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Results for “ERYTHROCYTE AGGREGATION, INTRAVASCULAR”

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At least 55 records · Page 3Linked to original sources
PubMed1994

[An experimental analysis of the development of local capillary stasis].

Micro-application of NaCl induced a local slowdown to full stoppage of the blood flow in the lamina of individual capillaries in the Wistar rats mesenterium. The blood stasis resulted from local disturbances of the blood rheological properties. The erythrocyte aggregates obstructed the capillaries leaving no space for the parietal plasma layer. The findings suggest the intravascular erythrocyte aggregation to be the immediate cause of the blood flow disturbances and the blood stasis in the microvascular lumina.

Animals↗
PubMed1997

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.

Animals↗
PubMed1976

[Microcirculatory changes in the cheek pouch mucosa of hamsters in the dynamics of experimental traumatic shock].

Acute experiments conducted on hamsters demonstrated significant disturbances of the microcirculation in the mucosa of the cheek pouch during a severe traumatic shock after a standardized mechanical injury of the hip. All the animals died in the course of the first 24 hours after this trauma. If the animals died not earlier than in one hour after the trauma the microcirculation changes were distinctly phasic in character; particularly there was seen a phase of temporary relative adaptation and stabilization of the peripheral circulation, invariably followed by the phase of decompensation, the terminal phase and death. In cases with a rapid lethal issue in the course of one hour no distinct phasic character of the microcirculation changes was observed, but there was a more or less rapid aggravation of all he indices. In difference from the majority of other investigators, no marked intravascular erythrocyte aggregation was seen by the authors in the experiments described.

Animals↗
PubMed1976

[Changes in mesenteric microcirculation in rats following repeated skin burns].

Acute experiments were conducted on rats; repeated extensive burn of a convalescent who formerly sustained the burn disease was better tolerated, led tono fatal outcome and was accompanied by moderate microcirculatory disturbances. The smae burn was accompanied in intact rats by a severe shock followed by death, intravascular aggregation of erythrocytes and significant microcirculatory disturbances leading to disturbance of tissue nutrition. It is supposed that the results obtained could serve as an indirect proof that toxemia played an important role in the genesis of intravascular aggregation of erythrocytes in burn shock.

Animals↗