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Results for “ERYTHROCYTE AGGREGATION, INTRAVASCULAR”

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PubMed1982

Intravascular aggregation after acute intracranial hypertension by epidural balloon compression in cats.

The authors have studied the effect of acute intracranial hypertension produced by placement of an epidural balloon (control group) in cats, on cerebral perfusion, evoked responses, and hematological parameters. These elements were measured in similarly injured animals which underwent isovolemic hemodilution with dextran 75, after relief of intracranial hypertension. Four hours after balloon deflation, perfusion was markedly impaired in 30% of the control group, and was reduced to 11% in the dextran-infused group. The suppressed N1 amplitude of somatosensory evoked responses on the compression side, the reduced platelet aggregability, and the erythrocyte-deformability by intracranial hypertension were all significantly more restored in the dextran-infused group after decompression. The percentage of platelets with volumes between 21.75 and 48.75 cu mu (normal 9.75 to 12.75 cu mu) significantly increased after decompression. Activation of platelets during intracranial hypertension leads to an increase in platelet volume from platelet aggregation, and correlates with a decrease in platelet aggregability. It was also suggested that reduction of erythrocyte deformability was not caused by erythrocyte aggregation. The authors emphasize the role of intravascular factors such as vascular obstruction by platelet aggregates, and difficulty in passage of erythrocytes through capillaries due to reduced deformability, in the disturbance of the microcirculation following acute intracranial hypertension. The protective effect of dextran 75 by inhibition of platelets as well as hemodilution is stressed.

Animals↗
PubMed1977

Stabilization of flow properties of blood with phenylbenzo-gama-pyrone derivatives (flavonoids).

An investigation conducted on erythrocytes suspension in plasma revealed an instability caused by apparent sensitivity of erythrocytes to aggregation due to slight changes in normal plasma constituents. There is evidence that low level intravascular aggregation and so-called normal erythrocyte sedimentation rate (ESR) of apparently healthy people may be caused by undue sensitivity of erythrocytes to aggregation by plasma constituents as they vary within accepted normal ranges. Certain flavones, particularly methoxylated compounds, which may occur in the diet, increase resistance of erythrocytes to aggregation by shifts in plasma constituents. The stabilizing and apparent regulatory action of flavonoids on parameters important in the rheology of blood supports the concept that these compounds are necessary in the diet.

ABO Blood-Group System↗
PubMed1996

Erythrocyte aggregation and erythrocyte deformability modify the permeability of erythrocyte enriched fibrin network.

Intravascular thrombus formed under low shear conditions consists of red cells enmeshed within a fibrin network. Since red cells reduce the permeability of fibrin network by surface drag and by volume occupancy the significance of red cell aggregability and deformability in network permeability needs examination. In this study networks were developed by the addition of thrombin to washed red cells suspended in platelet free plasma. The effects of the polymers polyvinylpyrrolidone (PVP) and poloxamer 188 on network permeability were compared to gauge the influence of red cell aggregation. Both polymers increase network permeability by an action on fibrin polymerisation but PVP alone enhances red cell aggregation. PVP was found to increase network permeability significantly both by increasing the permeability of the fibrin component of the network and by increasing red cell aggregation and thus reducing red cell surface drag. In separate experiments red cells were pre-treated with heat, glutaraldehyde, or diamide to reduce cell deformability. Decreased cell deformability caused significant reductions in network permeability. This was ascribed to the reduced aggregability of hardened red cells. Red cell aggregation during coagulation enhances molecular transport through modifying the network. This may have implications for the penetration of fibrinolytic agents.

Blood Coagulation↗
PubMed1984

Pathogenicity of cationized albumin in the dog: renal and extrarenal effects.

The effects of 21 cationized serum albumin samples of various degrees of cationization on renal function were studied in the dog. The samples were perfused intra- aortically to obtain preferential perfusion of the left kidney in 25 dogs. Standard clearance techniques were used, associated in six dogs with sieving studies of 125I-labelled polyvinylpyrrolidone (125I-PVP) and with an extensive morphological study in 15 dogs. Renal effects were observed. (a) Renal effects in left kidneys. The perfusion with weakly cationized albumin (group 1) produced moderate proteinuria associated with the deposition of cationized albumin on the anionic sites of the basement membrane. Glomerular filtration rate (GFR) was unaltered. Perfusion with highly cationized samples (group 2) produced more severe proteinuria and a significant decrease in GFR. Glomerular permeability to 125I-PVP increased. Perfusion with the four samples of highest pI (group 3) was followed by anuria. (b) Renal effects in right kidneys. A retarded mild proteinuria appeared only in group 2 and group 3 animals without alteration of GFR. All the kidneys (group 1 included), with the exception of two (group 3), showed deposition of the protein in the anionic sites. The following extrarenal effects were observed essentially in group 2 and group 3 animals: erythrocyte agglutination and haemolysis, platelet aggregation and thrombocytopenia, and a decrease in plasma fibrogen level due to fibrinogen precipitation. These effects produced progressive obstruction in the glomerular capillaries, thus explaining the occurrence of anuria. The structural damage in group 2 and group 3 left kidneys bears remarkable resemblance to that observed in the fulminant form of the human so-called 'haemolytic-uraemic syndrome'. The neutralization alone of the fixed negative charges in the glomerular wall appears to produce only mild proteinuria, whereas the various extrarenal effects combine to produce more severe proteinuria associated with functional alteration and vascular obstruction.

Acute Kidney Injury↗
PubMed2004

[Hemolytic-uremic syndrome].

Hemolytic-uremic syndrome (HUS) is the most common cause of acute renal failure in children below 3 years of age. It is defined by a triad of symptoms which associates hemolytic anemia with fragmented erythrocytes, thrombocytopenia and acute renal failure. Three types of HUS can be distinguished: typical HUS, also called diarrhoea-associated (D+HUS), very rare atypical HUS (D-HUS) and secondary HUS (drug induced, C+HUS, in patients receiving marrow transplantation, etc.). The common event among these entities appears to be vascular endothelial cell injury, which induces mechanical destruction of erythrocytes, activation of platelet aggregation and local intravascular coagulation, especially in the renal microvasculature. D+HUS represents 90% of HUS in children. Evidence of exposure to verotoxin (VT), shiga toxin (ST) producing Escherichia coli (VTEC or STEC) has been demonstrated in many countries in about 85% of cases. Serotype O157:H7 is the most frequent. Early and accurate supportive treatment and early start of dialysis is the major importance and allows a current mortality rate below 5%-10%. Vital prognosis is compromized in cases with multivisceral involvement. After 15 years or more of apparent recovery, 20 to 60% of patients have residual renal symptoms, with up to 20% having chronic renal insufficiency (CRI) or end-stage renal disease (ESRD). Atypical HUS represents less than 10% of HUS in children. Some of these cases (familial) are associated with low C3 levels, hereditary deficiency of factor H or with mutations in factor H gene. The deficiency of von Willebrand factor cleaving protease, as reported in adults with thrombotic thrombocytopenic purpura (TTP), is not present in D+HUS.

Hemolytic-Uremic Syndrome↗
PubMed1979

Heterotoxicity of human serum. IV. Role of the alternative complement pathway and natural antibody in the lethal toxicity of human serum for mice.

The toxic and often lethal reaction caused by intravascular injection of fresh human serum (FHS) was studied in mice. Decomplementation experiments indicated that the alternative complement pathway plays an essential role in the production of 'serum shock'. In vivo activation of human factor B and C3, following the administration of FHS into mice, was detected by immunoelectrophoresis. Absorption experiments suggested that natural antibodies were not required for toxicity, although they may amplify the lethal potential of normal sera by feedback mechanisms of C activation. Injections of FHS caused intravascular hemolysis of mouse erythrocytes and platelet aggregation in mice. The relationship of these observations to the mechanism(s) underlying lethality will be discussed in the following article.

Animals↗
PubMed1983

[Central problems in the general pathology and pathologic anatomy of shock].

From the results of detailed clinico-anatomical studies of traumatic, exotoxic, burn, cardiogenic, bacterial, hemorrhagic, and other kinds of shock (1500 observations) and the data of the literature, the paper analyses some disputable aspects of shock: the role of neurogenic factors and vasomotor disorders in its pathogenesis, shock and collapse relationship, possibilities of shock diagnosis at autopsy, the concept of shock organ and shock cell. The importance in the pathoanatomic diagnosis of shock of hemodynamic disorders (sequestration of blood in the microcirculatory bed, shunting of the bloodstream in vital organs) and of hemocoagulation (liquid state of cadaver blood, DIBC) as well as of rapid mobilization of glycogen from tissue depots (liver) and circulatory-hypoxic injuries to the internal organs. The specific features of the individual kinds of shock are determined by different combinations of the above signs or predominant involvement of some internal organ. The lack of a single complete definition of the shock organ concept is indicated. The importance in the pathogenesis of shock of hemodynamic disorders, complications of the main disease, and pathology of therapy (the third factor) is emphasized.

Disseminated Intravascular Coagulation↗
PubMed1987

[Reactivity of the microcirculation bed of the small intestine mesentery in experimental dehydration in rats].

The state of mesenteric microcirculatory bed has been studied in male rats 3, 6 and 12 days after the beginning of alimentary dehydration. It has been revealed that vascular, intravascular and extravascular changes were of particular importance. Spastic reactions of arterioles and precapillary arterioles, the activation of arteriolo-venular shunting and the reduction in capillary circulation accompanied by diminution of all microvascular diameters were among the most marked vascular phenomena. The intravascular changes were represented by decreased blood flow rate, erythrocyte aggregation and leucocyte adhesion. The extravascular phenomena were characterized by the appearance of local hemorrhages.

Animals↗
PubMed1982

Early tissue damage in ethchlorvynol-induced alveolar edema in rabbit lung.

The purpose of this study was to examine the morphologic changes that occur in the early stages of intraalveolar edema. Anesthetized rabbits were intravenously administered a bolus of 40 mg/kg of ethchlorvynol, a mild hypnotic known to induce respiratory distress syndrome in humans and laboratory animals when given intravenously. After 15 min their lungs were fixed for transmission electron microscopy. Examination revealed variable amounts of irregularly distributed intraalveolar edema with erythrocytes and fibrin strands that coexisted with modest or nonexisting interstitial edema suggesting that primary hemorrhagic alveolar flooding had taken place. Most alveolar epithelial and endothelial cells appeared normal except in localized areas. In lungs fixed by vascular perfusion, in which normal capillaries were flushed, obstructions were noticed in alveolar corner capillaries. These areas were identified by light microscopy and selectively sectioned for electron microscopy. They contained intravascular cell-fibrin aggregates consisting of plugs of degranulated platelets, fibrin, erythrocytes, and leukocytes. Endothelial and epithelial cells in the vicinity of the plugs showed variable degrees of injury. In places the damage was so severe that vascular and alveolar spaces were separated only by the basal lamina. Our work shows the previously unnoticed existence of capillary microemboli or microthrombi in a well-known experimental model of respiratory distress syndrome and suggests extravasation of blood elements through discrete sites of cell injury associated with the fibrin-platelet aggregates rather than diffuse increase of permeability as cause of early alveolar flooding.

Animals↗