Microcirculatory stasis induced by hemorheological disorders: further evidence.

OBJECTIVE: Reinvestigate the microcirculatory alterations immediately responsible for blood rheological disorders and blood stases, which are related to red blood cell (RBC) aggregation in capillaries. METHODS: Blood rheological disorders were produced by significantly intensified intravascular red blood cell aggregation in the intestinal mesentery of Wistar rats and in the cerebral cortex of Chinchilla rabbits, either systemically (by intravascular administration of high molecular-weight dextran) or locally (by increase of high-molecular compounds in blood plasma inside individual or groups of capillaries). RESULTS: Under conditions where the microvascular lumina were not decreased and the arteriolovenular pressure gradients got even higher, the significantly enhanced intravascular RBC aggregation resulted in the slowing down of blood flow in the microvessels to a full stop. CONCLUSION: A significant increase in microvascular RBC aggregation results in local hemorheological disorders, which is, in all probability, related to derangement of the blood-flow structuring in microvessels.

Blood flow structuring and its alterations in capillaries of the cerebral cortex.

Various manifestations of blood flow structuring were investigated in rabbit cerebral cortex capillaries, which possess the most narrow lumina of all parts of the body. Blood flow structuring in the capillaries was characterized by the presence of a stable and comparatively large parietal plasma layer, which changed insignificantly under control and ischemic conditions, but disappeared when blood stasis developed inside the capillaries. The axial core of the blood flow in the capillaries, which occupied almost two-thirds of the intracapillary volume under normal conditions, consisted of significantly deformed (stretched along the microvessels' axes) and nonaggregated erythrocytes. During ischemia the shape of the erythrocytes did not change appreciably; only the blood plasma intervals between them increased significantly, demonstrating reduction of the local hematocrit. During primary blood stasis caused by enhanced intravascular erythrocyte aggregation, typical blood flow structuring became significantly disturbed: red cells filled the whole, or almost the whole, capillary lumina and did not leave visible space for plasma inside the microvessel lumina. We concluded that normal blood flow structuring is a deciding factor in the blood rheological properties of microvessels. Its disturbance, caused by fast accumulation of erythrocytes in the capillary lumina, results in blood rheological disorders and in a slow down to a full stop of the blood flow, despite a preserved arteriolovenular pressure difference.

[The variously directed reactions of the pial and cortical arterial branches in postischemic hyperemia in the cerebral cortex]. / Raznonapravlennye reaktsii pial'nykh i korkovykh arterial'nykh vetvlenii pri postishemicheskoi giperemii v kore golovnogo mozga.

In adult rabbits, functional behaviour of pial and cortical (radial) arteries was rather different: the pial arteries showed regular dilatation while the lumen of the cortical arteries underwent regular reduction. Despite the different responses of the arterial segments, the vascular resistance diminished entailing an increase of local blood flow in the cerebral cortex.

[Effect of sympathectomy on responses of pial arteries during acute deficiency of cerebral blood supply]. / Vliianie simpatéktomii na reaktsii pial'nykh arterii pri ostrom defitsite krovosnabzheniia golovnogo mozga.

The dilatatory responses of small pial arteries including their active segments (sphincters at off-shoots, precortical arteries), to blood supply deficiency in the cerebral cortex were compared in control and sympathectomized rabbits. The sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls. The vasodilatation was much less obvious in sympathectomized than in control animals. This was associated with (and probably caused by) a considerable rise in histochemically detected serotonin activity of the pial arteries walls. After recovery of blood supply to the brain the constriction of the pial arterial active segments restricting the excessive cerebral blood flow, was significantly reduced due, probably, to the sympathetic deprivation. Therefore, the sympathetic control plays an important part in pial arterial responses regulating the adequate blood supply of the cerebral cortex.