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At least 253 records · Page 14Linked to original sources
PubMed1991

Role of leukocytes in the activation of intravascular coagulation in patients with septicemia.

To elucidate the role of leukocytes in intravascular coagulation in patients with septicemia, plasma levels of thrombin-antithrombin III complex (TAT), soluble fibrin monomer complex (SFMC) and fibrinogen (Fbg) were determined in 33 patients with septicemia. Twenty of 33 patients revealed marked leukopenia caused by suppression of hematopoiesis by the administration of chemotherapeutic agents for the treatment of hematological malignancies; the total leukocyte count of these patients was less than 1,000/microliters. Thirteen of 33 patients showed normal or increased leukocyte counts. Plasma levels of TAT and SFMC in septicemic patients without leukopenia were significantly higher than in patients with leukopenia. Although plasma TAT and SFMC levels correlated well with the number of leukocytes, a more significant positive correlation was found between the number of monocytes and the levels of TAT and SFMC. Plasma levels of Fbg were significantly lower in patients without leukopenia than in patients with leukopenia. No significant correlation was found between the number of leukocytes and the levels of Fbg. However, a significant negative correlation was found between the number of monocytes and the levels of Fbg. TAT levels did not correlate with the number of platelets. The fibrinolytic system was activated only in septicemic patients without leukopenia, which may be explained by secondary fibrinolysis following leukocyte-activated coagulation. These findings suggest that leukocytes, in particular monocytes, may play a critical role in the pathogenesis of intravascular coagulation in septicemia.

Antithrombin III↗
PubMed1981

Role of splenic red pulp in endotoxin-induced disseminated intravascular coagulation.

As an extension of our studies on vascular responses to endotoxemia, we evaluated sequential ultrastructural lesions of splenic red pulp and correlated these lesions with coagulation changes observed in rhesus monkeys following infusion with endotoxin either as a single bolus (10 mg. per kg.) or at a continuous rate of 10 mg. per kg. per hour for periods up to 16 hours. Controls included monkeys infused with Ringer's lactate solution. Progressive reactions of the splenic cords included increased phagocytic activity of macrophages in association with aggregation and degranulation of platelets and prominent fibrinous deposits characteristically abutting basement membranes of endothelial and reticular cells. The sinuses demonstrated endothelial damage, platelet-fibrin microthrombi obstructing interendothelial slits, and severe engorgement with entrapment of erythrocytes by tactoids of fibrin. The thrombotic lesions of the red pulp developed earlier than similar lesions in hepatic sinusoids, and they were accompanied by progressive thrombocytopenia and disseminated intravascular coagulation. The findings suggest that the unique microcirculation of the spleen is an early target and trigger of endotoxin-induced microthrombosis. It is proposed that phagocytosis of endotoxin by splenic phagocytic cells and associated inflammatory events result in disruption of reticular cells and endothelium leading to massive microthrombosis with breakdown of the splenic filter. In addition, rapid activation of coagulation mechanisms in the red pulp as well as liver sinusoids may promote the development of thrombocytopenia and disseminated intravascular coagulation in endotoxic shock.

Animals↗
PubMed1986

[Leukocyte-thrombocyte interactions in chronic myeloleukemia and erythremia].

An effect of the leucocytes of patients with chronic myeloproliferative diseases on the formation of cellular microthrombi in vitro was studied. A high degree of correlation between the amount of leucocytes and the rate of mixed cell leucocyte-thrombocyte aggregation was shown. The clinical signs of enhanced leucocyte-thrombocyte interactions in patients were disorders of microcirculation and intravascular microthrombus formation. It was shown that leucocytes could compensate the manifestations of thrombocytopenia and thrombocytopathy in chronic myeloproliferative diseases. The main types of leucocyte-thrombocyte interactions were singled out. An important role of erythrocyte hemolysis in the initiation of leucocyte-thrombocyte contacts was established. It was proposed that an increased amount of leucocytes especially in noticeable "rejuvenation" of their structure, should be regarded as one of the humoral factors of thrombogenicity in chronic myeloproliferative diseases.

Adult↗
PubMed1991

Cyclic changes of blood echogenicity in high-frequency ultrasound.

Ultrasound images from human arteries obtained in vivo with an intravascular 30 MHz ultrasound imaging device show that blood echogenicity changes during the cardiac cycle. Quantitative measurements of blood echogenicity during the cardiac cycle suggest that these variations may be related to changes in the state of erythrocyte aggregation, which are induced by varying shear rate.

Blood Flow Velocity↗
PubMedDate not supplied

[Relationship between thrombinemia and free radical processes in the blood].

Thrombin introduced in doses causing disseminated intravascular coagulation (DIC) has been studied for its effect on lipid peroxidation processes (POL) in plasma, erythrocytes and thrombocytes in rats. The vitamin-antioxidant complex is determined to decrease manifestations of DIC and POL intensity. Combined effect on thrombocytes is clearly marked: vitaminization results in diminishing thrombocytopenia caused by thrombinemia and decreasing their aggregation. In vitro thrombin activates POL in blood due to direct contact with erythrocytes and thrombocytes. Thrombocytes are more perceptible to thrombin action. The results analysed suggest that thrombinemia and POL interact as follows: activation of thrombinogenesis causes POL activation resulting in further thrombinogenesis activation etc. We have assumed that an anticoagulant that is not an antioxidant, or an antioxidant that does not directly influence thrombinogenesis may break the cycle or reduce it.

Animals↗