Blood advancing in living capillaries (5 to 10 m in diameter) and in the adjoining arterioles and venules (10 to 25 m in diameter) itself represents a specific substance hardly comparable with fluids in a usual understanding of this term. Its greatest part comprises the deformed red blood cells (RBCs) whose size is similar to luminal diameters of the microvessels. The RBCs (comprising great majority of the forming elements in microvessels) are disposed in the normal flow not chaotically, but in a certain order that was identified therefore as "blood flow structure (or structuring) in microvessels" [1][2][3].The specific regime of the RBCs flow in blood vessels changes from larger to smaller luminal diameters. Thus in vessels larger than 0.2 mm, the blood flow can be treated as a homogenous suspension with little error. By contrast, in arterioles or venules smaller than 25 m, and especially in capillaries (whose diameters are smaller than 8 m in humans), the RBCs are not uniformly dispersed, especially because of the presence of a parietal plasma layer containing no cells; thus the blood flow is specifically structured (Fig. 1). Disorders of this kind inevitably lead to the disturbance of normal blood rheological properties in the microvessels.Japanese Journal of Physiology Vol. 51, No. 1, 2001 19Japanese Journal of Physiology, 51, 19-30, 2001 Key words: RBC axial flow, parietal plasma layer, RBC aggregation, RBC deformation, plasma viscosity. Abstract:The review article deals with phenomena of the blood flow structure (structuring) in narrow microvessels-capillaries and the adjacent arterioles and venules. It is particularly focused on the flow behavior of red blood cells (RBCs), namely, on their specific arrangements of mutual interaction while forming definite patterns of self-organized microvascular flow. The principal features of the blood flow structure in microvessels, including capillaries, include axial RBC flow and parietal plasma layer, velocity profile in larger microvessels, plug (or bolus) flow in narrow capillaries, and deformation and specific behavior of the RBCs in the flow. The actual blood flow structuring in microvessels seems to be a most significant factor in the development of pathological conditions, including arterial hypertension, brain and cardiac infarctions, inflammation, and many others. The blood flow structuring might become a basic concept in determining the blood rheological properties and disorders in the narrow microvessels. No solid theoretical (biorheological) basis of the blood flow structuring in microvessel has been found, but in the future it might become a foundation for a better understanding of the mechanisms of these properties under normal and pathological conditions in the narrowest microvessels 5 to 25 m large. It is also a topic for further biorheological research directed to find the background of actual physiopathological phenomena in the microcirculation.

The major conceptions of cerebral blood flow (CBF) control developed in the 19th and 20th centuries are listed. The systems of CBF regulation are considered from the viewpoint of automatic control. In the classification of CBF regulation mechanisms, 4 types are identified. The effectors of CBF regulation, i.e. the specific arterial segments through which each type of regulation is accomplished, were found to be mainly the major arteries of the brain and the small pial arteries rather than the intracerebral arterioles. Review of controlling influences on these effectors of regulation, (myogenic, humoral and neurogenic), show that priority should be given to neurogenic mechanisms. Several criteria governing efficiency of CBF regulation are proposed. Review of interactions of different types of CBF regulation shows that there may be both synergistic and antagonistic relationships. Information about the processes is important for medical practice.

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We have investigated the pial arterial microcircles formed by the consecutive ramifications and anastomoses of minute pial vessels on the surface of the cerebral neocortex in various vertebrate species, representatives of various levels of phylogenic development. We found that the pial arterial microcircles became gradually more complex in the following order: hen < rabbit < cat < dog < monkey. The gradual development of microcircles involves various features in these species: (a) They become formed predominantly of smaller pial arterial branches whose vasomotor activity is much higher as compared with that of the larger ones; (b) each circle occupies a smaller area, and hence the number of circles per surface of neocortex increases; (c) the density of arterial branches feeding the circles increases despite the smaller size of the latter; (d) the number of offshooting precortical and radial arteries penetrating the cortex increases; (e) the areas of neocortex fed by individual radial arteries get gradually smaller. Thus, the development of the pial arterial bed contributes more and more toward precise spatial regulation of an adequate blood supply to increasingly smaller areas of neocortical tissue as we rise toward higher levels in phylogeny.

Abstract:Vascular Mechanisms Controlling a Constant Blood Supply to the Brain ("A utor emulation") • The segmental resistance in the major arteries of the brain and the respective smaller cerebral arteries carrying blood from the circle of Willis was computed (with a mathematical method developed recently) using the inlet and outlet pressures of the internal carotid arteries, as well as the venous pressure in the brain sinuses of dogs. Under the conditions of stepwise changes of the perfusion pressure the following localization of "autoregulatory" responses of the cerebral arteries has been found: changes in the inlet pressure of the internal carotid artery produced corresponding changes of its vascular resistance resulting in a relative constancy of the outlet pressure of the artery, i.e., pressure in the circle of Willis; resistance changes in the smaller brain arteries were evident only when the alterations of the perfusion pressure were too big and the major arteries were unable to eliminate the disturbance. The responses of the internal carotid arteries were eliminated when their muscular layer was maintained normal, but deprived of the nervous control (when the arteries were continuously perfused with blood or oxygenated Ringer-Krebs bicarbonate solution shortly after the death of the animal). Thus, evidence was obtained that the vascular responses were brought about by a nervous and not by a purely muscular mechanism, as is usually assumed.