischemic nitric oxide production in gerbil striatum.

The production of nitric oxide (NO) in gerbil striatum during ischemia and reperfusion was monitored by measuring total NO metabolites in dialysates, and the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal NO synthase, and N(G)-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of NO synthase, were examined. The effects of these agents on ischemic neuronal damage were histologically evaluated 7 days after transient ischemia for 5 or 10 min. 7-NI and L-NAME decreased the NO production to similar extents in non-ischemic gerbils. 7-NI inhibited the increased NO production after 5 min of ischemia, and partly attenuated the increase in NO production after 10 min of ischemia, but had no effect on the increase after 15 min of ischemia. L-NAME completely abolished the increased NO production after different durations of ischemia. The extent of ischemic neuronal damage by 5-min ischemia was aggravated by either 7-NI or L-NAME, while damage by 10-min ischemia was marked in all groups. These results indicate that neuronal and endothelial NO synthases make different contributions to the post-ischemic NO production and the histological outcomes in gerbil striatum.