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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↗
PubMed1992

Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited.

We have investigated the role of leukocyte-endothelial cell interactions in a rabbit model of hemorrhagic vasculitis. Microvascular injury was produced in the skin by intradermal injection of Salmonella typhosa endotoxin followed 20 h later by intravenous zymosan, which activates complement. Hemorrhagic necrosis develops in the "prepared" skin sites which is characterized by microthrombi, neutrophil aggregation, platelet and fibrin deposition, and massive extravasation of erythrocytes. Hemorrhage in these Shwartzman-like lesions was quantitated by 99mTc-labeled autologous erythrocytes. Inhibition of the hemorrhagic response was obtained with mAb reactive with ICAM-1 as well as mAb against the leukocyte CD18 when either was administered intravenously just before intravenous zymosan challenge. This observation suggests that an intravascular event occurring in response to complement activation is required for the development of hemorrhagic vasculitis. We hypothesize that agents which successfully prepare the skin for the Shwartzman response after their intradermal injection do so by promoting increased intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Activation of complement then induces CD11/CD18 expression on circulating leukocytes thus producing an intravascular CD11/CD18-ICAM-1 (leukocyte-endothelium) adhesion event. Inhibition of intravascular leukocyte-leukocyte aggregation with mAb against CD11b (Mac-1) showed partial inhibition of hemorrhage, while mAb against CD11a (LFA-1) showed no inhibitory activity. This type of cytokine-primed, neutrophil-dependent vascular damage may be a model of human vasculitic processes where microvascular damage is produced in the absence of immune-complex deposition.

Animals↗
PubMedDate not supplied

[Vasoactive drugs and microcirculation in old age].

Within a series of studies on microcirculation in the aged, the conjunctival vessels were investigated by means of the intravital microscope in the course of intravenous infusion or prolonged administration of various drugs (xanthinol nicotinate, buflomedil, CPD-choline). During and after the treatment a better perfusion of the small conjunctival vessels (terminal capillary network) was observed, as well as the appearance of collaterals and a reduction of intravascular red cell aggregation. On the basis of these results a further direct demonstration of the vasoactive effect of the drugs under study could be given.

Aged↗
PubMed1989

Morphologic characterization of acute injury to vascular endothelium of skin after frostbite.

Cyclo-oxygenase inhibitors and free-radical scavengers protect the skin against necrosis induced by frostbite. However, the tissue component(s) that determine the evolution of skin necrosis and the mechanism of this pharmacologic protection are not precisely defined. We have studied freezing injury to rabbit ears by serial biopsies examined by light and electron microscopy. The morphologic evidence of skin injury due to freezing was localized exclusively in the endothelial cells, particularly in the arterioles. Within 1 hour, the entire microvasculature demonstrated endothelial damage. Intravascular platelet aggregation occurred just after thawing and closely paralleled the endothelial cell injury. Very few neutrophils were seen initially (at 10 minutes). By 1 hour, leukocyte aggregates were present, and they further increased at 6 hours. Swelling of the interstitium started 10 minutes after thawing, while extravasation of erythrocytes began to appear by 6 hours. Parenchymal elements of skin were relatively free of damage. In the ear cartilage, the chondrocytes showed evidence of damage immediately after freezing. The administration of superoxide dismutase (SOD) during thawing (reperfusion) did not qualitatively alter any of the initial morphologic changes induced by freezing. We conclude that the endothelial cell is the initial target of injury induced by freezing, an initial injury that is mediated by a non-free-radical-mediated mechanism. It is likely that this acute injury ultimately compromises blood flow and leads to skin necrosis.

Animals↗
PubMed1987

Lung morphological and permeability changes induced by intravascular coagulation in dogs.

The objectives of this study were to describe the morphological alterations of the pulmonary microvasculature in anesthetized dogs infused intravenously with alpha-thrombin (111-233 NIH U/kg) and to measure the protein reflection coefficient (sigma d), an index of pulmonary vascular permeability to proteins. Quantitative electron microscopy of lung biopsies from a group of four dogs showed an increase in the volume density of the alveolar interstitium and an increase in intravascular fibrin at 30 min after the thrombin infusion. The pulmonary microvascular endothelium was often swollen, blistered, highly vacuolized, or rarefied when close to or in contact with fibrin but appeared normal when not closely associated with fibrin. Fibrin-endothelial interactions often included projections of endothelium surrounding fibrin, the presence of fibrin within endothelial cells, 10- to 15-nm bridges connecting fibrin and endothelium, and disruption of the endothelial plasmalemma in contact with fibrin. Alveolar epithelial cells were unaffected by the thrombin infusion. Pulmonary lymph was collected from an afferent lymphatic to the left tracheobronchial lymph node in a second group of five dogs anesthetized with pentobarbital sodium intravenously. Thrombin increased pulmonary lymph flow by sevenfold and also increased the extravascular lung water-to-bloodless dry lung weight ratio. Left atrial pressure was elevated after thrombin infusion until a filtration-independent state was approached for the calculation of sigma d. Thrombin decreased sigma d from a normal value of 0.62 +/- 0.02 to 0.53 +/- 0.02. Thus thrombin-induced intravascular coagulation in dogs produced focal disruptions of the microvascular endothelium associated with intravascular fibrin and increased the pulmonary vascular permeability to proteins.

Animals↗
PubMed1986

Intravascular hemolytic transfusion reaction without detectable antibodies: A case report and review of literature.

A case of intravascular hemolytic transfusion reaction without detectable antibodies occurring in a 55-year-old male is reported. Specificity for the C antigen in the Rh system was demonstrated by technetium-99m red cell survival studies. A cell-mediated mechanism of hemolysis was suspected and investigated. Previously reported cases are reviewed and discussed. The entity of intravascular hemolytic transfusion reaction associated with minimal symptoms and no detectable antibodies deserves further investigation.

Antigens, Surface↗
PubMed1986

Complement and neutrophil-mediated injury of perfused rat lungs.

It has previously been shown that systemic complement activation in rats leads to acute lung injury. We have now employed an ex vivo model of perfused rat lung which allows a more detailed examination of the role of circulating blood elements and pulmonary vascular pressure changes in the acute lung injury that occurs following cobra venom factor (CVF)-induced complement activation. In whole blood perfused lungs CVF infusion resulted in lung leukocyte sequestration, pulmonary vascular constriction, and acute lung injury. Lung injury was measured by quantitating the accumulation of [125I]-bovine serum albumin in lung parenchyma and alveolar lavage fluid. A histologic analysis of CVF-induced lung injury revealed the development of intravascular aggregates of platelets and accumulation of neutrophils, extensive bleb formation of pulmonary capillary interstitial endothelial cells, and interstitial and intraalveolar edema and intraalveolar hemorrhage. Experiments in lungs perfused with salt solution to which various blood elements were added showed that the development of lung injury was dependent on neutrophils and the interaction of CVF with heat-labile plasma components. The lung injury was not dependent on the presence of platelets or the pulmonary artery pressor response. Addition of catalase or erythrocytes to the lung perfusate significantly attenuated the acute lung injury. Like the development of lung injury, the pulmonary artery pressor response was dependent on the interaction of CVF with heat labile plasma components and neutrophils. The increase in PA pressure was not attenuated by the addition of catalase to the lung perfusate. These studies suggest that intravascular activation of the complement system leads to an acute microvascular injury which is dependent on neutrophils and the production of toxic oxygen metabolites. Pulmonary vascular constriction occurs independently of the associated lung injury and does not appear to be dependent on hydrogen peroxide production.

Animals↗
PubMed1997

Increased haemorrhagic risk after repeated infusion of highly substituted medium molecular weight hydroxyethyl starch.

Infusion of the large volumes of high molecular weight hydroxyethyl starch (HES) has been know to lead to coagulation disorders. Medium molecular starch is considered a safe alternative, even after repeated administration. In 10 patients with cerebrovascular diseases, a 10-day hemodilution was carried out using 10% HES 200/0.62. Initially, a loading dose of 500 ml was administered once over 45-60 min, followed by 500 ml maintenance dose per day for 10 days. Its high intravascular molecular weight (120,000 D) showed that cleavage of the starch is slowed due to the higher degree of substitution. The continuous increase of HES-serum concentration to 27.7 mg/ml gave evidence of a cumulation of poorly degradable molecules. Although this caused a prolonged volume effect, plasma viscosity and erythrocyte aggregation were influenced in an unfavourable way. The negative effects were not evident in their influence on the coagulation system. Under therapy, a significant 42.8% increase (p < 0.01) in activated partial thromboplastin time occurred. Factor VIII:C, von Willebrand ristocetin co-factor and von Willebrand factor antigen dropped during the therapy below the hemostasiological limit of 30% (p < 0.01), and in some patients below 10%. A high degree of substitution, particularly after repeated infusion, leads to a cumulation of large molecules that are difficult to break down and which unfavourably affect rheological and hemostasiological parameters.

Blood Coagulation↗
PubMed1985

Clearance of radioactive xenon in evaluating microcirculation in patients with ischaemic heart disease.

In 158 patients with chronic ischaemic heart disease (IHD), the state of microcirculation was investigated, using local 133Xe clearance. With growing severity of the disease, muscular blood flow decreased. Local disturbances were accompanied also by changes in central haemodynamics (decrease in cardiac index, slow-down of blood flow in the pulmonary and systemic circulations, increased peripheral resistance), which were established by radiocardiography using 131I-labelled albumin. A distinct relationship was found between muscular blood flow and the intensity of intravascular microcirculatory disturbances (microthrombosis, intravascular thrombocyte aggregation, arteriolo-venular anastomoses). The authors recommend the use of 133Xe clearance for microcirculation study in patients with chronic IHD.

Adult↗
PubMed1977

Microembolism in experimental septic shock. Distribution of platelets and fibrinogen after intravenous injection of disintegrated Pseudomonas bacteria to dogs.

Platelets were labelled with 51Cr, fibrinogen with 125I and erythrocytes with 59Fe. Disintegrated Pseudomonas bacteria were injected intravenously and radioactive measurements were made on whole blood; tissue biopsies and clottable fibrinogen. After the infection there was an immediate but transient increase of 51Cr activity in the lung concomitant with a decrease in platelet count and 51Cr activity of blood. In the liver there was a less pronounced increase of 51Cr activity. The fibrinogen concentration decreased slightly, paralleled by the 125I activity of whole blood and of clottable fibrinogen, whereas the 125I activity in the lung and liver remained fairly constant. There was no changes of 51Cr activity or 125I activity in biopsies from muscle, pancreas, small intestine, kidney or spleen. During the experiment (3h) there were no signs of significant disseminated intravascular coagulation other than platelet aggregation. A consumption of fibrinogen related to the formation of fibrin plugs could not be detected. After injection of disintegrated Pseudomonas bacteria reversible platelet aggregates were formed and temporarily trapped in the pulmonary microcirculation. This microembolism might induce tissue damage and could be of importance for the development of septic pulmonary complication.

Animals↗
PubMed1979

Importance of microcirculatory alterations in the initial hypertensive, oligoanuric phase of acute post-infective glomerulonephritis in infancy.

By applying the blood gas analysis to the venous blood of 17 children affected by DPGN, the authors have observed an increase of the PvO2 and a reduction of the PvCO2 in the oligoanuric and hypertensive phase, which is attributed to a minor utilization of O2. The authors relate a probable cellular respiratory defect with the initial skin tumefaction in these cases. This respiratory dysfunction would be due to intravascular red cell aggregation, to the reduction of perfusion of the exchange vessels and to the passage of the blood through preferential circuits.

Acute Disease↗